SAMJ Vol 104, No 10 (2014)

OCTOBER 2014

VOL. 104 NO. 10

NCDs – the looming epidemic

647, 675, 680

Preventing diabetic blindness

661, 700

Migrant health

663

Glucocorticoids and lipid metabolism

671

Sexual health of adolescents Cardiovascular risk in urban South Africans CME: Atopic dermatitis

676, 687 691 705-714

HOW MUCH IS ENOUGH TO GET THE BIG FAMILY HOME

&

STILL GROW YOUR INVESTMENT PORTFOLIO?

How much is enough? An age-old question that needs a new answer. Old Mutual Wealth has it and it’s called Integrated Wealth Planning. It’s a wealth map that puts you and your goals at its core, helping you plan how much is enough for you – for now, for your life and for your legacy. Contact your Financial Adviser about your Old Mutual Wealth Integrated Wealth Plan .

Call 0860 WEALTH (932584) or go to www.howmuchisenough.co.za

ADVICE | INVESTMENTS | WEALTH

Old Mutual Wealth is brought to you through several Licenced Financial Services Providers in the Old Mutual Group who make up the elite service offering 10015764JB/

/E

OCTOBER 2014

VOL. 104 NO. 10

GUEST EDITORIAL

647

Non-communicable diseases in South Africa: A challenge to economic development K Hofman

648

EDITOR’S CHOICE

CORRESPONDENCE 650

Use of the Xpert MTB/RIF assay in the diagnosis of tuberculous meningitis: A cautionary note A I Bhigjee

650

Hydroxyethyl starches in severe burns D den Hollander

651

Professional competence – adding reflective elements to case reports R P Abratt

651

The ‘Marketplace’ – a novel conference teaching and learning model B Cheema

Ebola: SA has no outbreak ‘laurels’ to rest on Dismal obs/gynae training contributing to maternal deaths - Motsoaledi New partnership stands to save millions of women and children BHF and Government – ‘I’ll change if you’ll change’

CONSULTING EDITOR JP de V van Niekerk, MD, FRCR DEPUTY EDITOR Bridget Farham, BSc (Hons), PhD, MB ChB

SCIENTIFIC EDITOR Ingrid Nye, BSc TECHNICAL EDITORS Paula van der Bijl, BA, HDipLib Emma Buchanan, BA NEWS EDITOR Chris Bateman | Email: chrisb@hmpg.co.za HEAD OF PUBLISHING Robert Arendse PRODUCTION COORDINATOR Bronlyne Granger ART DIRECTOR Brent Meder

SAMJ FORUM

661

OPINION Preventing diabetic blindness: A priority for South Africa K J Hofman, C Cook, N Levitt

663

Healthy migration: A public health and development imperative for south(ern) Africa J Vearey

665

ISSUES IN PUBLIC HEALTH Low levels of physical activity in female adolescents cause overweight and obesity: Are our schools failing our children?

M N Mokabane, M M Mashao, M van Staden, M J Potgieter, A Potgieter

668

CLINICAL ALERT Varicose veins: Look before you strip – the occluded inferior vena cava and other lurking pathologies T Mokoena

671

The influence of glucocorticoids on lipid and lipoprotein metabolism and atherosclerosis I L Ross, A D Marais

DTP & DESIGN Carl Sampson

EDITORIALS 675

SANHANES: A unique survey series in the health landscape D Labadarios, O Shisana, T Rehle, L Simbayi

676

The sexual and reproductive health needs of youth in South Africa – history in context M E Beksinska, L Pillay, Cecilia Milford, J A Smit

678

Orphans, HIVE and HAND: Who are the watch-keepers?

K Walker, M Inglis, G Norton, R Sher, D Zieff, T McCann, P Roux

Monitoring of non-communicable diseases such as hypertension in South Africa: Challenges for the post-2015 global development agenda C Day, P Groenewald, R Laubscher, S Chaudhry, N van Schaik, D Bradshaw

645

ONLINE MANAGER Gertrude Fani DISTRIBUTION MANAGER Edward Macdonald | Tel. 021-681-7085 HEAD OF SALES AND MARKETING Diane Smith | Tel. 012-481-2069 Email: dianes@samedical.org PROFESSIONAL ADVERTISING Bronlyne Granger | Tel. 021-681-7000 E-mail: bronlyne.granger@hmpg.co.za HMPG BOARD OF DIRECTORS Prof. M G Veller (Chair), Prof. M Lukhele, Dr M Mbokota, Prof. A A Stulting, Dr M R Abbas, Dr G Wolvaardt ASSOCIATE EDITORS Q Abdool Karim, A Dhai, N Khumalo R C Pattinson, A Rothberg, A A Stulting, J Surka, B Taylor, M Blockman ISSN 0256-9574

RESEARCH 680

EDITOR EMERITUS Daniel J Ncayiyana, MD (Groningen), FACOG, MD (Hon), FCM (Hon)

EDITORIAL SYSTEMS MANAGER Melissa Raemaekers, BSc (Hons), PhD

IZINDABA 653 656 658 659

EDITOR Janet Seggie, BSc (Hons), MD (Birm), FRCP (Lond), FCP (SA)

October 2014, Vol. 104, No. 3

Publisher website: www.hmpg.co.za SAMA website: www.samedical.org Journal website: www.samj.org.za

687

Meeting the sexual and reproductive health needs of high-school students in South Africa: Experiences from rural KwaZulu-Natal J A Frohlich, N Mkhize, R C Dellar, G Mahlase, C T Montague, Q Abdool Karim

691

Comparability of total cardiovascular disease risk estimates using laboratory and non-laboratory based assessments in urban-dwelling South Africans: The CRIBSA study N Peer, C Lombard, K Steyn, T Gaziano, N Levitt

696

Detecting virological failure in HIV-infected Tanzanian children E M Mgelea, R Kisenge, S Aboud

700

Quality assurance in diabetic retinal screening in South Africa S Cook, R T Staff, K A Goatman, J A Olson, and the Scottish Diabetic Retinopathy Screening collaborative

CONTENTS LISTED IN Index Medicus (Medline) Excerpta Medica (EMBASE) Web of Knowledge Biological Abstracts (BIOSIS) Science Citation Index (SciSearch) Current Contents/Clinical Medicine SAMJ SUBSCRIPTION RATES Local subscriptions R1 144.00 p.a.

Foreign subscriptions R2 580.00 p.a.

Single copies R95.00 Members of SAMA receive the SAMJ only on request, as part of their membership benefit.

Subscriptions: Tel. 012-481-2071 E-mail: members@samedical.org

CONTINUING MEDICAL EDUCATION

705

GUEST EDITORIAL Atopic dermatitis W Sinclair, R J Green

706

REVIEW Aetiopathogenesis of atopic dermatitis H F Jordaan, G Todd, W Sinclair, R J Green

28 Main Road (Cnr Devonshire Hill Road), Rondebosch, 7700 Tel. 021-681-7200.

E-mail: publishing@hmpg.co.za Website: www.hmpg.co.za

710

ARTICLES Epidemiology of atopic dermatitis G Todd

Please submit all letters and articles for publication online at www.samj.org.za

711

Diagnosis of atopic dermatitis: From bedside to laboratory W Sinclair, J Aboobaker, R J Green, M E Levin

712

Education and specialist referral of patients with atopic dermatitis R J Green, A Pentz, H F Jordaan

713

Non-pharmacological treatment modalities for atopic dermatitis G Todd, A Manjra, W Sinclair, M Levin, R J Green

714

Topical and systemic pharmacological treatment of atopic dermatitis A Puterman, H Lewis, W Sinclair, R J Green

General approach to and summary of the guideline for the management of atopic dermatitis* R J Green, W Sinclair

The SAMJ is published monthly by the Health and Medical Publishing Group (Pty) Ltd, Co. registration 2004/0220 32/07, a subsidiary of SAMA.

© Copyright: Health and Medical Publishing Group (Pty) Ltd, a subsidiary of SAMA

*Available online only

PROFESSIONAL ADVERTISING

CPD QUESTIONS

Use of editorial material is subject to Creative Commons Attribution – Noncommercial Works License 3.0. http://creativecommons. org/licenses/by-nc/3.0

Plagiarism is defined as the use of another’s work, words or ideas without attribution or permission, and representation of them as one’s own original work. Manuscripts containing plagiarism will not be considered for publication in the SAMJ. For more information on our plagiarism policy, please visit http://www.samj.org.za/index. php/samj/about/editorialPolicies Printed by FA Print

Xxxxxxx Photo and text: Eric Nathan Email: eric@ericnathan.com

646

October 2014, Vol. 104, No. 3

GUEST EDITORIAL

Non-communicable diseases in South Africa: A challenge to economic development The economic development of a nation depends in part on the health of its population. Addressing the non-communicable disease (NCD) epidemic is critical to a virtuous cycle of improved public health outcomes and better economic growth. Decreasing premature mortality from NCDs is now on the post-2015 development agenda. The accumulated losses to South Africa (SA)’s gross domestic product between 2006 and 2015 from diabetes, stroke and coronary heart disease alone are estimated to cost the country US$1.88 billion.[1] Employers face additional costs in the form of high staff turnover and absenteeism, because these conditions are not only a source of morbidity but a leading cause of death in our working-age population.[2] Obese workers cost their employers 49% more in paid time off than their non-obese colleagues.[2] Workplace wellness programmes are growing and show promise, but the urban poor, who are particularly vulnerable, have little access to them. Families of the deceased suffer catastrophic costs, with two-thirds of poor households being underinsured against funeral costs, and are dependent on either a regular wage earner or a grant reci­pient.[3] The NCD epidemic in SA is an even greater burden because it is occurring concurrently with an ageing HIV-positive population.

By 2030, NCDs will account for five times as many deaths as communicable diseases in low- and middle-income countries.[4] The World Health Assembly has agreed to aim to reduce premature mortality from cardiovascular and chronic respiratory disease, cancer and diabetes by 25% by 2025.[5] This ‘25 × 25’ strategy embraces six risk factors and their social determinants. By tackling tobacco use, harmful alcohol use, salt intake, hypertension, raised blood glucose and diabetes, and obesity, mortality in SA could be reduced by about 20%, but more importantly, premature disability and death could be significantly delayed.[5] A balance between population-based alongside individual-level strategies is well recognised in the SA National Department of Health (NDoH) Strategic Plan for the Prevention and Control of NonCommunicable Diseases 2013-17.[6] Preventing and postponing NCDs is appreciably more effective and considerably less costly than treatment of those who become sick.[7] Worldwide, governments support an array of levers that include regulatory, fiscal and legislative options.

In SA the NDoH has promulgated mandatory salt regulations, beginning in 2016. This will save a total of 6 400 lives from stroke, 4 300 from non-fatal stroke, and cut hospitalisation costs by ZAR300 million annually.[8] Similarly, a potential SA tax on sugary drinks would cut the number of obese people by 220 000 in 3 years.[9] Occasionally, industry and not government sets the precedent … Tesco, a leading food retailer in the UK, has banned junk food from its checkout aisles.[10] Targeting patients with multiple lifestyle risk factors by secondary prevention is another tactic, but even under the best of circumstances, efficacious behavioural or drug interventions involve complex implementation challenges. Shifts are needed to counter the marketing of calorie-dense and nutrient-poor products. Healthy messaging, targeting discretionary intake of salt and sugar and encouraging regular physical exercise, especially for girls and women, is needed. Responsible government interventions must create an environ­ment in which rich and poor alike are empowered to make healthy choices. With fewer sick people to support, our health system could focus on providing better-quality care.

Several new institutional models might be considered to promote prevention. One is a multi-stakeholder national health commission that engages other sectors, including trade and industry, agriculture, education, sports, and arts and culture.[11] Margaret Chan, director of the World Health Organization, says: ‘Governments cannot assume that NCDs are a health problem and that the health sector can manage on its own. We cannot.’[12] A second might involve the creation of an independent-of-government health promotion foundation (HPF) –

647

such organisations have successfully impacted on population health in many countries from Australia to Thailand.[13] HPFs work in collaboration with government, research institutions and civil society by using media campaigns, raising social awareness and providing support to families. Finally, we need a priority-setting agency that assesses cost-effectiveness, acceptability and feasibility of a range of interventions; the UK National Institute for Health and Care Excellence (NICE) and counterparts in South Korea and Thailand are examples.[13] Ultimately, to successfully reduce premature mortality from NCDs, accurate monitoring of the burden and the outcome of interventions is critical. This is reinforced by Day et al.[14] in this edition of the SAMJ. According to Health Minister Dr Aaron Motsoaledi, ‘Health budgets will break because of the cost of amputations, artificial limbs, wheelchairs and cardiac surgery.’[15] To ensure that social and human development indicators in SA are not further compromised, more funding must be allocated to expand robust health and costing data to include NCDs. In addition to facilitating transparency and accountability, regular, updated quality metrics that are readily accessible and comprehensible will enable the provincial health departments to accurately plan, budget and evaluate their activities.

Such institutional and policy interventions have the potential to harness public health as the basis of inclusive economic growth. Given the huge divide of health and inequality that characterises our current development trajectory, addressing the NCD epidemic could not be more urgent.

Karen Hofman Director, PRICELESS-SA (Priority Cost Effective Lessons for Systems Strengthening – SA), Medical Research Council/University of the Witwatersrand Rural Public Health and Health Transitions Research Unit (Agincourt), South Africa, and Health and Population Division, School of Public Health, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa karen.hofman@wits.ac.za 1. Abegunde DO, Mathers CD, Adam T, Ortegon M, Strong K. The burden and costs of chronic diseases in low-income and middle-income countries. Lancet 2007;370(9603):1929-1938. [http://dx.doi.org/10.1016/S0140-6736(07)61696-1] 2. Van Nuys K, Globe D, Ng-Mak D, et al. The association between employee obesity and employer costs: Evidence from a panel of US employers. Am J Health Promot 2014;28(5):277-285. [http://dx.doi. org/10.4278/ajhp.120905-QUAN-428] 3. Collins DL, Leibbrandt M. The financial impact of HIV/AIDS on poor households in South Africa.

AIDS 2007;21(Suppl 7):S75-S81. [http://dx.doi.org/10.1097/01.aids.0000300538.28096.1c] 4. Mathers C, Fat DM, Boerma JT. The Global Burden of Disease: 2004 Update. Geneva: World Health Organization, 2008. http://www.who.int/healthinfo/global_burden_disease/GBD_report_2004update_full.pdf (accessed 18 July 2014).

5. Atun R. Decisive action to end apathy and achieve 25 × 25 NCD targets. Lancet 2014;384(9941):384385. [http://dx.doi.org/10.1016/S0140-6736(14)60728-5] 6. National Department of Health. Strategic Plan for the Prevention and Control of Non-Communicable Diseases 2013-17. Pretoria: NDoH, 2013.

7. Cecchini M, Sassi F, Lauer JA, et al. Tackling of unhealthy diets, physical inactivity, and obesity: Health effects and cost-effectiveness. Lancet 2010;376(9754):1775-1784. [http://dx.doi.org/10.1016/S0140-6736(10)61514-0] 8. Hofman, KJ, Tollman SM. Population health in South Africa: A view from the salt mines. Lancet Global Health 2013;1(2):e66-e67. [http://dx.doi.org/10.1016/S2214-109X(13)70019-6] 9. Manyema M, Veerman L, Sartorius B, Chola L, Tugendhaft A, Hofman KJ. Potential impact on obesity of a 20% tax on sugar sweetened drinks in South Africa. PLoS One 2014;9(8):e105287.

10. Smithers R. Tesco bans sweets from checkouts in all stores. The Guardian, 22 May 2014. http://www.theguardian. com/business/2014/may/22/tesco-bans-sweets-from-checkouts-all-stores (accessed 28 July 2014).

11. 2014/15 Budget Vote speech by the Deputy Minister of Health, Dr Mathume Joe Phaahla. NDoH, 23 July 2014. http://www.gov.za/speeches/view.php?sid=47041 (accessed 18 July 2014).

12. Chan M. WHO Director-General opening remarks at high-level meeting on noncommunicable diseases. UN General Assembly high-level meeting on the comprehensive review and assessment of the progress achieved in the prevention and control of noncommunicable diseases. 2014. http://www. who.int/dg/speeches/2014/noncommunicable-diseases/en/ (accessed 18 July 2014).

13. Perez A, Ayo-Yusuf OA, Hofman KJ, et al. Establishing a health promotion and development foundation in South Africa. S Afr Med J 2013;103(3):147-149. [http://dx.doi.org/10.7196/samj.6281] 14. Day C, Groenewald P, Laubscher R, Chaudhry S, van Schaik N, Bradshaw D. Monitoring of noncommunicable diseases such as hypertension in South Africa: Challenges for the post-2015 global development agenda. S Afr Med J 2014;104(10):680-687. [http://dx.doi.org/10.7196/SAMJ.7868] 15. Lawrence F. Alarm as corporate giants target developing countries. The Guardian, 23 November 2011. http://www.theguardian.com/global-development/2011/nov/23/corporate-giants-target-developingcountries (accessed 18 July 2014).

S Afr Med J 2014;104(10):747-648. DOI:10.7196/SAMJ.8727

October 2014, Vol. 104, No. 10

She needs a professional treatment to a discreet problem . . .

Bacterial Vaginosis is more common than thrush.1,2 Many women may mistakenly believe that all vaginal discharges are caused by thrush, and therefore may treat inappropriately. Characterised by a thin, white discharge and unpleasant musty or fishy smell, left untreated, Bacterial Vaginosis may pose a serious threat to a woman’s health (e.g. increased risk of acquiring HIV and STDs, adverse pregnancy outcomes).1,2

Metrogel V is the Gynaecologists’ preferred choice in the treatment of Bacterial Vaginosis.3

vaginal gel metronidazole 0.75% 2

References: 1. Ries AJ. Treatment of Vaginal Infections: Candidiasis, Bacterial Vaginosis, and Trichomoniasis. J Am Pharm Assoc. 1997:NS37(5):563-569. 2. The Centers for Disease Control and Prevention. Sexually Transmitted Diseases Treatment Guidelines 2010. MMWR2010:59[RR-12]:56-57. 3. Impact Rx. Script Data – Jan 2012.

Scheduling status: S2 Proprietary name (and dosage form): MetroGel V Vaginal Gel. Composition: Metronidazole 37.5 mg/5 g. Preservatives: Methyl hydroxybenzoate 4.0 mg/5 g, Propyl hydroxybenzoate 1.0 mg/5 g. Pharmacological classification: A 20.2.6 Antimicrobial: Medicines against protozoa. Indications: MetroGel V is indicated for the treatment of bacterial vaginosis. Registration number: 33/20.2.6/0243 [Act 101/1965] Name and business address of applicant: iNova Pharmaceuticals (Pty) Ltd. Co. Reg. No. 1952/001640/07, 15e Riley Road, Bedfordview. Tel: 011 087 0000 www.inovapharma.co.za For full prescribing information, refer to the individual package inserts as approved by the medicines regulatory authority.

Further information is available on request from iNova Pharmaceuticals. IN823/13.

EDITOR’S CHOICE

CME: Atopic dermatitis

No other skin disease places such demands on resources, time and the human spirit as atopic dermatitis. Simplistically seeing atopic dermatitis as ‘an allergy’ is long outdated, as the complexity of this condition becomes more and more apparent as new information is published. All healthcare workers involved in the management of atopic dermatitis should take note of these guiding principles and try to implement them in clinical practice wherever possible.

The approach for this issue is novel, in that the articles have been compiled from a guideline on the management of this condition rather than publishing the guideline as a stand-alone supplement.

As a result the topic is tackled in a way that particularly benefits the generalist, who receives clear and up-to-date information that is immediately useful in a clinical consultation.

The guideline, edited by Werner Sinclair and Robin Green, was developed in an attempt to improve the outcomes of treatment of this condition, which has such a major impact on the quality of life of sufferers. Understanding the disease will also help to eliminate unnecessary investigations, unnecessary and inappropriate interventions, and the use of unsubstantiated treatment modalities.

Non-communicable diseases (NCDs)

The burden of disease analysis shows that NCDs have become the largest cause of years of life lost (YLL) in South Africa (SA) (32% of YLL in 2009). This month’s SAMJ carries coverage of the NCDs – SA’s next looming epidemic, which poses a significant challenge to our economic development.[1] Extensive routine information systems exist for key infectious diseases as well as maternal and child health, but minimal information is available on NCDs. The South African National Health and Nutrition Examination Survey (SANHANES-1) is expected to provide rich data for evaluation of NCDs.[2] Day et al.[3] show that the proportion of years of life lost due to NCDs is highest in SA’s metros and least-deprived districts, with all (except Mangaung) showing high age-standardised mortality rates for ischaemic heart disease, cerebrovascular disease (CVD) and hypertensive disease. Furthermore, the prevalence of hypertension has increased since 1998, a national household survey in 2010 showing a prevalence of >40% in adults aged ≥25 years.

Acknowledging that the burden of disease relating to NCDs would continue to rise if left unchecked, the SA National Department of Health released its Strategic Plan for the Prevention and Control of Non-communicable Diseases 2013-17 in August 2013, laying out national goals and targets (Table 1, p. 681).

Day et al. admit that more work is needed to refine NCD monitoring in SA, to enable the ten goals of the national strategic plan to be assessed. The priority targets for NCDs need to be integrated into national health planning processes, and surveillance requires integration into national health information systems. Finally, a greater focus on integrated chronic care within primary healthcare is needed at all levels to meet requirements for the effective management of NCDs.

Healthy migration

Prevention and management of NCDs should include the migrant population, to which Vearey alerts us.[4] The rest of the Southern African Development Community faces an increasing NCD burden.

Healthy migration is good for development, but current preven­tion, testing and treatment responses in public health systems – particularly for chronic conditions – fail to engage with migration. In SA, public health responses fail to address internal and cross-border movement, and non-nationals face challenges in accessing healthcare. Of

648

particular concern is the lack of nationally and regionally co-ordinated strategies to ensure continuity of treatment for chronic conditions.

Cardiovascular disease

Treatment of CVD risk factors has traditionally been based on the presence or absence of a single risk factor, such as hypertension, hyperlipidaemia or diabetes, without considering the continuous relationship between blood pressure, glucose and cholesterol levels, and cardiovascular risk. While this approach appears straightforward, it may result in committing some individuals with only a small cardiovascular risk to years of unnecessary treatment or, conversely, failure to treat individuals with an overall higher risk. This is because a combination of several slightly elevated risk factors may result in a much higher total risk than a single, more strikingly raised factor.

Given the enormous burden of CVD and the high costs of management, Peer et al.[5] believe that it is essential to prioritise costeffective approaches that target high-risk individuals. This approach is particularly recommended as a cost-effective strategy in developing regions, such as our own, with scarce resources. In this CRIBSA study, CVD risk was high in unemployed men, the poorest women and less-educated adults, which suggests that CVD management needs to target these vulnerable groups.

Glucocorticoids, lipid and lipoprotein metabolism and atherosclerosis

Glucocorticoid treatment should be undertaken for appropriate indications, but in some instances special attention should be given to management of dyslipidaemia, as long-term survivors of treatment are likely to encounter atherosclerosis. Patients managed with glucocorticoids should have their cardiovascular risk assessed, especially if long-term treatment is planned. While the impact of glucocorticoids on atherosclerosis is unclear and some apparently favourable changes have been reported in high-density lipoprotein metabolism, very-low-density lipoprotein and low-density lipoprotein responses seem unfavourable.[6]

Sexual and reproductive health needs of adolescents

There are strong associations of high HIV rates with high incidences of sexually transmitted infections (STIs), high rates of unplanned teenage pregnancy, and poor educational and economic outcomes.

As age of sexual debut is considered important in these associations, adolescence has been recognised as a critical period for sexual and reproductive health (SRH), beyond HIV prevention. Despite the obvious need for SRH facilities and a supportive legal framework, adolescent-focused services are scarce, and young people face a number of barriers to accessing such services. A study carried out under the auspices of the Centre for the AIDS Programme of Research in South Africa (CAPRISA) of the Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, suggests that integrating SRH services into schools may overcome many of these barriers.[7] The authors describe an SRH service model developed for high-school students, and its implementation in 14 high schools in rural SA. The programme comprised in-school group SRH information and awareness sessions in tier 1, in-school individual SRH counselling and customised counselling and testing in tier 2, and referrals to in-school fixed, in-school mobile, or public sector primary SRH clinics in tier 3. This SRH service provision pilot proved acceptable to the community and seems feasible for scale-up. Further work is required to understand interschool variability in uptake and identify additional service needs of students.

October 2014, Vol. 104, No. 10

EDITOR’S CHOICE

Preventing diabetic blindness

Diabetes is the third leading cause of blindness in SA, from retinopathy and cataracts, and accounts for 8 000 new cases of vision impairment every year.[8] International examples show that camera screening for diabetic vision impairment is successful on a national scale. In 1980, 2.4% of Iceland’s population was legally blind, but by 2005 the prevalence had dropped to 0.5%! The decline was attributed to the availability of treatment and preventive measures. In SA, screening for retino­ pathy at primary care level is almost non-existent, despite current guidelines recommending annual screening. In addition, ophthalmic treatment in the form of laser therapy and operations requires referral to tertiary centres. In 2007, a pilot study in Cape Town evaluated the impact of mobile fundus photography to screen for diabetic retino­ pathy.[9] Following the screening, an ophthalmic specialist reviewed the photographs and referred patients as needed. This proved effective and allowed a single technician to screen about 10 000 patients annually, suggesting that scale-up is feasible. Screening via camera alone cost ZAR189 per person with further costs, including follow-up operation procedures, ranging from a lower limit of ZAR10 500 to an upper limit of ZAR23 327 per blindness case averted.

The SA government provides support through monthly disability grants for the blind, totalling ZAR12 120 per year per blind person.

The ZAR10 500 per blindness case averted is less than the expense of one year of a disability grant. Prevention of blindness would also extend the number of working years for every diabetic patient.

Although the SA pilot project was performed in an urban setting, similar projects in rural communities in Australia and France have proved effective. Furthermore, smart-phone technology that might allow screening for diabetic retinopathy using mobile phones is now being tested elsewhere in Africa.

As National Health Insurance will not cover diagnostic procedures outside its approved guidelines and protocols, it is essential that

screening for diabetic retinopathy be considered for scale-up nationally. The use of mobile fundus cameras has huge savings potential compared with the current situation of diabetes treatment and disability coverage.

The ability to acquire and record high-quality retinal images is only the first step in early detection of diabetic retinopathy: effective interpretation is essential. Cook et al.[10] invited graders registered in the Ophthalmological Society of South Africa diabetic retinopathy screening programme to participate in an external quality assurance programme, and report their findings. Disparity in grader performance indicates room for improvement, and a high rate of referral to ophthalmology suggests that on average graders are performing safely, but with a high number of inappropriate referrals.

JS 1. Hofman K. Non-communicable diseases in South Africa: A challenge to economic development. S Afr Med J 2014;104(10):647-648. [http://dx.doi.org/10.7196/SAMJ.8727] 2. Labadarios D, Shisana O, Rehle T, Simbayi L. SANHANES: A unique survey series in the health landscape. S Afr Med J 2014;104(10):675-676. [http://dx.doi.org/10.7196/SAMJ.8842] 3. Day C, Groenewald P, Laubscher R, Chaudhry S, van Schaik N, Bradshaw D. Monitoring of noncommunicable diseases such as hypertension in South Africa: Challenges for the post-2015 global development agenda. S Afr Med J 2014;104(10):680-687. [http://dx.doi.org/10.7196/SAMJ.7868] 4. Vearey J. Healthy migration: A public health and development imperative for South(ern) Africa. S Afr Med J 2014;104(10):663-664. [http://dx.doi.org/10.7196/SAMJ.8569] 5. Peer N, Steyn K, Lombard C, Gaziano T, Levitt N. Comparability of total cardiovascular disease risk estimates using laboratory and non-laboratory based assessments in urban-dwelling South Africans: The CRIBSA study. S Afr Med J 2014;104(10):691-696. [http://dx.doi.org/10.7196/SAMJ.8125] 6. Ross IL, Marais AD. The influence of glucocorticoids on lipid and lipoprotein metabolism and atherosclerosis. S Afr Med J 2014;104(10):671-674. [http://dx.doi.org/10.7196/SAMJ.7979] 7. Frohlich JA, Mkhize N, Dellar RC, Mahlase G, Montague CT, Abdool Karim Q. Meeting the sexual and reproductive health needs of high-school students in South Africa: Experiences from rural KwaZuluNatal. S Afr Med J 2014;104(10):687-690. [http://dx.doi.org/10.7196/SAMJ.7841] 8. Hofman KJ, Cook C, Levitt N. Preventing diabetic blindness: A priority for South Africa. S Afr Med J 2014;104(10):661-662. [http://dx.doi.org/10.7196/SAMJ.8580] 9. Khan T, Bertram MY, Jina, R, Mash B, Levitt N, Hofman K. Preventing diabetes blindness: Cost effectiveness of a screening programme using digital non-mydriatic fundus photography for diabetic retinopathy in a primary health care setting in South Africa. Diabetes Res Clin Pract 2013;101(2):170176. [http://dx.doi.org/10.1016/j.diabres.2013.05.006] 10. Cook S, Staff RT, Goatman KA, Olson JA, and the Scottish Diabetic Retinopathy Screening collaborative.

Quality assurance in diabetic retinal screening in South Africa. S Afr Med J 2014;104(10):700-704. [http://dx.doi.org/10.7196/SAMJ.8678]

This month in the SAMJ ...

Mags Beksinska* is a Director at MatCH Research, a research division under the Wits Health Consortium in the Department of Obstetrics and Gynaecology at the University of the Witwatersrand, Johannesburg. She has worked in the field of sexual and reproductive health for almost 20 years, and her PhD focused on the relationship between hormonal contraception and bone mineral density in adolescents. She has a particular interest in barrier methods of HIV and pregnancy prevention for women and girls, with a focus on new condom and diaphragm development, where she is involved in clinical research in new designs. She provides technical assistance in barrier methods to the United Nations Population Fund, the World Health Organization and the International Organization for Standardization, and is involved in the National Department of Health condom co-ordination forum. * Beksinska M, Lavanya Pillay L, Milford C, Smit JA. The sexual and reproductive health needs of youth in South Africa – history in context. S Afr Med J 2014;104(10):676-678. [http://dx.doi.org/10.7196/SAMJ.8809]

649

October 2014, Vol. 104, No. 10

CORRESPONDENCE

Use of the Xpert MTB/RIF assay in the diagnosis of tuberculous meningitis: A cautionary note

To the Editor: The Xpert MTB/RIF (Cepheid) assay is a nucleic acid amplification test developed to detect mycobacterial tuberc­ ulosis (MTB) infection and rifampicin resistance. It is a closed system, requires minimal training to use, and produces a result in a few hours. When used as an initial diagnostic test replacing smear microscopy for pulmonary tuberculosis, the Xpert MTB/RIF has a pooled sensitivity of 88%.[1] The application of this test has been extended to extrapulmonary samples, including cerebrospinal fluid (CSF).

The World Health Organization (WHO) evaluated the results of 709 CSF samples tested with Xpert MTB/RIF in 16 studies using culture as a reference standard. Sensitivity varied widely, ranging from 51% to 100%.[1] Using a 3 ml volume of CSF and including a concentration step increased sensitivity.[1,2] The WHO recommends that the Xpert MTB/RIF should be the first test to be undertaken on CSF from patients with suspected tuberculous meningitis (TBM). However, caution is advised, as the following case illustrates.

A 43-year-old HIV-positive man was admitted to a peripheral hospital in South Africa with a 2-week history of headache and a more recent onset of slurred speech, inability to walk and impaired consciousness. A computed tomography scan of the brain showed mild hydrocephalus and basal enhancement. Lumbar puncture revealed an opening pressure of 4 cm H2O, yellow colour, lympho­ cytes 300/l, a protein level of 1.06 g/l and glucose level of 1.3 mmol/l. The Xpert MTB/RIF was negative. On the basis of this negative test result, initiation of antituberculosis (anti-TB) therapy was deferred and ceftriaxone was started. The patient was referred to the neurology unit at Inkosi Albert Luthuli Central Hospital in Durban 4 days later. He was noted to have a Glagow Coma Score of 8/15, meningism and normal optic fundi. He could move all his limbs. Anti-TB drugs and steroids were commenced, but he died within 3 hours of admission.

Ignoring the Xpert MTB/RIF result, this patient’s clinical, radiological and CSF profile is consistent with probable TBM. [3] As standard of care, he would have been started on anti-TB therapy and steroids while awaiting the other laboratory results.

The WHO, understandably, based its recommendation on studies done in research settings, where as much as 3 ml of CSF was used in at least one study.[2] For busy routine laboratories the extra step of concentration may be burdensome, and moreover they are unlikely to receive such a large volume of CSF. As this test for TBM becomes more widely available it will be requested at all levels of care by medical personnel who have varying degrees of clinical skill, knowledge and experience. Herein lies the concern. Clinicians need to understand that, as with other tests for diagnosis of TBM, the Xpert MTB/RIF is a good ‘rule-in’ test (i.e. specificity approaching 100%) but a poor ‘rule-out’ test (moderate sensitivity).[4] A negative test does not exclude TBM. Clinical judgement is required. Any delay in initiating therapy risks an unacceptable outcome for the patient.

The Xpert MTB/RIF test should be subjected to post-WHO recommendation scrutiny to determine how well it performs in routine clinical practice for the diagnosis of TBM. Ahmed I Bhigjee

Department of Neurology, Nelson R Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa bhigjee@ukzn.ac.za

650

1. WHO policy update. Xpert MTB/RIF assay for the diagnosis of pulmonary and extrapulmonary TB in adults and children. http://apps.who.int/iris/bitstream/10665/112472/1/9789241506335_eng.pdf (accessed 21 July 2014).

2. Patel VB, Theron G, Lenders L, et al. Diagnostic accuracy of quantitative PCR (Xpert MTB/RIF) for tuberculosis meningitis in a high burden setting: A prospective study. PLoS Med 2013;10(10):e1001536. [http://dx.doi.org/10.1371/journal.pmed.1001536] 3. Marais S, Thwaites G, Schoeman JF, et al. Tuberculous meningitis: A uniform case definition for use in clinical research. Lancet Infect Dis 2010;10(11):803-812. [http://dx.doi.org/10.1016/S14733099(10)70138-9] 4. Solomons RS, van Elsland SL, Visser DH, et al. Commercial nucleic acid amplification tests in tuberculous meningitis – a meta-analysis. Diag Microbiol Infect Dis 2014;78(4):398-403. [http:// dx.doi.org/10.1016/j.diagmicrobio.2014.01.002]

S Afr Med J 2014;104(10):650. DOI:10.7196/SAMJ.8735

Hydroxyethyl starches in severe burns

To the Editor: The Medicines Control Council of South Africa recently lifted the suspension on the use of all medicines containing hydroxyethyl starch (HES), with the exclusion of, among other contraindications, patients with severe burns. A circular from the KwaZulu-Natal Department of Health furthermore restricts the use of HES-containing products to specialist anaesthetists, advising the use of Gelofusine for the ‘general resuscitation of hypovolaemic patients in intensive care’ or for the ‘acute resuscitation of patients with severe, source-controlled haemorrhagic shock in theatre by a specialist anaesthetist’.[1] I submit that the exclusion of severe burns from the indications for the use of colloids, as well as the exclusion of consultant surgeons and emergency specialists from those who will be allowed to prescribe HES-containing products, indicates little insight into the evidence and the clinical situation at ‘the coalface’. It may have escaped the attention of pharmacologists that the majority of patients with hypovolaemic shock are resuscitated not by anaesthetists but by front-line clinicians such as those mentioned above.

The initial decision to suspend the use of HES-containing resuscitation fluids was based on three studies, the VISEP study,[2] the 6S study[3] and the CHEST study.[4] As was argued by Coetzee et al.,[5] among others, these studies were ‘seriously flawed and do not apply to the perioperative and acute resuscitation period’. The evidence against HES in burns resuscitation is even flimsier. Both the 6S study and the CHEST study excluded burns patients. The VISEP study included 30 patients with burns, and these were the subject of a post hoc analysis by Béchir et al.[6] (10 years after the study!); this analysis concluded that the application of hyperoncotic HES within the first 24 hours after severe burns ‘may be associated with fatal outcome and should therefore be used with caution’. Not only does the Béchir analysis suffer from the same drawbacks as the initial VISEP study, but analysis of data collected 10 years previously made it even more suspect. This is well borne out by the fact that the patients in the HES group were on average over 13 years older and had a higher prevalence of inhalation injury (both independent determinants of mortality in burns) than those who were resuscitated with saline alone.

An increasingly recognised complication of the resuscitation of patients with severe burns is the development of compartment syndromes, including that affecting the abdomen. A recent review of 50 publications including 1 616 patients quoted prevalences of 64.7 - 74.5% for intra-abdominal hypertension and of 4.1 - 16.6% for abdominal compartment syndrome. The mortality rate for abdominal compartment syndrome in patients with severe burns was 74.8%.[7] The development of compartment syndrome in burns patients is associated with total resuscitation volumes, and a reduction of the resuscitation volume in the Baxter (Parklands) formula from 4 to 3 ml/kg/% total body surface area has been proposed.[8,9] Vlachou et al.[10] found in a small study that patients with severe burns who

October 2014, Vol. 104, No. 10

CORRESPONDENCE

received part of their resuscitation fluid as HES required less fluid and showed less interstitial oedema than those who received their entire fluid requirements as crystalloid solution. Others have reported similar results with a variety of colloids, including a lower incidence of renal impairment with the use of colloids.[11,12] A review of fluid resuscitation in patients with severe burns concluded that ‘current best evidence supports recommendations to reduce fluid-volume administration through use of colloids or hypertonic saline’, especially if the required volumes would exceed a ‘volume ceiling’.[13] Although none of this provides level I evidence for the use of colloids or HES in early burn resuscitation, the scales are starting to tip in favour of the latter. Meanwhile, the evidence that HES is detrimental seems flimsy. Until large-scale studies are available, decisions to use colloids such as HES are best left to those who have made it their expertise to care for these complex cases.

Daan den Hollander

Clinical Director, Burns Unit, Inkosi Albert Luthuli Central Hospital, and Department of Surgery, Nelson Mandela School of Medicine, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa daanhol@ialch.co.za

Raymond P Abratt

1. Dlamini VC. Re: The Medicines Control Council (MCC) Lifting of Suspension on Medicines Containing Hydroxyethyl Starch. Index No. 08/2014/126. http://healthweb.kznhealth.gov.za/ pharmacy/circulars/2014/The_Medicines_Control_Council_MCC_Lifting_of_Suspension_On_ Medicines_Containing_Hyroxyethylstarch_04082014.pdf (accessed 17 September 2014).

2. Brunkhorst FM, Engel C, Blood F, et al. Intensive inulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008;358(2):125-139. [http://dx.doi.org/10.1056/NEJMoa070716] 3. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl starch 130/0.42 versus Ringer’s acetate in severe sepsis. N Engl J Med 2012;367(2):124-134. [http://dx.doi.org/10.1056/NEJMoa1204242] 4. Myberg JA, Finfer S, Bellome R, et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med 2012;367(20):1901-1911. [http://dx.doi.org/10.1056/NEJMoa1209759] 5. Coetzee A, Dyer RA, James MFM, et al. Evidence-based approach to the use of starch-containing intravenous fluids: An official response by two Western Cape university hospitals. Southern African Journal of Anaesthesia and Analgesia 2013;19(4):186-192.

6. Béchir M, Puhan MA, Neff SB, et al. Early fluid resuscitation with hyperoncotic hydroxyethyl starch 200/05 (10%) in severe burn injury. Crit Care 2010;14(3):R123. [http://dx.doi.org/10.1186/cc9086] 7. Strang SG, van Lieshout EMM, Breederveld RS, van Waes OJF. A systematic review on intraabdominal pressure in severely burned patients. Burns 2014;40(1):9-16. [http://dx.doi.org/10.1016/j. burns.2013.07.001] 8. Rogers AD, Karpelowsky J, Millar AJ, et al. Fluid creep in major pediatric burns. Eur J Pediatr Surg 2010;20(2):133-138. [http://dx.doi.org/10.1055/s-0029-1237355] 9. Pham TN, Cancio LC, Gibran NS. American Burns Association Practice Guidelines. Burn Shock Resuscitation. J Burn Care Res 2008;29(1):257-266. [http://dx.doi.org/10.1097/BCR.0b013e31815f3876] 10. Vlachou E, Gosling P, Moiemen NS. Hydroxyethylstarch supplementation in burn resuscitation – a prospective randomized controlled trial. Burns 2010;36(7):984-991. [http://dx.doi.org/10.1016/j. burns.2010.04.001] 11. Lawrence A, Faraklas I, Watkins H, et al. Colloid administration normalizes resuscitation ratio and ameliorates ‘fluid creep’. J Burn Care Res 2010;31(1):40-47. [http://dx.doi.org/10.1097/ BCR.0b013e3181cb8c72] 12. Dulhunty JM, Boots RJ, Budd MJ, Mulier MJ, Lipman J. Increased fluid resuscitation can lead to adverse outcomes in major-burn related patients, but low mortality is achievable. Burns 2008;34(8):1090-1097. [http://dx.doi.org/10.1016/j.burns.2008.01.011] 13. Azzopardi EA, McWilliams B, Yver S, Whitaker IS. Fluid resuscitation in adults with severe burns at risk of secondary abdominal compartment syndrome – an evidence-based systematic review. Burns 2009;35(7):911-920. [http://dx.doi.org/10.1016/j.burns.2009.03.001]

S Afr Med J 2014;104(10):650-651. DOI:10.7196/SAMJ.8897

Professional competence – adding reflective elements to case reports

To the Editor: Logbooks of procedures are helpful in determining the professional competence of trainees. There has been corres­pondence in the SAMJ on aspects of their use in South Africa – for example, the value of specifying the number of surgical operations in the logbook.[1,2] However, experience does not automatically translate into learning.

Reflection is needed to turn experience into learning. Logbooks of procedures may be complemented by case reports that are structured so as to contain a reflective element.

The College of Radiation Oncologists of South Africa has used structured case reports for the past 4 years, based on a model developed by the Royal Australian and New Zealand College of Radio­logy. These structured case reports include technical aspects of cases from both the

651

clinical and treatment points of view, as well as the potential benefits and toxicity of treatment. In addition, candidates describe both the lessons they have learnt and the candidate’s role in treating the case, to add a reflective element. A minimum of 20 structured case reports are produced during training, which are individually signed off and included in a larger learning portfolio.

The correspondence in the SAMJ does not make it clear whether it is practice to have the logbooks scrutinised by the examiners. It is appreciated that this can be logistically difficult. The College of Radiation Oncologists has dealt with this by having the candidates present their learning portfolios with structured case reports to their examiners one or more days before their oral examinations. The case reports are scrutinised, usually overnight, and the candidates then undergo an oral examination on the structured case reports. This is helpful in assessing the authenticity of the candidates’ practical and learning experience.

The experience with structured case reports has been helpful in both training and examining candidates, and the system could be extended and expanded.

President, College of Radiation Oncologists of South Africa raymond.abratt@uct.ac.za 1. Benatar SR. Professional competence and professional misconduct in South Africa. S Afr Med J 2014;104(7):480-482. [http://dx.doi.org/10.7196/SAMJ.8492] 2. Fagan J, Lindeque G, Benatar S. Professional competence in South Africa. S Afr Med J 2014;104(8):524. [http://dx.doi.org/10.7196/SAMJ.8703]

S Afr Med J 2014;104(10):651. DOI:10.7196/SAMJ.8808

The ‘Marketplace’ – a novel conference teaching and learning model

To the Editor: The word ‘marketplace’ brings to mind a bustling, colourful place where shoppers come to browse goods. The range of items on offer may vary from week to week and from market to market, but is usually led by one principle: what do the shoppers around here want to buy? The same principle of supplying a need can be applied to the ‘purchase’ of knowledge at medical conferences.

However, most conferences tend to offer solely didactic lectures with little opportunity for meaningful direct interaction between the delegates and experts/speakers.

Over the past few years, I have run a novel and highly popular teaching and learning event called the Paediatric Marketplace at the Emergency Medicine Society of South Africa conferences in Cape Town. The central idea is to have a dynamic, fun, interactive session based on a market-style environment, where delegates (shoppers) browse and chat with experts (stallholders), who tailor their teaching to individual needs.

Between ten and twelve market-stalls are set up on any topics of interest (e.g. cardiopulmonary resuscitation, triage, intraosseous line insertion, the ‘blue baby’, fluid management in children, cervical spine immobilisation, foreign body removal techniques, childhood poisoning, etc.). The stalls have eye-catching and inviting materials such as posters, interactive cases, quizzes, video material, radiology images, etc. Mannequins and/or equipment to demonstrate skills are available where appropriate. Delegates are free to browse at their own pace, and they will naturally stop and spend time at stalls that interest them.

In June this year the Paediatric Marketplace was invited to ‘go global’ with a large-scale event at the International Federation of Emergency Medicine (IFEM) Conference in Hong Kong (ICEM 2014). Our expert stallholders were members of the IFEM Paediatric

October 2014, Vol. 104, No. 10

CORRESPONDENCE

Emergency Special Interest Group (PEMSIG), and the co-organiser was Dr Ffion Davies (PEMSIG Chair). The event was a huge success, and it became clear that this innovative teaching and learning experience would be replicated at other conferences globally.

I would like to make a plea to those who may organise these events in the future to please respect and honour the integrity and ethos of the original concept by maintaining two core features: • Senior/expert stallholders. All stallholders need to be authorities or experts in their field. Delegates must be able to ask their ‘curved-ball’, burning or esoteric questions and receive meaningful, intelligent and expert answers. Junior staff and trainees, while invaluable as stall-assistants, are not appropriate solo stallholders as they are not able to adequately answer unexpected or unusual queries or assist all levels of delegates.

• Not for profit. A further core feature (and perhaps an ironic one) is that the Marketplace is entirely non-commercial. No

one is selling anything for money or profit. Expertise, skills and knowledge are being shared purely to help others in the field.

The trade is very much ‘two-way’, with meaningful exchange of accrued experience, wisdom and ideas between experts and delegates.

The Marketplace session is a vibrant, novel and interactive conference event where experts tailor their teaching to the needs of the delegate. Isn’t this what all learners in the education marketplace want?

Baljit Cheema

Paediatric Emergency Specialist, Division of Emergency Medicine, Faculty of Health Sciences, University of Cape Town, South Africa baljit.cheema@uct.ac.za S Afr Med J 2014;104(10):651-652. DOI:10.7196/SAMJ.8820

Correction

In the article ‘Mammographic screening for breast cancer in a resource-restricted environment’, which appeared on pp. 294-296 of the April 2014 SAMJ, and the reply to the letter by Pitcher et al. entitled ‘Mammography reporting at Tygerberg Hospital, Cape Town, South Africa’ on pp. 456-457 of the July issue, the authors should have been listed as J P Apffelstaedt and K Baatjes.

Taking care of your business so you can take care of your patients

For more information contact Wayne Campbell at: +27 (0) 72 424 6724 or +27 (0) 86 134 2544 wayne@medsolutions.co.za | www.medsolutions.co.za

IZINDABA

Ebola: SA has no outbreak ‘laurels’ to rest on South Africa (SA)’s record in handling the initial HIV/ AIDS pandemic (without anti­retroviral drugs) and the rapid spread of extensively drug-resistant tuberculosis (XDR TB) are major red flags warning that it may not have the capacity to face the deadly drug-defiant West African Ebola virus.

SA’s daily TB death rate is nearly ten times the average daily Ebola death rate across the four affected West African countries from March this year – a sobering compar­ ison when contemplating how we would handle an Ebola outbreak. Besides that, XDR TB kills 90% of its victims (multidrug-resistant (MDR) TB 50% – about the same as a West African Ebola victim’s survival chances).

among the hundreds of blood samples sent to the local National Institute for Communicable Diseases (NICD) for testing from throughout South African Development Community (SADC) member states, but the region is on high alert with emergency contingency plans for co-operation in detection, containment and awareness on ‘fast-track’, and a travel ban on all travellers from the affected countries in place.

Because of SA and her immediate neighbours’ geographical distance from West Africa – and the acute and severe nature of Ebola virus disease – officials claim it is ‘highly unlikely’ that cases will enter via land or sea. The highestrisk entry ports are OR Tambo International Airport in Gauteng and the nearby Lanseria Airport, from which all major medical air rescue company aircraft operate (two inter­ nationally). Travellers are being thermally screened at these airports and anyone with an elevated temperature questioned further, while OR Tambo has a modern emergency isolation/ transfer medical centre.

SA’s shaky track record on drug-defying diseases

Dr Andrew Medina-Marino, local disease surv­ eillance and laboratory systems expert, at a newly built isolation facility in Monrovia, Liberia, in August. Picture source: Dr Medina-Marino.

These analogies were drawn by an expert on disease surveillance and laboratory systems, Dr Andrew Medina-Marino, on his return to SA from Ebola-ravaged Liberia, one of the four West African countries across which the virus had claimed more than 1 900 lives among 4 000 suspected infections between early March and 3 September this year – and the pandemic is accelerating. A total of 2 200 infections were confirmed in the woefully inadequate mobile laboratories, with hundreds more people certain to die, as what is justifiably one of the world’s most-feared diseases has a nearly 50% current fatality rate. No Ebola cases have been confirmed

A retrospective look at SA’s XDR TB spread by Prof. Keertan Dheda, arguably the country’s leading expert on drug-resistant TB, at the National TB Conference in Durban in June, plus the lack of any communicable diseases regulation 6 years after the draft provisions were first published, add pinches of salt to ongoing public reassurances. Dheda, Professor of Medicine and Head of Pulmonology at the University of Cape Town (and one of the most published and cited TB academics in the country), estimates that several thousand local healthcare workers are currently TB-infected (the annual infection rate is 2 - 3%), while 140 people die of all types of TB every day.

Evidence that MDR TB is out of control is backed by known data; it has increased from 7 350 notified cases in 2007 to 14 161 in 2012.

Dheda told Izindaba: ‘We should be far more afraid of existing XDR TB than any fairly slim chances of an Ebola outbreak.’

While TB’s incubation period and mode of transmission are very different to Ebola’s (airborne spread v. bodily fluid and infected tissue spread), common denominators include infecting first-line primary healthcare workers, a dysfunctional public health system, low public awareness of basic infection control, and dismal, inappropriate education. At the Durban TB conference, Dheda made an impassioned plea for a nationally co-ordinated strategy to avoid the discharge of highly contagious

653

October 2014, Vol. 104, No. 10

‘therapeutically destitute’ TB patients back into a careless void, with uniquely tailored solu­tions including home-based or community care, plus multidisciplinary teams in modernday sanatoria.

If there’s a local outbreak, pray it’s small and localised – expert

Medina-Marino believes that general Ebola virus disease outbreak expertise and disease surveillance capacity in SA is probably insufficient to deal with ‘anything more than a small, geographically contained outbreak’.

Senior Technical Advisor (Disease Surveillance and Laboratory Systems) at the local Foundation for Professional Development (FPD), he believes that a scattered West African-type Ebola outbreak in our townships could quickly turn into a public health nightmare. (The West African outbreak is the first in the world to reach urban areas.) Our government would have to lean heavily on the mainly US-funded NICD to roll out epidemiological and outbreak control programmes. Medina-Marino returned from a month of voluntary work in Ebola-ravaged Liberia early this August, where he gained invaluable experience and witnessed some of the rampant contagion first-hand.

He believes that the widespread SA XDR TB epidemic is analogous to the West African Ebola outbreak when it comes to comparing public health responses in the absence of any available medical intervention.

His views, particularly about dysfunctional health systems, were echoed in principle by Prof. Sharon Fonn of the School of Public Health, University of the Witwatersrand, and co-director of the Consortium for Advanced Research Training in Africa, while Prof. Lucille Blumberg, head of the NICD’s Surveillance and Outbreak Response Unit, warned that any Ebola outbreak would rapidly expose any existing deficiencies in a public health system, with poverty and fear aggravating contagion.

With 150 healthcare workers dead among the more than 250 infected in the four (previously unaffected) West African outbreak countries, a graphic illustration of the ‘fear factor’ has already played out in SA. According to Dr Frew Benson, Chief Director of Communicable Diseases in the National Department of Health

IZINDABA

Beyond here lies death – without personal protection equipment. Picture source: Dr MedinaMarino.

(NDoH), local nurses treating an already negatively diagnosed but heavily pregnant Ebola suspect refused to ‘scrub in’ for her caesarean section, doing so only under orders when told she was uninfected. ‘You can imagine if we see more cases in SA, what the [caregiver] impact would be,’ he warned at an Ebola briefing at Wits University in late August.

West Africa outbreak ‘out of control’

The severity of the epidemic is illustrated by one startling fact: the confirmed case tally on 3 September was 10% more than all Ebola cases ever reported worldwide (2 000 people).

Medina-Marino spoke to Izindaba after reading our report on the state of SA’s Ebola prevention readiness, sharing his thoughts on interventions that would enable more effective detection and curtailment of any cases that might cross our borders. He is a veteran of the prestigious Centers for Disease Control in the USA, whose director Thomas Frieden warned on 2 September that ‘the window is closing’ on containing the West African epidemic, which he labelled ‘a global problem’. Medina-Marino was seconded to the FPD, where he took a permanent job 3 years ago. He said there was ‘no question’ but that SA had among the world’s best laboratory diagnostic capabilities, SA being one of only three countries asked by the World Health Organization (WHO) to send mobile diagnostic laboratories to West Africa. As one of the few doctors in SA with high-level outbreak response expertise, he volunteered to work cheek-by-jowl with colleagues from the world’s uncontested Ebola outbreak veteran, Médecins Sans Frontières (MSF). MSF has 700 staff in Guinea, Liberia, Sierra Leone and Nigeria.

Lindis Hurum, MSF emergency co-ordinator for Liberia’s capital, Monrovia, described the situation as ‘catastrophic’, with most of the city’s hospitals closed and decomposing and highly infectious bodies lying in streets and houses.

WHO Director-General Dr Margaret Chan declared the outbreak an international public health emergency, admitting that it was moving ‘faster than we can control it’. The WHO is being severely criticised by hugely overburdened MSF for its slow response (belatedly begun only after two deaths and seven confirmed cases in Lagos, Nigeria, the regional hub for international travel and business). Chan called for a global co-ordinated effort to combat what she termed ‘the largest, most severe and most complex outbreak in the nearly four-decade history of this disease’. MSF President Dr Joanne Liu said her organisation was ‘overwhelmed’ and could now offer ‘no more than palliative care’, needing 800 additional beds for MSF’s 160-bed Monrovian treatment centre alone. She said that rather than limit their responses to the potential arrival of an infected patient in their member countries, global health bodies ‘should be helping save lives in West Africa’.

SA’s poor track record in the early days of HIV and current XDR TB spread

Medina-Marino said that when it came to disease outbreaks, SA had already clumsily faced the ‘quite desperate’ HIV pandemic (initially without antiretroviral drugs) and was currently failing to curtail a burgeoning XDR TB pandemic because of the lack of appropriate facilities and care to contain and prevent the highly infectious disease, for which no proven drug treatment exists. The country’s response capacity (and expertise) remained focused on clinical care and treatment. When it came to identifying appropriate infection-risk factors and contact tracing, there was ‘still a lot of work to be done’. In his opinion, only the mainly externally funded NICD was properly prepared to respond to an outbreak. Regardless of what the country’s disease control officials said, SA did not have the capacity for fullscale investigations, especially for an outbreak anywhere near the scale of West Africa’s. It could ‘probably handle between one and three isolated cases’. ‘When things actually happen, the system breaks down very fast,’ he said. ‘All the money in the world’ could not make up for delayed and unco-ordinated responses.

Prof. Fonn said that while SA’s doctor-patient and nurse-patient ratios were better than those in the affected countries (SA has 8 doctors per 100 000 population v. half a doctor per 100 000 for Liberia and Sierra Leone, 1/100 000 for Guinea and 4/100 000 for Nigeria), there

654

October 2014, Vol. 104, No. 10

was no room for complacency. She called on the international community and countries to invest in the broader health system capacity and not respond to each event as if it were a crisis.

‘Curricula for medical students, nurses and doctors are inadequate and inappropriate (one basic example is not being taught how to put on and take off personal protection equipment without becoming infected). We don’t have systems for quick, effective communication between providers and tailored to the local burden of disease, should anything happen, let alone an Ebola outbreak,’ said Fonn. Public messaging campaigns should be conducted before any outbreak, to avoid spreading panic in the population, ‘so that when it happens, you’re reimporting an old message’, she added.

Simply responding to an epidemic was ‘totally inadequate’, she said, stressing that putting money into ‘the most cost-effective’ health programmes was an internationally and oft-repeated ‘mistake’. ‘What people don’t understand is that the healthcare system is the sea upon which health programmes float. Over and over, we put money into the ships and not into the sea,’ she said.

Blumberg stressed that once Ebola reached the cities it became very difficult to contain, the main enemies being poverty, fear and dysfunctional health systems. She said that the NICD’s mobile health laboratory in Liberia was ‘extremely busy’, with every second sample testing positive. Benson claims that 48 of SA’s health districts have received Ebola prevention and awareness training, while defence forces throughout the SADC region would be called in to curtail movement should an outbreak occur. Ebola-ready hospitals had been designated in every province, including one private sector hospital and two military hospitals (Medina-Marino questions how properly equipped they are). With the paucity of institutional training, basic healthcare worker protection training was being stepped up, while immigration officials were receiving twice-weekly updates and training and broader multi­sectoral awareness was being accelerated.

Vicious ‘circle of infection’

Benson said that strengthening SA’s screen­ ing capacity and facilities was essential. ‘An outbreak becomes a vicious circle; once the health system becomes affected it feeds into the outbreak itself,’ he admitted.

Asked what basic precautions should be taken by SA healthcare workers, MedinaMarino said that simply wearing gloves and asking patients whether they’d recently been in West Africa or in contact with someone from there would generally suffice. He chall­ enged Benson’s contention that people with

IZINDABA

Ebola were usually ‘very sick’ and typically presented to a hospital. In Medina-Marino’s experience one of the first places a person with Ebola symptoms went to was a primary or community health clinic (all 250 West African healthcare workers were infected in this way).

Here doctors and nurses were (initially) ‘not necessarily thinking this person has Ebola’ and interacted freely with patients, posing a major infection risk. Medina-Marino emphasised that there was ‘no need to panic’, but cautioned that there was ‘good reason’ for the SA govern­ ment to be better prepared.­

Because of SA and her immediate neighbours’ geographical distance from West Africa – and the acute and severe nature of Ebola – officials claim it is ‘highly unlikely’ that cases will enter via land or sea.

His ‘don’t panic’ message was echoed by Dr Charl van Loggerenberg, Regional Medical Director of International SOS (a 24/7 corporate medical assistance company that also includes the Air Rescue Africa air ambulance operation), who spoke to Izindaba on his return from an NDoH consultation of all relevant SA role players in the public and private sectors in Gauteng on 22 August. He revealed that the SA travel ban on passengers coming from any of the affected West African countries would not apply to medical air rescue companies, which already implemented the highest possible preand in-flight viral haemorrhagic fever (VHF) safety protocols and compliance with port health procedures for all clients. Van Loggerenberg said that the SA government wanted to use the global expertise of companies like his and Netcare 911 to help gather information and disseminate the best possible clinical pathways

and emergency health worker precautionary guidelines. He said that general and nursing practitioners in border areas were the ‘world’s best gatekeepers’, warning, however, that they should take robust travel histories from any patient presenting with fever associated even with mundane complaints such as toothache or earache. Netcare has developed a set of comprehensive clinical pathways that are used routinely as a precautionary measure by its emergency medical staff, doctors and hospital staff to assess any patient exposed to risk factors associated with VHF. Asked why he thought the situation in Liberia had deteriorated so quickly, Medina-Marino said the civil war had ‘decimated’ its’ health infrastructure, leaving the government starved of resources to deal with the scale of the outbreak.

Another aggravating factor was sociocultural: because of the war, communities distrusted any government intrusion, refusing health authorities permission to remove dead bodies.

In Liberia’s war-ravaged northern Barkadu district, communities actually barricaded themselves. Health officials, only admitted after a fortnight, discovered 20 bodies and 15 people near death. ‘Basically they didn’t believe Ebola was real and only called for help when they were scared witless. Similar stories abound in Sierra Leone and Guinea,’ he said. Another major issue was the unprotected washing, embalming or dressing of bodies as part of the pre-funeral rites. At burials many mourners also touched the body as a ‘final farewell’. ‘How do you tell these communities to stop their traditions?’ he asked. Another tragic and almost unavoidable problem was Ebola-infected children – if a child is vomiting or sick, how do you tell a mother or father not to touch them?

Ebola spread in war-torn Liberia ‘out of control’

By the time Medina-Marino left on 9 August, the situation in Liberia was ‘completely

out of control’. He said that the unique and unprecedented nature of the current widespread, urban West African outbreak (previous outbreaks in rural East Africa had been geographically ‘clustered’) meant there were ‘no models to deal with this’. He believes that the widespread SA XDR TB epidemic is analogous to the West African Ebola outbreak in terms of comparing public health responses in the absence of any available medical intervention.

Both Benson and Blumberg agreed that healthcare workers were at greatest risk.

Ebola, the onset of which is sudden and severe, is only infectious when its carrier is symptomatic and ill (and for some time after death). It typically only spreads via contact with bodily fluids and infected tissue. These include blood, vomit, faeces, sweat, saliva, tears, urine and (least likely, though feasible) semen. Unprotected home care settings, low hygiene awareness and the tradition of washing the newly dead mean that it wipes out entire families and communities, with the spread amplified in hospitals with poor infection control practices.

Thermal scanning more political than pragmatic

She said that thermal scanning at airports was relatively ineffective, as somebody incubating the virus could be asymptomatic.

Its ‘yield’ was infinitesimally low, and it was far more political than pragmatic.

Meanwhile, the SADC ministers of health plus the regional SADC and WHO officials held an emergency meeting in Johannesburg on 6 August to collaborate on critical Ebola detection, prevention and control strategies, releasing a lengthy statement of intent.

Izindaba has established that the four known Ebola cases air-lifted to the USA and Spain for treatment (one died, three were ‘improving’) were foreign healthcare workers and/or missionaries. Their treat­ment on home soil with the promising but experimental drug Z-Mapp (and that of a select few West African patients) sparked controversy, given that more than 1 900 Africans have died without access to existing (low) stocks. However, medical ethicists pointed to Z-Mapp’s untested nature, saying that public health measures should be paramount.

At the time of writing, the Ebola death toll in the then newly affected Democratic Republic of Congo had reached 31, albeit from a different strain to that in West Africa.

Chris Bateman chrisb@hmpg.co.za

Dr Medina-Marino with a volunteer helper and Ebola survivor (he presented early). Picture source: Dr Medina-Marino.

655

October 2014, Vol. 104, No. 10

S Afr Med J 2014;104(10):653-655.

DOI:10.7196/SAMJ.8894

IZINDABA

Dismal obs/gynae training contributing to maternal deaths – Motsoaledi The local standard of training in obstetrics and gynaecology has dropped so dramatically that ‘an ordinary caesarean section is now like brain surgery for most interns’, says national health minister Dr Aaron Motsoaledi. His claim, made at the South African Medical Association (SAMA)’s Millennium Development Goals (MDGs) conference in Durban at the end of August, was bolstered by one of the world’s top maternal mortality researchers, Prof. Jack Moodley, Chairperson of the National Committee on Confidential Enquiries into Maternal Deaths in South Africa (SA) and editor of ten local ‘Saving Mothers’ reports.

caesarean section (CS) deaths was a worrying trend, and urged the newly appointed district clinical specialists to ‘take a more handson role in training people’. Clinical heads of academic units should also urgently ensure that interns and medical officers were better versed in performing CSs: ‘in fact we’ll insist that specialists take an intern through a C-section [in future]. If you ask any specialist if they’ve trained an intern, the answer usually is “I’m too busy”. I’m not sure if they’re too busy in limited private practice (RWOPS),’ he added. Top medical academics consulted by Izindaba said that neither a community service officer nor a medical officer should be required to perform a CS in the public sector unless fully equipped and trained. ‘Otherwise you’re just asking for trouble,’ said one.

RWOPS controversy flares up again

World authority on maternal health, Emeritus Professor Jagidesa (‘Jack’) Moodley. Picture: Chris Bateman.

Moodley, the SA doyen of hypertensive disorders during pregnancy, told delegates that the latest (yet to be released) mater­ nal mortality data show a worrying new trend – a spike in the number of mothers dying in consultant-served regional hospitals v. district hospitals (where this would be more predictable). ‘I don’t know whether it’s a function of RWOPS-induced lack of consultants or just the paucity of consultants, or a combination of both,’ he added (RWOPS stands for remunerative work outside the public sector). He said that an increase in

The mere linkage of RWOPS to possible increased maternal deaths in regional hospitals – while the country’s horrific overall maternal death rate declines at a pace that will fall way short of the MDG target by the end of next year – is akin to pouring petrol on the coals of a long-simmering controversy in the medical profession. Motsoaledi firmly believes that the increase in maternal deaths at regional hospitals is at least partly due to consultants often not being available to train and supervise interns, junior doctors and registrars in crowded public sector maternity wards – because they’re too busy in private practice doing RWOPS. He told the SAMA doctors that he had decided he would have to speak urgently with the deans of medical schools, especially in the fields of obstetrics, gynaecology and anaesthetics, and promised to release a report within the next two months. ‘Unless we deal with these issues, we’ll lose the battle all over again,’ he added.

Moodley confided to Izindaba after his presen­ tation that what aggravated the unavailability of doctors in the public sector (but perhaps improved the junior learning curve) was the practice of consultants taking juniors with them to conduct RWOPS.[1] The minister and his chief maternal deaths advisor are arguably the most pivotal medical professionals in the much-needed acceleration in saving pregnant women’s lives. Motsoaledi said last year that RWOPS was costing lives[2] – but this is the first time

656

October 2014, Vol. 104, No. 10

any of his confidential enquiry committee’s unreleased data have been linked to his claims. Asked for his ‘diagnosis’ of the decline in healthcare worker training standards as he left the conference, he shot back: ‘One word: RWOPS!’

Medical schools deans still pondering RWOPS

Motsoaledi is currently awaiting compre­ hensive recommendations from the Committee of Deans of Medical Schools on how to prevent abuse of the RWOPS system after the issue ruptured into the public domain half way through last year – with some provincial health MECs mounting near witch-hunts, accompanied by specialist resignations, official threats and nearslanderous accusations on both sides.[2,3] A cloud still hangs over scores of consultants under investigation in various provinces, with several senior provincial officials and health politicians stubbornly resisting any suggestion of ‘wiping the slate clean’ in return for an undertaking by the profession to act promptly and decisively against future offenders.

He criticised the private sector for its predominant lack of maternal mortality and morbidity review meetings or auditing systems.

The biggest change to the easily and widely abused current set-up will probably be a standardised protocol across provinces with line managers being held directly responsible for ensuring consultants work their minimum 56 hours per week (40 hours plus 16 hours of paid overtime). Motsoaledi, if satisfied, is expected to table such amendments in parliament as a white paper for final enactment, a process that could take 2 years or more.

Not only is RWOPS (as practised by some) causing dissension and fall-out among doctors themselves and costing the state hundreds of millions of rands in, for example, botched CSs and adverse birth-related events, but some line managers are reluctant to confront longserving senior colleagues, effectively ‘turning a blind eye’ and resulting in abusive RWOPS practice becoming close to the norm in several regional and tertiary hospitals.[4] The system was introduced 14 years ago in an effort to

IZINDABA

recruit and retain clinical skills in the public health sector, especially among the more senior specialists who were not earning good salaries at the time. However, this changed in 2009 when the government reviewed salary packages, introducing the controversial Occupation-Specific Dispensation (OSD), which significantly bumped up the incomes of the most junior and the more senior doctors.

The latest salary scales, updated in April last year, show that a newly qualified specialist will earn R747 674 per annum plus R200 000 per annum for 16 hours of commuted overtime each week. After 5 years the annual salary will be around R854 751 plus R200 000 overtime.

This has lent weight to accusations that absences from public sector consultancy posts (where up to 80% of the population is served) are motivated by financial greed.

‘We came out of the starting blocks late’ – Motsoaledi

Motsoaledi expressed regret at his depart­ ment’s having only followed the recommen­ dations of the three ministerial committees (confidential enquiries into the commonest causes of maternal, perinatal and under-5 deaths, set up in 2002) in 2009. ‘We came very late out of the starting blocks,’ he admitted.

Moodley and his fellow researchers found that HIV/AIDS, obstetric haemorrhage and hypertension are the three main causes of maternal deaths. A full 40% of all maternal deaths are due to HIV, making screening of all HIV-positive pregnant women for pneumonia and tuberculosis a top priority. Obstetric hemorrhage, while highly preventable, was ‘a battle we can’t seem to win’. Moodley singled out deaths due to haemorrhage associated with CSs, saying this ‘might imply’ that too many CSs were being done (an overall rate of 25% in the public sector and 65% in the private sector). What he said he was certain about was that more complications were likely with CSs. In the public sector his teams’ research showed the procedure to be associated with poor surgical technique: ‘so we’re not training our doctors well to do CSs’, he stressed. Decisions about when to do the procedure were probably made too late, resulting in death or disability for the mother and/or infant, he added. SA’s private sector should have a maternal mortality rate similar to that in the UK (8.2/100 000 women), ‘as our equipment and resources here are as good, if not better’. However, the local private sector maternal mortality rate stood at about 40/100 000 women. He criticised the private sector for its lack of maternal mortality and morbidity review meetings or auditing systems. ‘I’ve been going around cajoling them to report all maternal deaths and giving them

SAMA Chairperson Dr Mzukisi Grootboom, Health Minister Dr Aaron Motsoaledi and SAMA President Prof. Ames Dhai. Picture: Chris Bateman.

reasons why we want to record,’ he added. His experience from these visits was that doctors did not attend peer review meetings.

Asked for his ‘diagnosis’ of the decline in healthcare worker training standards as he left the conference, national health minister, Dr Aaron Motsoaledi shot back ‘One word: RWOPS!’ Moodley appealed to SAMA to ask itself how it could get private doctors to attend such meetings and learn from their faults – and to urge doctors to attend the Essential Steps Management of Obstetric Emergencies (ESMOE) course, plus encourage the team training of doctors and nurses. Combined, these measures had the potential to reduce maternal deaths dramatically. Moodley said the entire point of his talk was to explore how his audience and the healthcare profession in general could help reduce maternal deaths ‘without apportioning blame and dishing out punishment’.

Maternal deaths highly preventable

‘We’re here to learn, and hopefully minimise future maternal deaths,’ he said, stressing that in 60% of these deaths there was an avoidable factor – with this figure in anaesthetics and obstetric haemorrhage standing at 90% and 80%, respectively. Moodley warned against the high risk of ‘single-operator CSs’ in district hospitals, where many GPs conducted spinal blocks. The argument is often made that the critical shortage of doctors (and anaesthetists) means this is virtually unavoidable. Moodley’s answer is to reassign CSs to centralised hospitals. ‘There are some hospitals that do so few CSs that they shouldn’t be doing them at

657

October 2014, Vol. 104, No. 10

all,’ he warned. Motsoaledi said that although Moodley’s committee had made ‘the three Hs famous’, he had another two to add. These were healthcare worker training and health system strengthening.

The maternal mortality MDG goal is to reduce the maternal mortality ratio by threequarters between 1990 and 2015. Maternal deaths per 100 000 live births in SA stood at 150 in 1998, climbing to a peak of 312 in 2009 before dropping to 269 in late 2010 – as the findings of Moodley’s team began to be acted upon. SA’s MDG target for next year is 38, which Motosaoledi describes as ‘a possible or impossible dream’.

Prof. Ames Dhai, SAMA President and Head of the Steve Biko Centre for Bioethics at the University of the Witwatersrand, said that Moodley’s presentation showed either a ‘lack of care or negligence’ among doctors.

‘We don’t have sufficient role models in our academic institutions to ensure professionalism and we concentrate too much on the clinical aspects,’ she added.

SAMA chairman Dr Mzukisi Grootboom said that the drop in training standards was a ‘serious challenge’ which SAMA would be taking up to ensure ‘that those who come after us are educated to make the profession relevant’.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2014;104(10):656-657.

DOI:10.7196/SAMJ.8905 1. Bateman C. RWOPS abuse ‘eroding ethical standards of juniors’.

S Afr Med J 2013;103(8):505-506. [http://dx.doi.org/10.7196/ SAMJ.7165] 2. Bateman C. RWOPS abuse – Government’s had enough. S Afr Med J 2012;102(12):899-901. [http://dx.doi.org/10.7196/ SAMJ.6481] 3. Bateman C. RWOPS clampdown – a crisis in the offing. S Afr Med J 2013;103(6):361-364. [http://dx.doi.org/10.7196/ SAMJ.7029] 4. Bateman C. RWOPS – light at the end of a dusty tunnel. S Afr Med J 2013;103(12):888. [http://dx.doi.org/10.7196/SAMJ.7693]

IZINDABA

New partnership stands to save millions of mothers and children Two of several health inno­ vations that could save the lives of millions of mothers and babies will probably reach the South African (SA) market first – years ahead of schedule – because of a new partnership between the government, the South African Medical Research Council (MRC) and a leading international NGO. With postpartum haemorrhage the lead­ ing cause of maternal mortality worldwide, the first innovation is a breathtakingly simple improvement on the first-line preventive medicine currently in use – the heat-sensitive injectable oxytocin. The intended product, a pill formulation, solves the longstanding dilemma of storage and supply chain management of liquid oxytocin in rural and/ or under-resourced areas, where most of the deaths occur. Not only will the prospective heat-stable ‘under-the-tongue’ fast-dissolving oxytocin pill be easier to store and manage, but less-skilled healthcare workers will be able to administer it, enabling quicker, better and more accessible prevention and treatment all round. The fixed-dose presentation has proved highly successful in animal studies and can withstand temperatures of up to 40oC for several months, making it ideal for tropical and subtropical climates, where most maternal deaths occur.

Cutting R&D-to-market time by two-thirds

Developed by PATH, international non-profit leader in global health innovation, this is but one example of how products and devices can benefit from a health innovation accelerator initiative and partnership. PATH has now teamed up with SA’s Department of Science and Technology and the MRC to apply the same booster principles locally, prioritising key gaps in maternal and infant health. PATH are specialists in accelerating innovation for vaccines, drugs, diagnostics, devices, systems and services, typically applying their knowledge and channelling funding to cut research and development-to-market time by up to twothirds. On average, it takes up to 15 years for a product to reach the market. SA’s track record and successes in these fields make it the ideal partner, enabling PATH to accelerate clinical trials and regulatory approval and bring products to scale far sooner than would otherwise have been the case.

MRC President Prof. Glenda Gray, Dr Ayo Ajayi, PATH’s Vice-President of International Development, and Dr Nonhlanhla Dlamini, Chief Director of Child, Adolescent and School Health, NDoH. Picture: Chris Bateman.

One local example of why PATH has quietly invested over R3.5 million in MRC activities over the past 3 years is a Stellenbosch University medical school-developed dev­ ice called the ‘Umbiflow’, a mobile and highly versatile Doppler waveform analyser measuring placental insufficiency in small-for-gestational-age babies in the third trimester. In MRC President Prof.

Glenda Gray’s estimation, this would be the second of the two accelerated innovations to hit the local market first. Priceless in enabling early identification of potential birth problems and almost certain to generate major savings by avoiding unnecessary upward referrals, the Umbiflow was developed by the MRC and the Council for Scientific and Industrial Research (CSIR) under a grant from the former Innovation Fund, a Department of Science and Technologyfunded vehicle established to support local innovation. The machine detects blood flow within the umbilical cord, ascertaining placental function via a hand-held probe (similar to a sonar scan), but is connected with a USB cable to any Windows-based computer. By installing the necessary software, an integrated 3G card enables a mobile internet connection and automatic upload of exam results to a central server for remote expert support and electronic health record management. PATH will help accelerate the project even further, supporting continuing evaluation and subsequent implementation in antenatal facilities country-wide, with potential adoption by health systems across the African continent.

658

October 2014, Vol. 104, No. 10

Leading by example with life-changing products and meds

Speaking at the launch of the MRC-PATH Global Health Innovation Accelerator (GHIA), Dr Ayo Ajayi, PATH’s vice-president of international development, lauded SA’s culture of innovative research dating back to Chris Barnard’s first human-to-human heart transplant in 1967. He summed up PATH’s mission as ‘to get the best ideas and solutions and to translate and implement them where they can do the most good’, taking innovations to scale to tackle the greatest health needs.

He said that SA’s deep expertise in vaccine development, drugs and devices made it the ideal partner to ‘add the multiplier effect’ by doing what PATH did best: getting involved in the middle stages of development, or the value chain. Globally PATH had reached 290 million people through various technological innovations so far, one of the most impressive being a meningitis A vaccine to which 153 million people across the 26 African countries where the disease is prevalent have had access over the past 4 years – its Indian manufacturer willing and able to churn it out for under 50 cents a dose. With the help of the World Health Organization, the vaccine was produced at one-tenth of the ‘normal’ research and development costs-to-market.

Another notable PATH success story is the vaccine vial monitor, a tiny sticker put on vials of vaccine that changes colour when exposed

IZINDABA

to heat. Healthcare workers can tell at a glance whether heat-sensitive drugs are damaged.

Ajayi said that more than five million stickers had been used worldwide so far.

Why we need life-saving innovation for mothers and babies

Speaking at the 8 August launch of the GHIA, Dr Nonhlanhla Dlamini, Chief Director of Child, Adolescent and School Health in the National Department of Health, illustrated just how badly needed effective new solutions are.

She said that one-third of the country’s under5 child mortality figures were due to just three newborn causes: prematurity, infection and birth asphyxia. ‘If we can get a handle on these, we can overcome newborn deaths,’ she asserted. Broader under-5 mortality causes included diarrhoea, pneumonia, AIDSrelated illnesses and tuberculosis. She said that 65% of children who died in SA were malnourished, prompting the current African Union-funded infant and young child feeding policy. Recent innovations that were proving a huge success included the locally developed human papillomavirus vaccine, currently being administered with parental permission

to all girls in grade 4 at state schools (3 000 SA women a year die of this cancer). The subdermal contraceptive implant was also being offered to girls who could legally opt to use it (from the age of 12). Of the one million women who fell pregnant in SA annually, 8% were girls below the age of 18. These minors were giving birth to 80 000 unplanned babies annually, contributing to 36% of all maternal deaths, with their youth contributing to fatalities. Dlamini said that other new vaccines added to the preventive arsenal (in 2009) were the rotavirus and pneumococcal vaccines. Their efficacy was vividly illustrated by the MRC’s own rapid mortality survey this year, which showed a drop in the under-5 mortality rate from 56/1 000 children in 2009 to 41/1 000 in 2012.

Local products making global impact

Dr Phil Mjwara, Director-General in the Depart­ ment of Science and Technology, said among the projects currently being piloted was an earlywarning computer system for infectious diseases in Limpopo Province, including meningitis and water-borne diseases. Several companies had been born out of research efforts, including

Kapa Biosystems, which had developed rea­ gents and kits for a number of DNA analysis applications such as real-time polymerase chain reaction (PCR) and high-fidelity PCR and molecular diagnostics. This company, which now exports its products, had expanded its local manufacturing base and research and development operations. Another major success story was Altis Biologics, which is on the verge of registering its regenerative biological implants as a fast and safe alternative to surgery for bone trauma patients. The injectable product was one of the most commercially viable and promising innovations he’d seen, winning the 2014 Innovation Prize Africa Award. Mjwara said that his department’s collaboration with PATH and the MRC would ‘benefit us tremendously as we seek to address the challenges of know­ ledge translation for South Africans’. The initial focus of the partnership would save ‘millions’ of vulnerable women and children in the country, he added.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2014;104(10):658-659.

DOI:10.7196/SAMJ.8887

BHF and Government: ‘I’ll change if you’ll change’ While government and private healthcare funders urged one another to make internal changes to enable faster progress towards a more equitable healthcare system, some concrete evidence of vitally needed partnership did emerge from the 15th annual Board of Healthcare Funders (BHF) conference.

Firstly, the 24 - 27 August conference in Durban, attended by over 900 delegates from all sectors of the healthcare funding industry, heard that the government’s new Essential Drugs List (EDL) Committee will include representatives of the private healthcare funding industry to finally obtain consensus on just which essential medicines should be available to patients.

Secondly, a blueprint on how the National Department of Health (NDoH) can partner with the private healthcare funding sector in conducting economic evaluations of products to save both sectors time and money (and avoid longstanding unnecessary duplication) has been drawn up – by no less than the NDoH itself.

National Health Minister Dr Aaron Motsoaledi

also pleaded with delegates to ‘embrace change’, warning that they would be hardest hit by the ‘exploding’ epidemic of non-communicable diseases if they failed to introduce health promotion and disease prevention measures.

Government promises National Health Commission

Motsoaledi said that reducing risk factors such as smoking, alcohol abuse, obesity and lack of exercise would be the focus of a National Health Commission he would be setting up in the near future. Chaired by Deputy President Cyril Ramaphosa, and assisted by the country’s top healthcare academics, business executives from the private and public health sectors and civil society, the commission would advise him on the most effective ways to stop the country’s escalating disease burden. This will be a groundbreaking first – given that some of the top medical aids he was addressing are world leaders in wellness and disease prevention programmes and have been itching to share their expertise for years. Motsoaledi

659

October 2014, Vol. 104, No. 10

said that inefficiencies in the private and public sectors were caused by different things. While he was ‘trying’ to resolve the poor quality of care in the public sector, ‘exorbitant fees’ in the private sector rendered it too expensive – and therefore inefficient. He either failed to discuss, or deliberately avoided discussing, the long-awaited White Paper on National Health Insurance (he did say that universal health coverage was a ‘global phenomenon’ and there was ‘no walking away from it’). Nor did he venture into the political quicksand of the complexities behind high private sector costs, possibly because stalled government regulation (and deregulation) are chief among them.

Christoff Raath, joint CEO of Insight Actuaries and Consultants, had no such aversion.

Unchain us, so we can help cover lives – top actuary

Hammering home now-persistent private sec­ tor pleas, Raath singled out the 25% sol­ vency rate medical schemes must adhere to, the hugely expensive current Prescribed

IZINDABA

Christoff Raath, joint CEO of Insight Actuaries and Consultants.

Minimum Benefits (PMBs), and the selfsustaining requirement that makes it illegal for schemes to implement risk and income cross-subsidies across options. He said without such cross-subsidisation and ‘some form’ of mandatory cover, the requirements for open enrolment, community rating and full payment of PMBs were threatening the very sustainability of the medical scheme industry.

If just cross-subsidisation and mandatory cover were implemented or allowed, medical schemes could more easily ‘come to the party’, helping facilitate some form of universal coverage towards an overall National Health Insurance (NHI) goal. Illustrating just how much pressure the private sector could take off its public counterpart (while helping achieve greater healthcare access and equity), he said that medical schemes had the ability to cover between two and four million additional lives.

However, the current regulatory environment allowed very little scope for further growth or innovation, actually impeding the expansion of coverage to the 83% of the population that is not insured, and adding to the burden on state healthcare facilities.

Incremental change: beyond the ‘big reform mindset’

Echoing a theme punted by actuarial colleagues at last year’s Hospital Association of South Africa (HASA) congress, Raath said that government’s decision to suspend its initial healthcare reforms halfway through its planned trajectory towards universal coverage (with the introduction of the NHI plans negating everything else) had resulted in ‘an incomplete, semi-designed system in which health cover is becoming increasingly unaffordable’. There was no incentive for growth, as the risks for growth in the current not-for-profit environment outweighed the potential benefits of growth.

Expanding on the 25% solvency requirement,

he said it impacted directly on affordability and growth because new or growing medical schemes could only achieve such reserve levels by raising premiums. He estimated that last year alone, between 1.5% and 2% of medical schemes’ total contribution increases could be attributed to having to meet this solvency requirement. He said that between the country’s two biggest medical schemes, Discovery Health and GEMS, around R24 billion was needed to meet this requirement.

Raath said that even the Council for Medical Schemes agreed there was no scientific basis for the 25% solvency requirement, which he said made the situation ‘very distressing’.

PMB conditions, per member per month, cost an estimated R550 - 1 000, negatively affecting healthcare affordability. Citing the Low Income Medical Scheme (LIMS) study in 2006, he said that people in low-income groups wanted and could afford to pay between R150 and R200 (R280 and R300 in today’s prices) for a primary care package – including GP visits, optometry, medication and dental – and that they preferred a primary care package to tertiary cover. The government’s attempt to move towards universal coverage would require a complete reconsideration of PMBs, which he described as ‘unaffordable, prone to abuse from providers’ and not meeting the needs of lower-income groups. Raath urged the private healthcare industry to ‘look beyond the big reform mindset’ and instead implement incremental improvements that allowed it to move in the direction of government’s objective of universal coverage.

Regulate reimbursement, bring back our ‘gatekeepers’

Dr Anban Pillay, NDoH Deputy DirectorGeneral: Health Regulatory and Compliance Management, singled out for criticism the lack of any current incentives to provide primary care benefits and the virtually unlimited private hospital benefits, saying that SA was unique in this respect. ‘Where else are patients allowed direct access to high-cost specialists without any referral?’ he asked, urging medical schemes to consider returning the ‘gatekeeper’ function to primary healthcare providers. He said that two of the main cost drivers were the lack of a proper patient referral system and the absence of a regulated reimbursement model.

Aligning PMBs to the proposed NHI system’s focus on primary health, harmonisation of treatment guidelines for disease management, using public hospitals in selected cases and increasing access to primary healthcare medicines were all ‘rich with opportunity’ for public-private partnership. This would address

660

October 2014, Vol. 104, No. 10

cost and efficiency issues in both sectors, Pillay added, saying that an effective primary healthcare system could reduce hospital use and lead to lower premiums for members. ‘You should also consider a system where schemes partner with government to deliver PMBs’, he suggested. The current demarcation process provided ‘huge opportunities’ for medical schemes to increase their memberships – if they were able to design options catering for the needs of the broader public and affordable to those who previously bought low-cost insurance products to cover their medical expenses.

Dr Anban Pillay, the NDoH’s Deputy DirectorGeneral: Health Regulatory and Compliance Management.

‘Waves of change, oceans of opportunity’ – BHF’s Zokufa

Dr Humphrey Zokufa, Managing Director of the BHF, said that evaluations of the prospective EDL committee would not be enforced but rather treated as an objective tool that could be used ‘as a departure point for fairness in benefit design’. Asked about the government’s failure to implement the Risk Equalisation Fund and letdown on introducing mandatory membership, his response was diplomatic (the conference theme was, after all, ‘Waves of Change, Oceans of Opportunity’): ‘We don’t want to position the BHF in such a way that it works against the waves of change, but rather works with it to ensure that decisions are going in the right direction.’ In doing so, the BHF would be in a position to see the ‘oceans of opportunities’ ahead. He urged both sectors to build bridges rather than increase tension by seeing themselves as two separate entities. The ‘way forward’ would be through public-private partnerships and the creation of centres of excellence that rendered affordable treatment of previously high-cost diseases, he concluded.

Chris Bateman chrisb@hmpg.co.za S Afr Med J 2014;104(10):659-660.

DOI:10.7196/SAMJ.8886

TJDR (CT) 40674/E

WE’RE OBSESSED WITH THE FUTURE. AT MEDICLINIC, OUR DECISIONS ARE CALCULATED. OUR ACTIONS ARE CONSIDERED. WE SHARE EXPERT KNOWLEDGE AND COLLECTIVE SKILL FROM OUR HOSPITALS AROUND THE WORLD. WITH THIS KNOWLEDGE, WE CAN CONTRIBUTE TO A FUTURE HEALTH SYSTEM IN WHICH VERIFIABLE, COST-EFFECTIVE QUALITY HEALTHCARE WILL NOT BE COMPROMISED.

EXPERTISE YOU CAN TRUST. SOUTH AFRICA • SWITZERLAND • UAE • NAMIBIA www.mediclinic.co.za

FORUM

OPINION

Preventing diabetic blindness: A priority for South Africa K J Hofman, C Cook, N Levitt Karen Hofman is a medical graduate of the University of the Wit­watersrand, Johannesburg, South Africa, and a paediatrician. She is Director of PRICELESS SA (Priority Cost Effective Lessons for Systems Strengthening), focused on ‘best buys’ in public health and based at the Medical Research Council/Wits Rural Public Health Unit (Agincourt) in the School of Public Health, Faculty of Health Sciences, University of the Witwatersrand.

Colin Cook is a graduate of the University of Cape Town, South Africa, and Morris Mauberger Professor of Ophthalmology in the Department of Surgery, Faculty of Health Sciences, University of Cape Town and Groote Schuur Hospital, Cape Town. Dinky (Naomi) Levitt, also a UCT graduate, is Head of the Division of Diabetes and Endocrinology in the Department of Medicine at UCT and Groote Schuur Hospital and Director of the Chronic Diseases Initiative for Africa, Cape Town.

Corresponding author: K J Hofman (karen.hofman@wits.ac.za)

The prevalence of diabetes in South Africa is increasing rapidly, and diabetes is a significant cause of blindness. Diabetic complications can induce a cycle of poverty for affected families. Early detection of retinopathy and appropriate management can prevent blindness. Screening for retinopathy using a mobile retinal camera is highly cost-effective, with costs of screening and follow-up treatment being less than the expense of one year of a disability grant. Such a programme is a prime example of a ‘best buy’ that should be part of the national diabetes care package.

S Afr Med J 2014;104(10):661-662. DOI:10.7196/SAMJ.8580

Around 300 million people worldwide are affected with diabetes, and this number is forecast to increase to over 550 million by the year 2030.[1] Of those affected, 80% live in low- and middle-income countries (LMICs).[1] In South Africa (SA), the prevalence of type 2 diabetes rose from 5.5% in adults in 2000 to 9.0% in 2009. Currently approximately 2 million South Africans live with type 2 diabetes, with a projected 115 000 new cases per year.[1] It is of concern that about 55% of people with diabetes are likely to suffer from diabetic retinopathy.[2] Diabetes is the third leading cause of blindness in SA, with retinopathy and cataracts[2] accounting for 8 000 new cases of vision impairment every year. In a 2010 survey in Cape Town, diabetic retinopathy was responsible for 8% of blindness and 11% of severe visual impairment.[3] In LMICs, including SA, diabetic blindness creates a poverty cycle that disables breadwinners and burdens caregivers. The fact that timely treatment of diabetic retinopathy can reduce the risk of visual impairment by 90%[2] implies a need for screening and early detection. The Ophthalmology Society of South Africa has recommended a strategy for diabetic retinopathy screening using a validated grading system, an internet-based database and tracking system, and a patient-held ‘scorecard’.[4] In 2007, a pilot study in Cape Town evaluated the impact of mobile fundus photography to screen for diabetic retinopathy.[5] Following the screening, an ophthalmic specialist reviewed the photographs and if necessary referred the patient. This proved effective and allowed a single technician to screen about 10 000 patients annually, suggesting that scaleup is feasible.

Despite this, a systematic review revealed a lack of information on the cost-effectiveness of using mobile fundus cameras as a screening method.[6] In response, PRICELESS-SA and collaborators measured the prevalence of type 2 diabetes and its associated complications in SA based on 2009 data.[7] Using these estimates together with data from the pilot project, modelling was performed on the cost and consequences of using a mobile fundus camera in a primary care setting.[7] Screening via camera alone cost an average of ZAR189 per person, including followup operation procedures, ranging from a lower limit of ZAR10 500 to an upper limit of ZAR23 327 per case of blindness averted.

661

Relevance to policy

Advocacy for preventive screening of diabetic retinopathy intersects early stages in the development of SA’s National Health Insurance (NHI). As the NHI will not cover diagnostic procedures outside its approved guidelines and protocols, it is essential that screening for diabetic retinopathy be considered for scale-up nationally and therefore for inclusion in these guidelines. At present, screening for retinopathy at primary care level is almost non-existent, despite current guidelines recommending annual screening.[6,8] In addition, ophthalmic referral and treatment in the form of laser therapy and operations are reserved for the tertiary care sector.[9] Difficulty of access to screening and treatment of diabetic blindness is exacerbated by the 55% of diabetic patients who remain undiagnosed.

The government provides support through monthly disability grants for the blind, totalling ZAR12 120 per year per blind person.[10] In comparison, the cost-effectiveness study showed that the ZAR10 500 per blindness case averted is less than the expense of one year of a disability grant. Prevention of blindness would also extend the number of working years for every diabetic patient. The use of mobile fundus cameras has huge savings potential compared with the current situation of diabetes treatment and disability coverage.

International comparisons

Canadian researchers found fundus cameras to be cost-effective compared with their alternative specialist-based programme. Camera screening saved 67 sight-years at US$3 900 per sight-year, while the alternative programme saved only 56 sight-years at US$9 800 per sightyear.[11] Although the SA pilot project was performed in an urban setting, similar projects in rural communities in Australia[12] and France[13] proved to be effective. US researchers[14] have also built a prototype mobile fundus camera that will cut costs significantly and potentially make screening for diabetic blindness even more cost-effective. Smartphone technology that might allow screening for diabetic retinopathy using mobile phones is now being tested elsewhere in Africa.[15] International examples show that camera screening for diabetic vision impairment is successful at a national scale. Such systematic screening

October 2014, Vol. 104, No. 10

FORUM

has been established in Iceland for over 30 years. In 1980, 2.4% of Iceland’s population was legally blind, but by 2005 the prevalence had dropped to 0.5%.[16] Similarly, Israel’s prevalence of preventable blindness dropped by half from 33.8/100 000 in 1999 to 16.6/100 000 in 2008.[17] These declines can be attributed to the availability of treatment and preventive measures and illustrate the importance of implementing treatment guidelines for diabetic vision impairment.

In sub-Saharan Africa, countries have utilised other alternatives by task-shifting cataract operations from ophthalmologists to nonphysician cataract surgeons (NPCSs). NPCSs in Kenya, Tanzania and Ethiopia, for example, performed over 77 000 operations in 2000 - 2004.[18] Results showed no difference between specialised ophthalmologists and NPCSs in respect of the quality of surgeries conducted.[19] Although the use of NPCSs is not widely accepted, they represent a cost-effective alternative solution. Laser treatment for diabetic retinopathy by appropriately trained doctors at secondary level and district hospitals would be a feasible solution to deal with diabetic retinopathy-related blindness in SA.

‘Best buys’ for policy makers

Under the current economic circumstances, every ZAR must work more effectively, efficiently and equitably. In order for the SA government to discern a ‘best buy’ among cost-effective options, it needs access to valid, reliable and comparable information on costs and consequences of policy alternatives. International examples do provide useful information, but this must be complemented by local context-specific evidence. Prevention interventions offer particularly good value, as they produce the largest gain.

Conclusion

The use of mobile fundus cameras to screen for diabetic vision impairment is a paradigm of an innovative approach to achieve economies of scale to reduce preventable blindness effectively on a national level. The use of mobile fundus cameras would interface well with the screening strategy recommended by the Ophthalmology Society of South Africa. One of the challenges for the evolving NHI

is how value for money and affordability can be balanced across competing priorities. This approach is one example of a ‘best buy’ that could potentially be incorporated in a diabetes care package.

1. Bradshaw D, Norman R, Pieterse D, Levitt NS. Estimating the burden of disease attributable to diabetes in South Africa in 2000. S Afr Med J 2007;97(8):700-706.

2. Bertram MY, Jaswal AV, Van Wyk VP, Levitt NS, Hofman KJ. The non-fatal disease burden caused by type 2 diabetes in South Africa, 2009. Glob Health Action 2013;6:12944. [http://dx.doi.org/10.3402/gha.v6i0.19244] 3. Cockburn N, Steven D, Lecuona K, et al. Prevalence, causes and socio-economic determinants of vision loss in Cape Town, South Africa. PloS One 2012;7(2):e30718. [http://dx.doi.org/10.1371/ journal.pone.0030718] 4. Cook S. Diabetic retinopathy – the Ophthalmology Society of Southern Africa screening programme.

S Afr Med J 2013;103(7):449-451. [http://dx.doi.org/10.7196/samj.7136] 5. Mash B, Powell D, Du Plessis F, Van Vuuren U, Michalowska M, Levitt N. Screening for diabetic retinopathy in primary care with a mobile fundal camera – evaluation of a South African pilot project.

S Afr Med J 2007;97(12):1284-1288.

6. Jones S, Edwards RT. Diabetic retinopathy screening: A systematic review of the economic evidence.

Diabet Med 2010;27(3):249-256. [http://dx.doi.org/10.1111/j.1464-5491.2009.02870.x] 7. Khan T, Bertram MY, Jina, R, Mash B, Levitt N, Hofman K. Preventing diabetes blindness: Cost effectiveness of a screening programme using digital non-mydriatic fundus photography for diabetic retinopathy in a primary health care setting in South Africa. Diabetes Res Clin Pract 2013;101(2):170176. [http://dx.doi.org/10.1016/j.diabres.2013.05.006] 8. Guideline Committee. 2012 SEMDSA guideline for the management of type 2 diabetes mellitus.

Journal of Endocrinology, Metabolism and Diabetes of South Africa 2012;17(1):S1-94.

9. Department of Health, Republic of South Africa. Strategic Plan for the Prevention and Control of NonCommunicable Diseases 2013-7: 57. Pretoria, 2013. http://www.hsrc.ac.za/.../NCDs%20STRAT%20 PLAN%20%20CONTENT% (accessed 15 August 2014).

10. Department of Social Development. Disability Grant. http://www.dsd.gov.za/index.php?option=com_ content&task=view&id=112 (accessed 15 August 2014).

11. Maberley D, Walker H, Koushik A, Cruess A. Screening for diabetic retinopathy in James Bay, Ontario: A cost-effectiveness analysis. CMAJ 2003;168(2):160-164.

12. Spurling GKP, Askew DA, Hayman NE, Hansar N, Cooney AM, Jackson CL. Retinal photography for diabetic retinopathy screening in Indigenous primary health care: The Inala experience. Aust N Z J Public Health 2010;34(S1):S30-S33. [http://dx.doi.org/10.1111/j.1753-6405.2010.00549.x] 13. Beynat J, Charles A, Astruc K, et al. Screening for diabetic retinopathy in a rural French population with a mobile non-mydriatic camera. Diabetes Metab 2009;35(1):49-56. [http://dx.doi.org/10.1016/j. diabet.2008.07.002] 14. Tran K, Mendel TA, Holbrook KL, Yates PA. Construction of an inexpensive, hand-held fundus camera through modification of a consumer ‘point-and-shoot’ camera. Invest Ophthalmol Vis Sci 2012;53(12):7600-7607. [http://dx.doi.org/10.1167/iovs.12-10449] 15. Peek Vision. Eye care: Everywhere. http://www.peekvision.org (accessed 25 August 2014).

16. Zoega GM, Gunnarsdóttir Þ, Björnsdóttir S, Hreiðarsson ÁB, Viggósson G, Stefánsson E. Screening compliance and visual outcome in diabetes. Acta Ophthalmol Scand 2005;83(6):687-690. [http:// dx.doi.org/10.1111/j.1600-0420.2005.00541.x] 17. Skaat A, Chetrit A, Belkin M, Kinori M, Kalter-Leibovici O. Time trends in the incidence and causes of blindness in Israel. Am J Ophthalmol 2012;153(2):214.e1-221.e1. [http://dx.doi.org/10.1016/j.ajo.2011.08.035] 18. Courtright P, Ndegwa L, Msosi J, Banzi J. Use of our existing eye care human resources : assessment of the productivity of cataract surgeons trained in eastern Africa. Arch Ophthalmol 2007;125(5):684-687. [http://dx.doi.org/10.1001/archopht.125.5.684] 19. Yorston D, Foster A. Audit of extracapsular cataract extraction and posterior chamber lens implantation as a routine treatment for age related cataract in east Africa. Br J Ophthalmol 1999;83(8):897-901. [http://dx.doi.org/10.1136/bjo.83.8.897]

Accepted 26 June 2014.

This month in the SAMJ ...

Candy Day* is a Technical Specialist in Information Dissemination at the Health Systems Trust. She is a pharmacist with a master’s degree in clinical pharmacology and subsequent training in medical informatics through the International Training in Medical Informatics Fellowship and other courses.

Over the past 18 years Candy has worked on developing information resources in the field of public health.

The current focus of her work includes monitoring and evaluation, data analysis, health systems performance assessment, and maintaining a dynamic web-based repository of South African health and related indicators.

She collaborates with international and local experts such as the World Health Organization, National Treasury, National Department of Health, Health Economics Unit and Medical Research Council. * Day C, Groenewald P, Laubscher R, Chaudhry S, van Schaik N, Bradshaw D. Monitoring of non-communicable diseases such as hypertension in South Africa: Challenges for the post-2015 global development agenda. S Afr Med J 2014;104(10):680-687. [http://dx.doi.org/10.7196/SAMJ.7868]

662

October 2014, Vol. 104, No. 10

FORUM

OPINION

Healthy migration: A public health and development imperative for south(ern) Africa J Vearey Jo Vearey, PhD, is a senior researcher with the African Centre for Migration & Society, School of Social Sciences, University of the Witwatersrand, Johannesburg, South Africa. With a commitment to social justice and the development of pro-poor policy responses, Jo’s current research explores international, regional, national and local responses to migration, health, and urban vulnerabilities.

Corresponding author: J Vearey (jovearey@gmail.com)

South Africa (SA), like the rest of the Southern African Develop­ment Community, has a high prevalence of communicable dis­eases, an increasing non-communicable disease burden, and diverse internal and cross-border population movements. Healthy migration is good for development, but current prevention, testing and treatment responses within public health systems – particularly for chronic conditions – fail to engage with migration. Understanding of migration is poor within sectors responsible for developing appropriate responses; negative, unsupported assumptions relating to the prevalence of cross-border migration, the spread of disease, and the burden on receiving health systems prevail. In SA, public health responses fail to address internal and cross-border mobilities, and non-nationals face challenges in accessing healthcare. Of particular concern is the lack of nationally and regionally co-ordinated strategies to ensure treatment continuity for chronic conditions. Co-ordinated, evidence-informed responses to migration, mobility and health are urgently needed. These will have developmental and public health benefits for all.

S Afr Med J 2014;104(10):663-664. DOI:10.7196/SAMJ.8569

Healthy migration is good for development, but migration is rarely managed in a healthy way.[1,2] Migration and mobility are recognised globally to be central determinants of health and as key concerns for public health programming, yet appropriate responses to population movements and health are lacking in the Southern African Development Community (SADC) region.[3-5] Given the historical and contemporary importance of population movements in the SADC, the high communicable disease – and increasing non-communicable disease (NCD) – burden in the region, and the knowledge that healthy migration is good for development, it is surprising that health responses do not sufficiently engage with, and respond to, migration and mobility. A large body of evidence acknowledges that the relationship between migration, mobility and health in the region is complex: while the migrant labour system was clearly implicated in the early transmission and spread of syphilis, tuberculosis (TB) and HIV (especially in relation to the ongoing systems of labour migration associated with the mines in South Africa (SA)), these dynamics have changed over time, and the association between movement and the spread of communicable diseases is less clear cut today.[4] However, prevention, testing and treatment programmes for common communicable diseases and NCDs in the SADC must be continuously available for those who move, both within countries and across borders. Key concerns in 2014 relate to the (lack of) effective management of chronic conditions for those who move. This has negative implications not only on the morbidity and mortality of a highly mobile population, but also on the healthcare systems and family structures that are forced to manage the costs associated with delayed healthcare seeking.

the world’s population are estimated to be cross-border migrants; this is also observed in SA, where – despite popular assumptions to the contrary – 3.3% of the country’s population are non-citizens.[6] Migra­ tion and movement are not homogeneous processes, and those who move form heterogeneous groups; it is exactly this complexity that public health responses in the SADC must engage with and respond to. Owing to the ways in which people move and the spaces they transit or at which they arrive, migrants may reside in – or pass through – spaces of vulnerability,[1,7,8] spaces that contain a combination of social, economic and physical conditions that may increase the likelihood of exposure to, and acquisition of, a communicable disease, or of developing an NCD. The daily stressors that may be experienced in these spaces are increasingly acknowledged to affect emotional wellbeing and mental health.[9]

The diversity of movement

Responding to migration and health

While the majority of people who move within the SADC do so within the borders of their country of birth, a smaller – yet import­ ant – number move across national borders. Globally, just over 3% of

663

Healthy migration?

Within the SADC region (as is often the case globally), healthseeking is an assumed reason for movement – yet evidence suggests otherwise; the majority move in search of improved livelihood opportunities, and to do so they need to be in good health.[5] An important phenomenon, the ‘healthy migrant effect’, is the common observation that recent arrivals are in better health than the local population, reflecting the positive selection of migrants – to move, an individual needs to be healthy.[10] However, this health benefit is seen to deteriorate, sometimes rapidly, as a result of the conditions in which migrants live and work. This is particularly the case in cities, and is mostly associated with the inability of migrants – both internal and cross-border – to access positive determinants of health in the city, a phenomenon known as the urban health penalty.[11]

When considering the development of appropriate responses to population movements and health in the SADC, it is essential that discussions do not get twisted (as they often do) into debates that

October 2014, Vol. 104, No. 10

FORUM

focus solely on cross-border migrants. As indicated above, the majority who move are internal migrants (i.e. national citizens of member states), and internal mobility is recognised as placing the greatest developmental challenges on national and local govern­ ments.[2] Despite this, the notion of ‘migration’ within the SADC region – including in SA – is often quickly (re)interpreted to refer exclusively to cross-border migration, leading to discussions of immigration management and border securitisation. When health is added to the equation, with unsupported assumptions relating to the health burden presumed to be presented by cross-border migrants and the communicable diseases they are assumed to spread, questions relating to whether non-citizens deserve public healthcare, and the rationing of healthcare services, prevail. As a result, population movement remains excluded from the development of improved health system responses to communicable and non-communicable diseases in the SADC, with negative public health consequences.

The policy context

In 2008, the World Health Assembly passed a Resolution on the Health of Migrants.[1] This resolution calls on member states (including SA) to improve responses to the health of migrants.

Meanwhile, in 2009, a Framework for the Control of Population Mobility and Communicable Diseases was drafted in the SADC. This calls for the development of a co-ordinated regional response to migration and health, including cross-border referral systems and financing mechanisms. However, SA is still to approve and ratify the framework. At the same time, the SADC HIV and AIDS Strategic Framework, 2009 - 2015, was finalised, highlighting the need to ensure that migrant and mobile populations are considered in regional responses to HIV. The year 2012 saw the ratification of the SADC Declaration on Tuberculosis in the Mining Sector, which clearly outlines the need for improved, co-ordinated regional responses to the migrant labour systems associated with SA mines, and HIV and TB.

SA responses

In SA, responses have mostly been restricted to discussions related to key populations (viewing migrants, particularly cross-border migrants, as such a group) and the country’s HIV response.

Additionally, a Migrant Health Forum (MHF) in Johannesburg (established in 2008) brings together various researchers and civil society representatives, including non-governmental, communitybased and international organisations, working on migration and health in the city. Different iterations of the MHF have, with the support of the International Organization for Migration and the Office of the Premier in Limpopo Province, been established in several districts in Limpopo.

Despite official recognition of the public health importance of ensuring timely access to health for all within legislative frameworks, non-nationals continue to face multiple, intersecting challenges when attempting to access public healthcare in SA.[1,5,12] Key challenges exist in how frontline staff – including security guards, receptionists and data clerks – engage with and treat non-nationals.

In 2014, these challenges have worsened (particularly in Gauteng Province), with increasing reports of incorrect fee classification

664

for higher levels of care being made, and upfront payment being demanded for emergency care. This appears to be in response to guidelines and posters circulated by the provincial Department of Health which demand up-front payment for all treatment and imply the need for frontline staff to act as immigration officials. These actions are unhelpful – not only in terms of the misapplication of policy and the associated extralegal implications of denying access to care, but in the negative public health consequences for all in SA and the additional costs and burdens associated with delayed healthcare seeking.

What is needed?

A growing body of evidence provided by researchers, civil society and international organisations emphasises the following: • Training on migration, mobility, health and development for all levels of staff in the Department of Health, including frontline staff, healthcare providers, facility managers, district and provincial health co-ordinators, and within the national department.

• Recognition of the importance of internal mobility within SA and other countries in the SADC region, and the development of migration-aware health systems.

• SA should lead the development of a co-ordinated regional response to migration, mobility and health.

• Effective implementation of current protective and progressive legislation relating to the right to health for non-nationals in SA. • Correct classification of non-nationals when being means tested for co-payment for healthcare.

• Implementation of national monitoring of the correct implementation of existing legislation within health facilities.

• Health passports or regionally recognised ‘road-to-health’ cards for all (a form of patient-held records).

• Referral letters for internal AND cross-border migrants.

• The establishment of local migrant health forums.

1. Vearey J, Nunez, L. Migration and Health in South Africa: A Review of the Current Situation and Recommendations for Achieving the World Health Assembly Resolution on the Health of Migrants.

Pretoria: International Organization for Migration, 2010.

2. Landau L, Segatti AWK. Human development impacts of migration: South Africa case study. Human Development Research Paper Series 2009;5. http://mpra.ub.uni-muenchen.de/19182/ (accessed 18 August 2014).

3. Deane KD, Parkhurst JO, Johnston D. Linking migration, mobility and HIV. Trop Med Int Health 2010;15(12):1458-1463. [http://dx.doi.org/10.1111/j.1365-3156.2010.02647.x] 4. Lurie MN, Williams B. Migration and health in southern Africa: 100 years and still circulating. Health Psychology and Behavioral Medicine: An Open-Access Journal 2014;2(1):34-40. [http://dx.doi.org/10.

1080/21642850.2013.866898] 5. Vearey J. Learning from HIV: Exploring migration and health in South Africa. Glob Public Health 2012;7(1):58-70. [http://dx.doi.org/10.1080/17441692.2010.549494] 6. StatsSA. Census 2011: Census in Brief. Pretoria: StatsSA, 2012.

7. Crush J. Spaces of Vulnerability: Migration and HIV/AIDS in South Africa. Southern African Migration Programme Migration Policy Series No. 24, 2002.

8. International Organization for Migration. Migration and Health in SADC: A Review of the Literature.

Pretoria: IOM, 2011.

9. Vearey J, Nunez L, Lakika D. Exploring the Psychosocial & Health Rights of Forced Migrants in Johannesburg: The Impact of ‘Daily Stressors’ on the Emotional Wellbeing of Forced Migrants.

Johannesburg: Centre for the Study of Violence and Reconciliation and African Centre for Migration & Society, University of the Witwatersrand, 2011.

10. Malmusi D, Borrell C, Benach J. Migration-related health inequalities: Showing the complex interactions between gender, social class and place of origin. Soc Sci Med 2010;71(9):1610-1619. [http://dx.doi.org/10.1016/j.socscimed.2010.07.043] 11. Vearey J. Migration, urban health and inequality in Johannesburg. In: Bastia T, ed. Migration and Inequality. London: Routledge, 2013:121-144.

12. Vearey J. Migration, access to ART, and survivalist livelihood strategies in Johannesburg. Afr J AIDS Res 2008;7(3):361-374. [http://dx.doi.org/10.2989/AJAR.2008.7.3.13.660]

Accepted 3 July 2014.

October 2014, Vol. 104, No. 10

FORUM

ISSUES IN PUBLIC HEALTH

Low levels of physical activity in female adolescents cause overweight and obesity: Are our schools failing our children?

M N Mokabane, M M Mashao, M van Staden, M J Potgieter, A Potgieter Nelly Mokabane is an MSc student in the Department of Physiology and Environmental Health, School of Molecular and Life Sciences, University of Limpopo, South Africa; Mercy Mashao is a junior lecturer in the Department, and currently registered for an MSc degree in Physiology; Marlise van Staden, PhD, is a senior lecturer in the Department, with a keen interest in obesity, and its causes and effects; Martin Potgieter, PhD, is an associate professor in the Department of Biodiversity, School of Molecular and Life Sciences, University of Limpopo; and Annelize Potgieter is manager of the Science Centre at the University of Limpopo.

Corresponding author: M van Staden (marlise.vanstaden@ul.ac.za)

The increasing prevalence of overweight and obesity among female adolescents is a global health problem. In developing countries such as South Africa, this increase is often associated with urbanisation and the adoption of a Western lifestyle. Two aspects of the Western lifestyle that contribute to the development of overweight and obesity are a decrease in physical activity levels and an increase in the consumption of energy-dense food, high in fats and refined sugar. Information on the prevalence of increased body fatness in populations in transition is scarce, but necessary for effective planning and intervention. Current indications are that there is a trend towards unhealthy behaviour among high-school girls, globally and in South Africa. Schools can play an important role in the prevention of overweight and obesity among schoolgirls. It is recommended that school governing bodies institute remedial action to prevent weight gain in children, especially girls.

S Afr Med J 2014;104(10):xxxx. DOI:10.7196/SAMJ.8577

Obesity develops rapidly during adolescence.[1] According to the World Health Organization (WHO), childhood obesity is a major global public health problem.[2] The prevalence of overweight and obesity is increasing rapidly in Africa; between 1990 and 2010, the number of overweight or obese children doubled.[3] Arm足 strong et al.[4] noted that there was an increase in overweight and obesity in South Africa (SA) from 1994 to 2004. According to the WHO,[5] females are more likely to be obese than males. This is especially true for black females in SA, who according to Martorell et al. [6] are often overweight or obese, or have abdominal obesity. In African culture increased body fatness is viewed as a sign of health and wealth. Mothers therefore tend to over-feed their infants, thereby increasing the risk of developing obesity.[7] Although traditional culture remains strong in many parts of SA, a transition is currently occurring between traditional and Westernorientated lifestyles.[8] This has potential consequences for overweight and obesity among black schoolchildren, especially girls, who live in periurban and urban environments. Their increase in body fatness increases the risk of development of chronic diseases of lifestyle such as hypertension, stroke, coronary heart disease and type 2 diabetes mellitus.[9]

Possible causes for increased body fatness in schoolgirls

Since increased body fatness is a consequence of a positive energy balance,[10] schoolgirls who use less energy than they consume will gradually become overweight and eventually obese. The two most obvious causes of increased body fatness in schoolgirls are probably a decrease in physical activity and an increased consumption of energy, both of which are associated with urbanisation and westernisation.[11]

665

Life in an urban setting has a severe negative impact on the amount of physical activity a child has the chance to enjoy.[12] In urban and peri足 urban regions, safety concerns contribute to the decrease in physical activity;[11] e.g. it is no longer safe for children to walk to school or to play in parks. Finances also contribute to the decreased physical activity level in children,[11] many parents lacking the money to allow their children to participate in organised sport activities.

Periurban communities often lack access to sports facilities in any case, and few schools in these environments have such facilities.[11] The result is that children grow up in an environment that is condu足cive to sedentary rather than physical activities.

The typical Western diet is high in energy-dense foods, fat and refined sugar[10] that easily lead to a positive energy balance. This is especially true in the presence of decreased physical activity.

During the process of urbanisation and westernisation, children (and adults) consume more snacks and convenience foods, which are very high in salt, fat, refined sugar and energy.[13] Part of the problem may be that the SA public is continually confronted with misleading and confusing dietary information.[10] Parents may not know what constitutes a healthy diet, or of the dangers associated with an unhealthy diet and the resultant increase in body fatness.

Many public schools have feeding or nutrition programmes, where children receive at least one meal per day at school. The meals are prepared at the school and the menu is often determined by what is available, rather than what constitutes a healthy diet. Another factor contributing to childhood obesity is the foods sold at the school snack shop,[13] which for many schools is an opportunity to increase income.

The selection of snacks tends to be based on popularity rather than dietary benefit.

Urbanisation and westernisation in SA are therefore setting the stage for an increasing prevalence of overweight and obesity in

October 2014, Vol. 104, No. 10

FORUM

schoolchildren, with the associated risks of development of a variety of chronic diseases of lifestyle.[10]

Case study

We recently undertook a study at a high school in a periurban area of the Polokwane Local Municipality, Limpopo Province. The study population comprised 56 black girls aged 13 - 19 years. They were not specifi­ cally selected to participate in the study, any girl who brought back a consent form signed by her parents/guardian being allowed to take part. Each girl also received a questionnaire (with questions on physical activity and snacking behaviour) that the parents/guardian completed. The weight and height of each girl was measured according to the internationally accepted methods described by Marfell-Jones et al.[14] The body mass index (BMI) was calculated using the formula kg/m2.

Table 1 shows that the girls consumed significant quantities of snacks (such as

sweets, biscuits and cake), between one and seven times per week, and beverages (e.g. cold drink or fruit juice), between two and six times per week. In addition, on average they spent a significant amount of time each day performing sedentary activities (refer to Table 1 for a list), and spent very little time being physically active (Table 1).

Fig. 1 shows the percentages of girls who fell into each of the BMI categories (as suggested by Reilly[15]). Of the girls, 67.8% had a normal BMI (>25 kg/m2), 12.5% were overweight and 3.6% were obese. The preva­ lence of over­weight and obesity in this young female population is a cause for concern, because overweight in adolescents frequently continues into adulthood. The longer these girls are exposed to the increased body fat, the higher their risk of developing complica­tions later in life.[16] Just over 16.1% of the girls were underweight/lean. The causes of underweight are usually poor nutrition or malnutrition and infections.[8,17] We did not investigate the causes for underweight in this study.

Table 1. Data on the study population Variables, mean (SD) Age (years)

15.4 (1.9)

Sweets such as chocolate bars, biscuits and cakes (n/week)

3.6 (2.9)

Any form of cold drink or fruit juice (n/week)

3.6 (2.0)

Sedentary activities* (hours/day)

2.0 (1.3)

Physical activities at home (hours/day)

1.2 (1.5)

Participating in organised sports (hours/day)

1.1 (1.1)

Weight (kg)

54.0 (11.6)

Height (m)

1.56 (0.06)

BMI

21.9 (3.7)

†

SD = standard deviation; BMI = body mass index (kg/m2). * Watching television, DVDs or videos; playing video games or cellphone games; using the computer/internet, e.g. to e-mail or chat online; reading and doing homework. † Playing, running around outside, climbing trees, kicking balls, riding a bicycle, swimming.

80 70 60 50 % 40

There was a negative but weak correlation (p=0.017) between age and being physically active at home, indicating that as these girls grow older, their physical activity levels decrease. This may be one of the causes for the strong positive correlation between age and BMI (p=0.001), as well as the weak negative correlation between BMI and time spent being physically active at home (p=0.41), and between BMI and participation in sport (p=0.009). There were also weak positive correlations between watching television and frequency of consuming sweets (p=0.13) and soft drinks (p=0.20), indicating that watching television is associated with snacking behaviour.

Furthermore, there was a weak positive correlation between time spent playing electronic games and watching television (p=0.009) and frequency of consuming sweets, biscuits and cakes (p=0.009), once again indicating the occurrence of unhealthy behaviours in the same girls.

What do we need to do?

The girls in our study were not selected on the grounds of their unhealthy behaviour.

The behavioural trends they displayed are probably typical of girls in this age group.

Taking into consideration that children spend a considerable amount of time at school, schools can play a very important role in promoting regular physical activity and the consumption of a healthy diet. It is recommended that schools introduce and promote sustained healthy physical activities during and after school hours via sports activities to counteract overweight and obesity, especially in girls. The establishment of safe community playgrounds would go a long way towards encouraging physical activity. Ideally, the above should be supplemented by counselling for weight loss and weight management in overweight and obese children. Furthermore, emphasis in the school curriculum must be placed on the health benefits of physical activity and a prudent diet. School snack shops should provide healthy alternatives to sweets and biscuits or cake.

Acknowledgements. The principal, teachers and children at the secondary school are acknowledged for participating in the study.

We also thank Dr V O Onywera for permission to use his questionnaire.

30 20 10 0 Underweight/lean

Normal

Overweight

Obese

BMI category

Fig. 1. Percentages of the girls in specific BMI categories. (BMI = body mass index.)

666

October 2014, Vol. 104, No. 10

1. Dietz WH. Critical periods in childhood for the development of obesity. Am J Clin Nutr 1994;59(5):955-959.

2. Anrig CDC. The obese child. Dynamic Chiropractic 2003;21(22):27-31.

3. De Onis M, Blossner M. Prevalence and trends of overweight among preschool children in developing countries. Am J Clin Nutr 2000;72(4):1032-1039.

FORUM

4. Armstrong MEG, Lambert MI, Lambert EV. Secular trends in the prevalence of stunting, overweight and obesity among South African children (1994-2004). Eur J Clin Nutr 2011;65(7):835-840. [http:// dx.doi.org/10.1038/ejcn.2011.46] 5. World Health Organization. Obesity: Preventing and Managing the Global Epidemic. Report of a WHO Consultation. Geneva: WHO, 2000:252.

6. Martorell R, Khan LK, Hughes ML, Grummer-Strawn LM. Obesity in women from developing countries. Eur J Clin Nutr 2000;54(3):247-252. [http://dx.doi.org/10.1038/sj.ejcn.1600931] 7. Mamabolo RL, Alberts M, Steyn NP. Prevalence and determinants of stunting and overweight in 3 year old black South African children residing in the central region of Limpopo Province, South Africa.

Public Health Nutr 2005;8(5):501-508. [http://dx.doi.org/10.1079/PHN2005786] 8. Tathiah N, Moodley I, Mubaiwa V, Denny L, Taylor M. South Africa’s nutritional transition: Overweight, obesity, underweight and stunting in female primary school learners in rural KwaZuluNatal, South Africa. S Afr Med J 2013;103(10):718-723. [http://dx.doi.org/10.7196/SAMJ.6922] 9. Kruger HS, Venter CS, Vorster HH. Obesity in African women in the North West province, South Africa is associated with an increased risk of non-communicable diseases: The THUSA study. Br J Nutr 2001;86(6):733-740. [http://dx.doi.org/10.1079/BJN2001469] 10. Vorster HH, Badhan JB, Venter CS. An introduction to the revised food-based dietary guidelines for South Africa. South African Journal of Clinical Nutrition 2013;26(3, Suppl):S5-S12.

11. Botha CR, Wright HH, Moss SJ, Kolbe-Alexander TL. ‘Be active!’ Revising the South African food based dietary guideline for activity. South African Journal of Clinical Nutrition 2013;26(3, Suppl):S18-S27.

12. Onywera VO, Adamo KB, Sheel AW, et al. Emerging evidence of the physical activity transition in Kenya. Journal of Physical Activity and Health 2012;9(4):554-562.

13. Story M, Nanney MS, Schwartz MB. Schools and obesity prevention: Creating school environments and policies to promote healthy eating and physical activity. Milbank Q 2009;87(1):71-100. [http:// dx.doi.org/10.1111/j.1468-0009.2009.00548.x] 14. Marfell-Jones M, Olds TS, Carter JEL. International Standards for Anthropometric Assessment.

Underdale, Australia: International Society for the Advancement of Anthropometry, 2006:57-59.

15. Reilly JJ. Assessment of obesity in children and adolescents: Syntheses of recent systematic reviews and clinical guidelines. J Hum Nutr Diet 2010;23(3):205-211. [http://dx.doi.org/10.1111/j.1365277X.2010.01054.x] 16. Whitaker RC, Wright JA, Pepe MS, Seidel KD, Dietz WH. Predicting obesity in young adulthood from childhood and parental obesity. N Engl J Med 1997;337(13):869-873. [http://dx.doi.org/10.1056/ NEJM199709253371301] 17. Jinabhai CC, Taylor M, Sullivan KR. Implications of the prevalence of stunting, overweight and obesity amongst South African primary school children: A possible transition. Eur J Clin Nutr 2003;57(2):358365. [http://dx.doi.org/10.1038/sj.ejcn.1601534]

Accepted 22 August 2014.

10333

Offering the perfect solution is only possible with deeper insight.

At Nedbank Business Banking your skilled relationship manager, backed by a team of specialists, is committed to nurturing close and lasting partnerships with our clients in the medical fraternity. This allows us to delve below the surface to give you carefully nuanced solutions that truly meet the needs of your healthcare business.

In addition we are also able to be of service to you, your staff and household.

For more information email us at medical@nedbank.co.za. nedbank.co.za

Nedbank Limited Reg No 1951/000009/06. Authorised financial services and registered credit provider (NCRCP16).

FORUM

CLINICAL ALERT

Varicose veins: Look before you strip – the occluded inferior vena cava and other lurking pathologies T Mokoena Prof. Taole Mokoena, MB ChB, DPhil, FRCS, is the Head of Surgery at the School of Medicine, University of Pretoria, South Africa, and the Pretoria Academic Hospital Complex. He is a keen observer of disease and has a wide-ranging interest in surgery.

Corresponding author: T Mokoena (taole.mokoena@up.ac.za)

Lower limb varicose veins are a common complication of bipedal human movement and deep-vein thrombosis. However, they may have unusual causes, e.g. forming as collaterals around an obstruction or resulting from vascular malformations. Surgery in these cases can be inappropriate or harmful. Five cases of lower limb varicose veins in which there was underlying pathology highlight the fact that cursory examination of patients with varicose veins and inappropriate special investigations can miss rare but significant underlying pathology.

Patients should be examined systematically, and varicose veins in unusual situations should alert the clinician. Inappropriate surgery can be harmful.

S Afr Med J 2014;104(10):668-670. DOI:10.7196/SAMJ.7979

There are many causes of dilated tortuous subcutaneous veins. The common varicose veins of the legs result from excessive blood flow due to incompetence of unidirectional valve systems. The latter are either primarily defective or overwhelmed by gravitational force in the prolonged upright position. The flow of blood in such veins is in the natural direction. Dilated veins may also be collaterals that allow flow of blood around an obstruction, such as the oesophageal collaterals in portal hypertension. Collaterals can also develop in the limbs when deep veins are occluded. Depending on the anatomical location, flow in these collaterals may be reversed.

Classic varicose vein surgery on the legs is aimed at removing the abnormal veins by stripping and addressing the incompetent flow channels by performing vein ligation. Surgery on collaterals around a venous obstruction may be inappropriate and even harmful, and surgery on varicose veins caused by arteriovenous (AV) malformations is also inappropriate. Five cases in which varicose vein surgery had been inappropriately performed or requested are presented. These situations could have been prevented by thorough clinical examination and consequent appropriate imaging studies.

Case 2

Case reports

Case 4

Case 1

A 41-year-old man was referred to the surgical outpatient depart­ment at Kalafong Hospital, Pretoria, South Africa, for management of an indolent leg ulcer and ‘lower limb’ varicose veins. On clinical examination, both legs and feet showed dystrophic skin changes with ulceration medially above the right ankle. There were varicose veins in both lower limbs, more marked on the right, and tortuous distended superficial inferior and superior epigastric veins on the trunk. The direction of flow in the latter was cephalad. The primary doctor had established patency and competence of the deep veins of the leg by Doppler studies and had referred the patient for vein stripping and ligation.

In view of the varicose veins on the trunk, further imaging was undertaken. This revealed occlusion of the inferior vena cava (IVC).

No surgery was performed.

668

A 46-year-old man presented with bilateral leg ulcers and unilateral lower limb varicose veins. Varicose vein stripping had been performed 2 years previously for varicose ulcers in one leg. Examination of the abdominal wall revealed varicosity of the superficial inferior epigastric veins arising at the groin, with cephalad flow. Venography confirmed IVC occlusion. He was treated non-operatively with local wound care and bilateral full-leg compression stockings.

Case 3

A 12-year-old boy presented with a longstanding lump over the right groin which became prominent and painful on straining. The referring practitioner considered it to be an inguinal hernia. However, on examination of the patient’s trunk it soon became evident that the lump was the distal extent of an abdominothoracic varicose channel arising from the right groin. A duplex Doppler scan of the lower limb and IVC failed to reveal the suspected venous occlusion. It was later demonstrated in the distal IVC by transfemoral venography, which also showed ascending lumbar vein collaterals draining into the proximal IVC. The cause of the occlusion was unknown, and no surgery was performed.

A 42-year-old female nurse presented with recurrent varicose veins after previous bilateral saphenous vein stripping performed elsewhere. On close examination, tortuous venous channels on the torso with femoroaxillary drainage were noted. Imaging of the IVC by venography revealed retrohepatic IVC occlusion. Further investigations confirmed a liver tumour in segment IV, which was confirmed to be a fibrolamellar hepatoma. It was managed by transarterial chemoembolisation, and a follow-up computed tomography scan of the liver showed that it has shrunk completely.

No further venous surgery was performed.

Case 5

A 29-year-old man with a lifelong history of varicosities of the left lower limb presented with painful swelling of that leg. He had

October 2014, Vol. 104, No. 10

FORUM

undergone surgery on the same leg 12 years earlier for removal of varicose veins. He had varicosities on the lateral and posterior aspects of both lower limbs as well as the gluteal region. There were dystrophic skin changes on the legs but no ulcers. There were no bruits over the varices. Arteriography showed extensive AV malformations of the popliteal, anterior and posterior tibial and peroneal vessels. The patient was managed with compression stockings. Fig. 1 depicts a similar case in which the AV malformation was unilateral. The patient first presented to us, was correctly diagnosed, and was managed similarly.

Discussion

Thrombosis of the deep veins of the lower limb and destruction of their valve systems is a well-recognised cause of varicose veins and their sequelae of dystrophic skin changes and ulceration.[1] That these varicosities can also arise from ‘reverse’ venous flow from IVC obstruction and resultant saphenofemoral incompetence requires emphasis. Cursory physical examination and inappropriately directed imaging in such cases may mean that underlying pathology is overlooked or misdiagnosed. The concern is that with more widespread use of modern technology such as ultrasound scanning in clinical medicine, long-established teaching and simple clinical tests are increasingly being ignored or unlearned.[2] This is particularly pertinent to primary family doctors, whose advice their patients tend, understandably, to trust more than that of an unknown specialist.

There is a growing tendency for patients to resist being subjected to a full physical examination, apart from their perceived area of pathology.[3] Reluctance in this regard on the part of doctors has also increased, especially in view of the increase in charges of improper conduct. However, clinical exami­ nation of the torso could reveal varicosities as depicted in Fig. 2, and alert the clinician to possible major intra-abdominal venous occlusion. In the five cases described above, the tortuous trunk vessels with reverse flow could be discerned clinically and should have prompted further investigation for occlusion of the IVC. If Doppler studies alone, often done by technical staff and in the absence of a thorough clinical assessment, are used to study deep limb veins, there is a risk that saphenous varicosities will be incorrectly attributed to saphenofemoral venous incompetence.

The most common cause of occlusion of the major veins in the abdomen is throm­ bosis.[4] The patients described here presented

Fig. 1. A patient with severe limb varicosities due to an arteriovenous malformation. These are located superiorly and laterally and not in the vena saphena magna area of distribution. Note also the overgrowth of the affected limb.

Fig. 2. A sketch illustrating the typical distribution of varicosities on the trunk in case of IVC obstruction. Blood flow is cephalad in such veins.

in a chronic phase with established varicose veins. It is likely that cases 1 and 2 were due to previous thrombosis. These patients presented in adulthood, and thrombophilias and congenital anatomical abnormalities are therefore unlikely. While thrombosis as the cause of their IVC occlusion could not be proven, another case clearly illustrated this pathology. A 47-year-old man was treated for acute iliofemoral thrombosis. Within a week of admission he developed prominent venous channels over the lower abdomen.

Suspected extension of the thrombosis to the IVC was confirmed by both ultrasound and venography. The patient was treated with full anticoagulation.

In case 3, the 12-year-old boy’s right groin swelling was under­standably mistaken for a hernia, especially because it became larger and painful on performing a Valsalva manoeuvre. The presence of prominent varicosities over the saphenofemoral junc­ tion (‘saphena varix’) is an uncommon condition that must be distinguished from a groin hernia.[1] However, careful clinical examination would have shown extension of the swelling onto the trunk and revealed

that the mass consisted of prominent veins.

The thrombosis in this case may have resulted from dehydration in earlier child­ hood, as severe dehydration may lead to IVC thrombosis in children.[4] Iatrogenic thrombosis from IVC cannulation for longterm parenteral nutrition and intravenous infusions has also been reported in this age group.

Isolated IVC thrombosis is sometimes associated with intra-abdominal malignancy, especially renal and pancreatic tumours, and these should be actively excluded. The case of hepatoma described above illustrates such a neoplastic cause. Thrombosis in cancer results from the hypercoagulability associated with malignancy and/or local compression or infiltration of veins.[5] Both these mechanisms were probably operative in this patient.

Case 5 illustrates a cause of limb varicosi­ ties that can be confused with extensive occlusion of the deep venous system. AV malformations of the type that contain AV fistulas (Klippel-Trenaunay-Parkes-Weber syndrome) also exhibit extensive venous tortuosities and recurrent varicosities.[6] As

669

October 2014, Vol. 104, No. 10

FORUM

can be seen in Fig. 1, the varicosities are unusually distributed on the leg (superior and posterior) and there is overgrowth of the affected limb. IVC occlusion should be sought in patients with such varicosities, but other causes such as an AV malformation should be entertained before saphenofemoral vein stripping is done.

Varicosities on the torso should be noted. Prominent veins on the flanks and lateral chest wall could be collaterals caused by IVC obstruction, as depicted in Fig. 2.

It should be noted that two of our patients had their minds set on immediate surgery, as their respective doctors had referred them for varicose vein stripping. Judicious varicose vein surgery can be contemplated for recalcitrant ulceration in such cases. However, cognisance must be taken of saphenous vein tributaries that provide bypass around IVC occlusion, because disruption of these channels can worsen venous hypertension.

Conclusion

There can be more to varicose veins of the legs than meets the eye. It is important that doctors examine their patients’ torsos carefully for prominent veins in all cases of lower limb varicosities and atypical groin hernias. IVC occlusion, or more rare causes such as AV

malformations, should be considered in such cases, and appropriate treatment recommendations made. Extra vigilance is called for when a patient has recurrent varicose veins following previous surgery.

While referral for directed surgery can be amicably received, this is not always appropriate.[7] Incorrect diagnosis and inappropriate referral can sour relationships between colleagues and with patients.

1. Morris PJ, Malt RA, eds. Oxford Textbook of Surgery. New York: Oxford University Press, 1994:503596.

2. Feddock CA. The lost art of clinical skills. Am J Med 2007;120(4):374-378. [http://dx.doi.org/10.1016/j. amjmed.2007.01.023] 3. Oliveria SA, Heneghan MK, Cushman LF, et al. Skin cancer screening by dermatologists, family practitioners, and internists: Barriers and facilitating factors. Arch Dermatol 2011;147(1):39-44. [http://dx.doi.org/10.1001/archdermatol.2010.414] 4. Harris RD. The etiology of inferior vena caval obstruction and compression. CRC Crit Rev Radiol Nucl Med 1976;8(1):57-86.

5. Young A, Chapman O, Connor C, et al. Thrombosis and cancer. Nat Rev Clin Oncol 2012;9(8):437-49. [http://dx.doi.org/10.1038/nrclinonc.2012.106] 6. Oduber CEU, van der Horst CMAM, Hennekam RCM. Klippel-Trenaunay syndrome: Diagnostic criteria and hypothesis on etiology. Ann Plast Surg 2008;60(2):217-223. [http://dx.doi.org/10.1097/ SAP.0b013e318062abc1] 7. Smith FC, Gwynn BR. Direct access surgery. Ann R Coll Surg Engl 1995;77(2):94-96.

Accepted 15 May 2014.

SciELO SA:[1] Ten most visited titles to date SciELO SA: Tn most visited titles to date South African Medical Journal

16%

South African Journal of Science

23%

South African Journal of Education Water SA South African Orthopaedic Journal 14%

3%

South African Journal of Animal Science South African Journal of Industrial Psychology

3%

Potchefstroom Electronic Law Journal

3% 4% 13%

4% 5% 12%

Journal of the Southern African Institution of Mining and Metallurgy Journal of the Southern African Institution of Civil Engineering Other titles in the collection

The ten most visited of the 45 titles in the SciELO SA Collection, as of 22 September 2014. A total of 3 195 757 articles had been viewed via the SciELO SA website, http://www.scielo.org.za/ 1. Veldsman S, Gevers W. Increased visibility and discoverability of South African health-related research. S Afr Med J 2014;104(4):287. [http://dx.doi.org/10.7196/SAMJ.7934]

670

October 2014, Vol. 104, No. 10

FORUM

CLINICAL ALERT

The influence of glucocorticoids on lipid and lipoprotein metabolism and atherosclerosis I L Ross, A D Marais Dr Ian Ross is a senior consultant endocrinologist attached to the Division of Endocrinology, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa, and Groote Schuur Hospital, Cape Town. His major interests are Addison’s disease, glucocorticoids, clinical thyroidology and thyroid cancer. He received his PhD from UCT on the clinical aspects of Addison’s disease. Prof. David Marais specialised in internal medicine, then received a Medical Research Council scholarship to study lipoprotein metabolism in medical biochemistry before resuming a consultant post in internal medicine at Groote Schuur Hospital. He joined the lipid clinic in 1984 and developed a diagnostic and research laboratory for dyslipidaemias. He headed the clinic from 1990 to 2012, when he joined the Depart­ment of Chemical Pathology, National Health Laboratory Service and Faculty of Health Sciences, UCT. He is also a member of the MRC Cape Heart Group.

Corresponding author: I Ross (ian.ross@uct.ac.za)

Glucocorticoids have multiple therapeutic uses, but their impact on lipid metabolism and cardiovascular disease risk is not always considered during long-term treatment. Genetic variations, environmental factors and the reasons for glucocorticoid treatment all influence the lipid profile and atherosclerosis. Responses to glucocorticoid treatment may therefore be variable and unpredictable. Despite the frequency with which pharmacological doses of glucocorticoids are used, surprisingly few publications examine their effects on lipid metabolism and atherosclerosis. Patients managed with glucocorticoids should have their cardiovascular risk assessed, especially if long-term treatment is planned. While some apparent favourable changes have been reported in high-density lipoprotein metabolism, very-low-density lipoprotein and low-density lipoprotein responses seem unfavourable. The impact of glucocorticoids on atherosclerosis, which is often viewed as an inflammatory process, is unclear. Glucocorticoid treatment should be undertaken for appropriate indications, but in some instances special attention should be given to management of dyslipidaemia, as long-term survivors of treatment are likely to encounter atherosclerosis.

S Afr Med J 2014;104(10):671-674. DOI:10.7196/SAMJ.7979

Lipid transport

Lipoproteins transport lipids in the circulation in four major pathways: (i) a postprandial (exogenous) pathway for chylomicrons; (ii) an endogenous pathway involving very-low-density lipoprotein (VLDL) for triglyceride (TG) transport from the liver; (iii) a lowdensity lipoprotein (LDL) pathway from a proportion of VLDL as a source of cholesterol for cells; and (iv) a reverse cholesterol transport pathway by high-density lipoprotein (HDL).[1] These pathways and the reported effects of glucocorticoids are shown in Fig. 1.

Exogenous TG pathway

Chylomicrons, comprising 85 - 90% TG and containing apolipo­ protein B (apo B)-48 (apoB48), apolipoprotein Ai (apoAi) and apolipoprotein Aiv (apoAiv), are produced in enterocytes, traverse the thoracic duct and ultimately reach the systemic circulation.

Lipoprotein lipase anchored on cells by heparan sulphate proteoglycans hydrolyses TG at the vascular endothelium, yielding non-esterified fatty acids (NEFAs) and remnants, proportionately richer in cholesterol esters. Chylomicron remnants are rapidly cleared by liver remnant receptors,[2] as a result of apolipoprotein E (apoE) acquired in the circulation. Dietary fat restriction will have a significant impact on severe hypertriglyceridaemia.

Endogenous TG pathway

VLDL is assembled on apolipoprotein B-100 (apoB100) and compri­ses 50% TG, 20% cholesterol esters, 15% phospholipids and 15% protein.

Secretion is enhanced by increasing delivery of NEFAs from adipose

671

tissue during starvation or in diabetes.[3] VLDL is also hydrolysed by lipoprotein lipase. These remnants and other small lipoproteins (LDL and HDL) can undergo hydrolysis of TG by hepatic lipase, forming progressively smaller particles. VLDL remnants are proportionately richer in cholesterol, and some form LDL.[1] The release of fatty acids from adipose tissue and their uptake in the liver will enhance VLDL production and may cause hypertriglyceridaemia.

LDL pathway

LDL contains the majority of cholesterol in the plasma. Its mass comprises 35% cholesteryl ester, 10% unesterified cholesterol (UC), 10% TG and 20% phospholipids. ApoB100 almost entirely accounts for the 25% of protein. Most circulating LDL is taken up by hepatocyte LDL receptors. Increased VLDL could increase LDLC while also resulting in modulation of particle size. This process requires cholesterylester transfer protein (CETP) to enrich with TG, after which hepatic lipase hydrolyses the TG. The plasma LDL concentration may also be raised by decreased clearance (by LDL receptors) in familial hypercholesterolaemia.

Reverse cholesterol transport

HDL is the smallest of the lipoproteins. About half is lipids (25% phospholipids and 15% cholesterylester, while UC and TG both constitute 5%). The remainder is chiefly apoAi and apolipoprotein Aii (apoAii). The liver and intestine secrete apoAi that may initiate particle formation, which may also result from lipolysis of TG-rich lipoproteins[4] when apoAi and the relative excess of phospholipids pinch off from the lipoprotein. Lecithin-cholesterol acyltransferase

October 2014, Vol. 104, No. 10

FORUM

increased in cultured rat hepatocytes exposed to glucocorticoids.[16] Transient down-regulation of LDL receptors in rats followed methylprednisolone admini­ stration, accounting for elevated LDL and TC.[17] Overall, animal models illustrate marked effects on HDL and some adverse effects on LDL, as well as differences between the drugs.

Ai HDL 3

LDL B100

CO 2 de novo synthesis

Ai

FA

CE

LDLR

HL

TG

liver

E remnant

LRP

B100/48

VLDL

C E

BA

adipose tissue FA

Cii

LPL

TG CE Ai B100

muscle LDLR

Ai

gall bladder

HDL 3 BA TG

C

FA C

adrenal gland

E

Ai

CM Cii TG C B48

HL LCAT

gut

C

CE TP

Ai CE/TG HDL 2

SRB1

ABCA1 CE

peripheral cells including macrophage

plasma

Fig. 1. Schematic view of lipoprotein metabolism including the effects of glucocorticoids. Adapted with permission from Marais.[1] (ABCA1 = adenosine binding cassette transporter A1; apoE = apolipoprotein E; Ai = apolipoprotein Ai; BA = bile acid; B100 = apolipoprotein B100; C = cholesterol; CE = cholesteryl ester; CETP = cholesterylester transfer protein; CM = chylomicron; Cii = apolipoprotein Cii; FA = fatty acids; HDL2 = high-density lipoprotein 2; HDL3 = high-density lipoprotein 3; HL = hepatic lipase; TG = triglyceride; LDL = low-density lipoprotein; LDLR = LDL receptor protein; LPL = lipoprotein lipase; LRP = low-density lipoprotein receptor protein; LCAT = lecithin cholesterol acyltransferase; SRB1 = scavenger receptor B1; VLDL = very-low-density lipoprotein.)

(LCAT) esterifies UC, using long-chain fatty acids from phospholipids. Cholesteryl esters migrate to the core, forming more mature spherical particles (HDL3) and later larger and less dense HDL. CETP transfers cholesteryl ester from HDL2 to TG-rich lipoproteins, permitting delivery of cholesterol to the liver, and in exchange HDL receives TG.[4] Hepatic lipase hydrolyses TG, regenerating smaller HDL3 particles. Exchange of TG into LDL similarly produces smaller particles. In HDL, esterification of UC permits more UC to be accepted from cells or other lipoproteins. HDL delivers cholesterol directly to the liver, leading to its excretion in bile.[5]

Lipid and lipoprotein changes with corticosteroids

Dyslipidaemia, hyperglycaemia and hypertension are the most significant cardiovascular adverse effects resulting from glucocorticoid therapy,[6] but mechanistic insights are incomplete. Documented changes in human lipid profiles on varying doses of prednisone[7-10] include elevated VLDL, TG and LDL cholesterol, and either increased or decreased HDL cholesterol.

Animal studies of lipid changes in steroid use

Hydrocortisone (single dose) administered to rabbits with athero­sclerosis raised TG

but not total cholesterol (TC),[11] sugges­ ting increased VLDL production or possi­ bly decreased metabolism. In rats, dexa­ methasone and triamcinolone (but not hydrocortisone) increased plasma TC and TG. [12] Hydrocortisone administered to rats at 100 µg/g of body mass reduced TC. Hydrocortisone, triamcinolone and dexa­methasone increased apoAi, with the greatest increases documented for triam­ cinolone and dexamethasone. Dexametha­ sone raised apoAiv the most, and triam­ cinolone caused the greatest increase in apoE, yet reductions in apoE levels occurred in rats receiving hydrocortisone.

[12] Methylprednisone admini­ stered to normal rats for 8 days increased TG and almost doubled TC,[13] probably owing to a reduction in lipoprotein lipase activity and decreased HDL choles­terol.[14] ApoE decreased with hydrocorti­ s one, either as a result of less hepatic secre­ tion or increased catabolism of apoE-containing lipoproteins, but lower production of apoE by extra­hepatic tissues has also been pro­ posed.[15] The brain, spleen and kidney produce apoE, aiding redistribution of cholesterol from cells with an excess of cholesterol to those requiring it.[15] ApoAi increased with most glucocorticoids, but especially with triamcinolone and dexamethasone, resulting in increased HDL cholesterol.[12,15] Hepatic apoAi mRNA

672

October 2014, Vol. 104, No. 10

Human studies with glucocorticoids

The impact of glucocorticoid hormones on lipoprotein metabolism can be examined in normal variation, acute and chronic dosing, replacement therapy, and hypercortisolism.

Positive correlations exist between LDL cholesterol and endogenous plasma cortisol in healthy men aged between 52 years and 67 years.[18] Glucocorticoids alter plasma lipids within 14 days.[10] Acute effects of 3 mg dexamethasone (twice daily simula­ ting acute stress) in young men included lower highly sensitive C-reactive protein levels and increased HDL cholesterol; LDL cholesterol, NEFA and TG were not altered.

[19] Glucocorticoids reduce hep­atic lipase and CETP, resulting in elevated HDL cholesterol after cardiac trans­plantation.[20] In the third National Health and Nutrition Examination Survey, gluco­ corticoid use was associated with higher HDL and lower TC/HDL cholesterol ratios.[21] Both glucocorticoid use and endogenous hypercortisolism (Cushing’s disease) resulted in elevated TC and LDL cholesterol. Glucocorticoid replacement in hypopituitary patients lowered VLDL, LDL cholesterol, LCAT and CETP. Based on animal and human studies, exposure to glucocorticoids may produce either increased or decreased HDL cholesterol. Changes in reverse cholesterol transport or other effects may modulate atherosclerosis. Some studies corroborate up-regulated hepatic LDL receptor activity, explaining a decrease in LDL cholesterol.

While glucocorticoids are known to have pleiotropic actions on physiological and pathological processes, lipoprotein responses and homoeostasis are varied, but are potentially atherogenic (Table 1).

Hypercortisolism stimulates the production of VLDL.[6] Subclinical Cushing’s syndrome has been associated with dyslipidaemia. Rheumatoid arthritis sufferers frequently have high TC and LDL cholesterol and decreased HDL cholesterol.

Untreated rheumatoid arthritis patients may have lower HDL cholesterol levels relating to inflammation and acute-phase response.

Treatment with glucocorticoids may dampen inflammation favourably, though

FORUM

Table 1. Changes in lipid and lipoprotein metabolism attributable to glucocorticoid treatment Lipid parameter

Increase

No change

Decrease

TC (composite of all lipoproteins)

Methyl-prednisolone administered for 8 days raised total cholesterol. Over-replacement of hypopituitary patients

In response to glucocorticoids in rats

In hypopituitary individuals

VLDLC (reflects most of fasting plasma TG)

Rabbits: increased TG by 80%; increased VLDLC

A short-term study showed no change in VLDL with glucocorticoids

Hydrocortisone in hypopituitary patients

One study with dexamethasone showed a neutral effect on LDLC

Corticotrophin decreased LDLC and apoB

Rodent increased VLDL size Decreased lipoprotein lipase activity responsible for increased TG Remarkably supraphysiological doses used LDLC (bulk of plasma cholesterol in humans)

Reduction in LDL-receptor mRNA

Human plasma cortisol proportional to LDLC: human study, Cushing’s disease LDL particle size

Increased small dense LDL

Decreased small dense LDL

HDLC (contains apoAi and substrate for LCAT and CETP)

Low-dose glucocorticoid in women with rheumatoid arthritis: apoAi unchanged, but HDLC increased by 15%

Promotes atherogenic ratio

ApoAi increased by 18% and HDLC increased by 28% following prednisone after 2 weeks ApoAi increased with hydrocortisone, triamcinolone and dexamethasone variably but only dexamethasone increased apoAiv in rats ApoAi increased after exposure to dexamethasone Increase of HDLC by 10% Increased phospholipids, only esterified cholesterol and apoE, reduced CETP and hepatic lipase, LCAT unchanged ApoAi significantly higher atheroprotective ratios in the elderly Increased after corticotrophin and dexamethasone in healthy humans In human hypopituitary patients TC = total cholesterol; VLDLC = very-low-density lipoprotein cholesterol; TG = triglycerides; VLDL = very-low-density lipoprotein; LDLC = low-density lipoprotein cholesterol; LDL = low-density lipoprotein; apo B = apolipoprotein B; HDLC = high-density lipoprotein; apoAi = apolipoprotein Ai; LCAT = lecithin-cholesterol-acyl-transferase; apoAiv = apolipoprotein Aiv; CETP = cholesterylester transfer protein.

this may not apply to atherogenesis.[7] A meta-analysis found an increase of cardiovascular and cerebrovascular disease by 59% and 50%, respectively, compared with the general population. Accelerated atherosclerosis in systemic lupus erythematosus has been attributed to the disease or to glucocorticoid therapy.

Hypopituitary patients on replacement therapy (hydrocortisone, thyroxine and sex steroids) are subject to increased morbidity and mortality from accelerated atherosclerosis. Optimally replaced patients had adverse lipid profiles, with increased TG, TC and LDL cholesterol compared with controls. Daily hydrocortisone supplementation of less than 20 mg/d in growth hormonereplaced patients had the least metabolic consequences.

673

Clinical approach to glucocorticoid treatment

Doctors considering glucocorticoid treatment in patients with chro­nic disorders should be aware that cardiovascular risk may increase. Chronic inflammatory conditions can predispose to vascular disease, and treatment may aggravate risk through dyslipoproteinaemia or other mechanisms.

Until further studies inform otherwise, prevailing guidelines should be followed. Risk calculations based on clinical parameters and lipid profiles as suggested guidelines offer the best guidance on the threshold for treatment, but may not be accurate. The premorbid lipid profile as well as levels during the illness may guide management. Exercise and dietary recommendations should be the norm.

October 2014, Vol. 104, No. 10

FORUM

Conclusions

Table 2. Dyslipidaemia and glucocorticoid treatment Primary ominant disorders, familial combined hyperlipidaemia, D familial hypercholesterolaemia, dysbetalipoproteinaemia ariably penetrant disorders, apoE2 homozygosity, lipoprotein V lipase deficiency Secondary Diabetes mellitus

Treatment of conditions requiring glucocorticoids together with disease-modifying agents is likely to prolong life expectancy and therefore raise the risk of cardiovascular disease. This risk is related at least in part to lipoprotein responses, as summarised in this article. More studies are required to evaluate cardiovascular risk in replacement and anti-inflammatory treatment, as well as the effects of different doses and forms of corticosteroid.

References. For a complete set of references, please contact the corresponding author.

Hypothyroidism Nephrotic syndrome Autoimmune, e.g antibodies to LPL Chronic inflammation (atherogenic lipoprotein phenotype) Glucocorticoid prescription Physiological increases in VLDL, LDL and HDL nti-inflammatory therapy (low and high dose); altered acuteA phase response Iatrogenic General effect Unmasking underlying lipid disorder ApoE2 = apolipoprotein E2; LPL = lipoprotein lipase; VLDL = very-low-density lipoprotein; LDL = low-density lipoprotein; HDL = high-density lipoprotein.

Detailed clinical assessments of a personal and family history of premature cardiovascular disease, physical signs and lipoprotein profiles will assist in the diagnoses listed in Table 2. Physical signs are not invariably present. Certain recessive disorders, e.g. dysbetalipoproteinaemia in subjects homozygous for apolipoprotein E2 (apoE2), manifest only when metabolic stress occurs. Partial lipoprotein lipase activity in heterozygotes may predispose to hypertriglyceridaemia. It is expected that glucocorticoid therapy will have a small impact on the lipoprotein profile in patients with normal genetic constitutions, while benefiting the chronic inflammatory condition. Occasionally, severe dyslipidaemia may be precipitated by glucocorticoid treatment, and in this setting special treatment with statins will be required for LDL hypercholesterolaemia, or fibrates for severe hypertriglyceridaemia. Successful treatment of the nephrotic syndrome with glucocorticoids will result in improved lipid profiles. Precipitation of diabetes by glucocorticoid therapy can affect the lipid profile and cardiovascular risk. Hypertension will similarly require a re-evaluation of risk and preventive actions to combat cardiovascular disease.

674

1. Marais AD. Lipids, lipoprotein metabolism and their derangements. SA Heart 2005;2(3):8-18.

2. Mahley RW, Huang Y, Rall SC Jr. Pathogenesis of type III hyperlipoproteinemia (dysbetalipoproteinemia): Questions, quandaries, and paradoxes. J Lipid Res 1999;40(11):1933-1949.

3. Adiels M, Olofsson SO, Taskinen MR, Boren J. Overproduction of very low-density lipoproteins is the hallmark of the dyslipidemia in the metabolic syndrome. Arterioscler Thromb Vasc Biol 2008;28(7):1225-1236. [http://dx.doi.org/10.1161/ATVBAHA.107.160192] 4. Davidson MH, Toth PP. High-density lipoprotein metabolism: potential therapeutic targets. Am J Cardiol 2007;100(11A):32-40. [http://dx.doi.org/10.1016/j.amjcard.2007.08.011] 5. Rader DJ, Alexander ET, Weibel GL, Billheimer J, Rothblat GH. The role of reverse cholesterol transport in animals and humans and relationship to atherosclerosis. J Lipid Res 2009;50(Suppl):S189-S194. [http://dx.doi.org/10.1194/jlr.R800088-JLR200] 6. McDonough AK, Curtis JR, Saag KG. The epidemiology of glucocorticoid-associated adverse events.

Curr Opin Rheumatol 2008;20(2):131-137. [http://dx.doi.org/10.1097/BOR.0b013e3282f51031] 7. Garcia-Gomez C, Nolla JM, Valverde J, Narvaez J, Corbella E, Pinto X. High HDL-cholesterol in women with rheumatoid arthritis on low-dose glucocorticoid therapy. Eur J Clin Invest 2008;38(9):686-692. [http://dx.doi.org/10.1111/j.1365-2362.2008.01994.x] 8. Becker DM, Chamberlain B, Swank R, et al. Relationship between corticosteroid exposure and plasma lipid levels in heart transplant recipients. Am J Med 1988;85(5):632-638. [http://dx.doi.org/10.1016/S0002-9343(88)80234-1] 9. Ettinger WH, Klinefelter HF, Kwiterovitch PO. Effect of short-term, low-dose corticosteroids on plasma lipoprotein lipids. Atherosclerosis 1987;63(2-3):167-172. [http://dx.doi.org/10.1016/0021-9150(87)90117-1] 10. Ettinger WH Jr., Hazzard WR. Prednisone increases very low density lipoprotein and high density lipoprotein in healthy men. Metabolism 1988;37(11):1055-1058. [http://dx.doi.org/10.1016/0026-0495(88)90067-4] 11. Scherbakova IA, Gerasimova EN, Perova NV, Titova VN, Koldaeva AP, Galakhova IE. [Effect of hydrocortisone on lipid composition of blood serum lipoproteins in the development of experimental atherosclerosis]. Vopr Med Khim 1975;21(6):589-595.

12. Staels B, van Tol A, Chan L, Verhoeven G, Auwerx J. Variable effects of different corticosteroids on plasma lipids, apolipoproteins, and hepatic apolipoprotein mRNA levels in rats. Arterioscler Thromb 1991;11(3):760-769. [http://dx.doi.org/10.1161/01.ATV.11.3.760] 13. Reaven EP, Kolterman OG, Reaven GM. Ultrastructural and physiological evidence for corticosteroid-induced alterations in hepatic production of very low density lipoprotein particles. J Lipid Res 1974;15(1):74-83.

14. Bagdade JD, Yee E, Albers J, Pykalisto OJ. Glucocorticoids and triglyceride transport: Effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. Metabolism 1976;25(5):533-542. [http://dx.doi.org/10.1016/0026-0495(76)90007-X] 15. Mahley RW. Apolipoprotein E: Cholesterol transport protein with expanding role in cell biology.

Science 1988;240(4852):622-630. [http://dx.doi.org/10.1126/science.3283935] 16. Lin RC. Effects of hormones on apolipoprotein secretion in cultured rat hepatocytes. Metabolism 1988;37(8):745-751. [http://dx.doi.org/10.1016/0026-0495(88)90009-1] 17. Hazra A, Pyszczynski NA, DuBois DC, Almon RR, Jusko WJ. Modeling of corticosteroid effects on hepatic low-density lipoprotein receptors and plasma lipid dynamics in rats. Pharm Res 2008;25(4):769-780. [http://dx.doi.org/10.1007/s11095-007-9371-8] 18. Nanjee MN, Miller NE. Plasma lipoproteins and adrenocortical hormones in men – positive association of low density lipoprotein cholesterol with plasma cortisol concentration. Clin Chim Acta 1989;180(2):113-120. [http://dx.doi.org/10.1016/0009-8981(89)90342-2] 19. Brotman DJ, Girod JP, Garcia MJ, et al. Effects of short-term glucocorticoids on cardiovascular biomarkers. J Clin Endocrinol Metab 2005;90(6):3202-3208. [http://dx.doi.org/10.1210/jc.2004-2379] 20. Atger V, Leclerc T, Cambillau M, et al. Elevated high density lipoprotein concentrations in heart transplant recipients are related to impaired plasma cholesteryl ester transfer and hepatic lipase activity. Atherosclerosis 1993;103(1):29-41. [http://dx.doi.org/10.1016/0021-9150(93)90037-U] 21. Choi HK, Seeger JD. Glucocorticoid use and serum lipid levels in US adults: The Third National Health and Nutrition Examination Survey. Arthritis Rheum 2005;53(4):528-535. [http://dx.doi.org/10.1002/art.21329]

Accepted 30 April 2014.

October 2014, Vol. 104, No. 10

Accredit your CPD activities: SA MEDICAL ASSOCIATION CPD LEVEL GUIDELINES Level

CRITERIA DESCRIPTION

DEFAULT UNITS

POINTS

1

Breakfast meetings or presentations

Hour

1

1

Formally arranged hospital or inter-departmental meetings or updates;

Hour

1

1

Case Study discussions/ Case Presentations

Hour

1

1

Formally organised special purpose teaching/learning ward rounds

Hour

1

1

Special purpose lectures/Seminars

Hour

1

1

Mentoring/Supervision activities/ Teaching and Training

Hour

1

1

Conferences, symposia, refresher courses, short courses, workshops

Hour

1

2

Principal Author of peer reviewed publication or chapter in book

Document/Presentation

15

2

Co-author of peer reviewed publication or chapter in book

Document/Presentation

5

2

Review of Article/Chapter in a book in book/journal

2

Principal presenter/author of a paper/poster congress/symposium/refresher course

Document/Presentation

10

2

Co-presenter/co-authors of a paper/poster at a congress/refresher course

Document/Presentation

5

2

Presenters of accredited Short Courses

Document/Presentation

10

2

Co-presenters of Short Courses

Document/Presentation

5

2

Interactive skills workshop with evaluation, presenter(10pts) participant(5pts)

Document/Presentation

2

MCQ in journals, including electronic - 70% pass rate

Per Questionnaire

3

2

Guest/occasional lecturer at a accredited institution

Per Lecture

3

2

Supervision of under/post graduates/interns - part time

Per Student

2 (max 16 in year)

3

2

External examiner of Master and Doctoral thesis on completion

Per thesis

5

2

Ethics workshops, lectures, seminars

Per Hour

2

2

Single modules of Masters degrees with part-time enrolment for non-degree purpose

On Completion

5

2

Professional interest groups (journal clubs)meet at least 6 times per year

Per Meeting

3

3

Post graduate degrees and diplomas

Qualification

30

3

Short courses - min 25 hours contact time

Qualification

30

3

Learning Portfolio’s

30

For further information contact: SAMA CPD Department: cpd@samedical.org 012Â 481 2082

EDITORIALS

SANHANES: A unique survey series in the health landscape Non-communicable diseases (NCDs), mainly cardiovascular diseases, cancers, chronic respiratory diseases and diabetes, represent a leading threat to human health and development. According to World Health Organization (WHO) statistics, these four preventable diseases are the world’s biggest killers, causing an estimated 35 million deaths each year – 60% of all deaths globally – with 80% in low- and middle-income countries.[1] Up to 80% of heart disease, stroke and type 2 diabetes and over a third of cancers could be prevented by eliminating shared risk factors, mainly tobacco use, an unhealthy diet, physical inactivity and the harmful use of alcohol.

Unless addressed with urgency, the mortality and disease burden from these health problems will continue to increase. The WHO projects that, globally, NCD deaths will increase by 17% over the next 10 years, and the greatest increase will be seen in the African region (27%).

In relation to NCDs, when Bradshaw et al.[2] conducted the first national burden of disease study for South Africa (SA) in 2000, they reported that 37% of deaths in this country were attributable to NCDs, many of which were associated with nutrition and lifestyle. In 2009, Mayosi et al.[3] concluded that the burden of NCDs in SA is ‘rising in rural communities, disproportionately affecting poor people living in urban settings, and resulting in an increase in the demand for care for chronic diseases’. In this regard, SA is undergoing an epidemio­ logical transition from communicable diseases to NCDs.[3] Recent and reliable estimates of population health parameters are therefore essential to understand the nature of the changing disease profile in the country and to translate such information into effective health promotion and disease prevention intervention programmes.

The 2012 South African National Health and Nutrition Examination Survey (SANHANES-1)[4] is the first of a series of surveys designed to assess the health and nutritional status of adults and children in SA. The collaborative network for the design and implementation of the survey, with the Human Sciences Research Council (HSRC) as the lead partner, included the National Department of Health (NDoH), the Medical Research Council, UNICEF, Stats SA, the Programme to Support Pro-poor Policy Development (PSPPD), and six universities (Free State, Limpopo, North West, Nelson Mandela Metropolitan, Stellenbosch and Western Cape). The survey was sponsored by the NDoH, the Department for International Development (UK) and the HSRC. Methodologically, SANHANES-1 provides baseline data on a representative sample of the population for future analysis over the longer term (longitudinal design of the survey), a policy approach initially adopted by the USA[5] (National Health and Nutrition Examination Survey (NHANES)) and more recently by other countries such as Canada[6] and China,[7] and in Europe.[8] The survey is unique in that it combines personal interviews with standardised physical examinations conducted by medical practitioners and nurses, diagnostic procedures and a variety of laboratory tests.

The completion of the SANHANES has facilitated both the detection and future tracking of the extent of current and emerging health priorities and the associated risk factors in the SA population of all ages. The SANHANES-1 findings provide the latest information on a broad range of health topics and associated risk factors that were beyond the scope of the previous national surveys in the health arena, and address the NDoH’s priority health indicators. The findings also provide national references for, among others, measurements such as height, weight and blood pressure, and are of interest to both health practitioners and researchers. The SANHANES-1 generated data

675

that can be used to develop health policy and health programmes and services. It also documented the health literacy of the nation, information that is vital for planning disease prevention and health promotion intervention programmes. In relation to NCDs, the survey documented the prevalence of obesity, dyslipidaemia, diabetes, impaired glucose homeostasis, hypertension (31.8%, when defined as blood pressure of systolic ≥140 mmHg or diastolic ≥90 mmHg, or currently on antihypertensive medication) and tobacco use, as well as perception of body weight, proxies of physical inactivity and poor dietary practices.[4] The latest evidence at the national level clearly indicates that SA indeed has a very significant burden of disease that is fuelled by a multiplicity of risk factors requiring multisectoral action and healthy public policies. Among the recommendations proposed in the report, the survey team strongly advocated the implementation and institutionalisation of the ‘Health in All Policies’ approach, as recently emphasised at the 8th WHO Global Conference on Health Promotion in Helsinki, Finland, in 2013.[9] This means implementation of healthy public policies within the framework of the National Development Plan – 2030 vision. The WHO’s recommended approach also means that other sectors’ policies and programmes must be consistent with the protection and promotion of public health.

Following the ministerial release, the SANHANES-1 report elicited extensive national and international coverage. Subsequent to the release of the report, there has been intensive demand for the survey’s data for policy formulation purposes from a number of national and provincial government departments, other than the NDoH, the Presidency, committees such as the National Surveillance System Committee and the Health Data Advisory and Coordinating Committee, academic institutions (including the Institute for Health Metrics and Evaluation, University of Washington), and NGOs and international organisations such as UNICEF, the World Bank and the WHO. While SANHANES-2 is being planned for implementation, a number of collaborative activities have been initiated for a more in-depth analysis of the SANHANES-1 data. The latter, as per HSRC policy, will be curated in due course and made available to the broader scientific community. It is also the intention to establish a specimen bank that will be made available for such use. Further, the SANHANES team is advising the National Food Technology Research Centre in Botswana on the design of the BOTSHANES survey, due to be conducted in the third quarter of 2015.

D Labadarios Executive Director: Population Health, Health Systems and Innovation, Human Sciences Research Council, Cape Town, South Africa Olive Shisana CEO, Human Sciences Research Council, Cape Town, South Africa Thomas Rehle Senior Programme Advisor, HIV/AIDS, STIs AND TB, Human Sciences Research Council, Cape Town, South Africa Leickness Simbayi Executive Director: HIV/AIDS, STIs AND TB, Human Sciences Research Council, Cape Town, South Africa Corresponding author: D Labadarios (dlabadarios@hsrc.ac.za)

October 2014, Vol. 104, No. 10

EDITORIALS

1. World Health Organization. 2008-2013 Action Plan for the Global Strategy for the Prevention and Control of Non-communicable Diseases. Geneva: WHO, 2008.

2. Bradshaw D, Groenewald P, Laubscher R, et al. Initial burden of disease estimates for South Africa, 2000. S Afr Med J 2003;93(9):682-688.

3. Mayosi BM, Flisher AJ, Lalloo UG, Sitas F, Tollman SM, Bradshaw D. The burden of noncommunicable diseases in South Africa. Lancet 2009;374(9693):934-947. [http://dx.doi.org/10.1016/ S0140-6736(09)61087-4] 4. Shisana O, Labadarios D, Rehle T, et al., and the SANHANES-1 Team. South African National Health and Nutrition Examination Survey (SANHANES-1): 2014 Edition. Cape Town: HSRC Press, 2014. http://www.hsrcpress.ac.za/product.php?productid=2314&cat=0&page=1&featured&freedownlo ad=1 (accessed 30 July 2014).

5. The National Health and Nutrition Examination Survey (NHANES), USA. http://www.cdc.gov/nchs/ nhanes.htm (accessed 30 July 2014).

6. The Joint Canada/United States Survey of Health (JCUSH). http://www.cdc.gov/nchs/nhis/jcush.htm (accessed 25 March 2013).

7. China Health and Nutrition Survey (CHNS). http://www.cpc.unc.edu/projects/china (accessed 29 August 2014).

8. European Health and Examination Survey. http://www.ehes.info/ (accessed 15 January 2014).

9. World Health Organization. Opening address, 8th Global Conference on Health Promotion, 10 June 2013, Helsinki, Finland. http://www.who.int/dg/speeches/2013/health_promotion_20130610/en/ (accessed 14 August 2014).

S Afr Med J 2014;104(10):675-676. DOI:10.7196/SAMJ.8842

The sexual and reproductive health needs of youth in South Africa – history in context Adolescence is a time of rapid transition, of significant emotional, physical and psychological changes.

These changes influence behaviour, in particular decisions to engage in risky behaviour, including sexual activity, alcohol consumption, smoking and taking drugs. Eighty-eight per cent of the 1.2 billion adolescents worldwide live in developing countries where access to sexual and reproductive health (SRH) services that could support them are often inadequate and fragmented.[1] Unplanned pregnancies can affect the health and wellbeing of adolescents, placing them at risk for morbidity and mortality related to unsafe abortion and childbirth, as well as limiting their educational and employment opportunities.

South African (SA) youth continue to be vulnerable, with an HIV prevalence of 7.3% reported for 15 - 24-year-olds in 2012.[2] A survey conducted in 2007 in four of the nine SA provinces showed that 19.2% of females aged 12 - 19 years had had at least one pregnancy, the majority of which were unwanted, while 5.8% of males in the same age group had impregnated a girl.[3] In addition, reported condom use by 15 - 24-year-olds in their most recent sexual encounter dropped from 85.2% to 67.5% for males and from 66.5% to 49.8% for females, according to two nationally representative surveys conducted in 2008 and 2012, respectively.[2] In 2008, the Youth Risk Behaviour Survey showed 30% of female learners reporting ever having had sex, with 24% reporting pregnancy.

[4] Fifteen per cent of the sexually active female learners reportedly did not usually use contraception, and 67% did not use condoms.

[4] In addition, 71% of the sexually active male learners did not use condoms,[4] and of the 4.4% of sexually active learners who had had a sexually transmitted infection (STI), only half had received treatment.

[5]

SA has a statutory commitment to address these problems,[5] so the state of youth SRH has not been ignored. Many government and nongovernmental organisation (NGO) initiatives have been implemented since SA’s transition to democracy, such as: • Policies addressing youth SRH (Table 1) • National media campaigns promoting awareness of HIV/AIDS among youth, e.g. the Soul City, Soul Buddyz and loveLife programmes • Peer education programmes, e.g. Old Mutual’s I Have Hope AIDS Peer Group Project (1993) and the Society for Family Health’s Abasha Phezulu Peer Helper project (1993) • Youth SRH service provision programmes, namely the National Adolescent Friendly Clinic Initiative (NAFCI) launched in 2001 and loveLife programmes • HIV prevention awareness programmes, e.g. the Stepping Stones HIV prevention programme.

676

The current guiding policy for youth SRH initiatives is the 2012 Integrated School Health Policy (ISHP), which outlines SRH care for youth. This policy states that all learners in secondary schools should receive SRH counselling, particularly risk behaviour counselling.

Dual-method contraception, HIV counselling and testing (HCT) and STI screening services are to be provided for sexually active learners by an on-site nurse or via referral to a healthcare facility offering the services.[5] However, provision of SRH preventive services (namely contraception and condom provision) in schools has been contested[6] in spite of the most recent youth HIV, STI and pregnancy statistics[4,5] and the 2005 SA Children’s Act (which enables youth aged >12 years to access SRH care services without parental consent and ensures confidentiality).[4]

Government-level school health programmes

In 1999, the Department of Education initiated the school health programme by establishing the National Policy on HIV and AIDS for Learners and Educators in Public Schools and Students and Educators in Further Education and Training Institutions.[7] As a result, the HIV and AIDS Life Skills Education Programme was implemented in 2000 with the aim of reducing the vulnerability of young people to HIV and AIDS and enhancing their knowledge and skills for responsible sexual behaviour decisions. The programme was implemented through Life Orientation (LO) subjects across all grades; however, evaluation studies identified challenges to this programme, such as insufficient LO teachers and lack of integration into the schools’ system and policies (among others).[7] The 2003 National School Health Policy (NSHP) was then implemented as a health promotion and preventive school-based initiative for youth, integrating school and other district health services. Some of the problems identified with the implementation of the NSHP included low service provision, suboptimal and inequitable nurse-to-school ratios, and the absence of referral services to respond to problems identified via screening assessments.[5] In 2009, the HIV and AIDS Life Skills Education Programme was revised, focusing among other things on risk behaviours such as unprotected sex and multiple concurrent sexual partners. Schoolbased support teams and school management teams were also established to aid implementation.[8] The ISHP was put into effect in 2012 to address the problems experienced with the NSHP. It is overseen collaboratively by the National Department of Health (DoH), the Department of Basic Education and the Department of Social Development. Offering higher-level support and increasing the number of schools included in the programme, the ISHP is expected to extend the range of services previously offered by the NSHP. However, with the expansion of services, concerns

October 2014, Vol. 104, No. 10

EDITORIALS

regarding implementation, feasibility, effective service delivery and sustainability have been raised.[6] The latest policy addressing youth SRH is the DoH’s integrated strategy on HIV, STIs and tuberculosis (TB), 2012 - 2016, which was rolled out in 2013.[7]

Research and evaluation of programmes and interventions

Questions about the implementation and efficacy of the above policies have far-reaching implications with regard to the state of youth SRH. Although limited, research studies have evaluated some of the initiatives, and there are various reports on the effectiveness of different youth SRH interventions.

Three years after the loveLife programme was initiated, a baseline study in all SA provinces revealed no significant differences in HIV and STI prevalence between youth living in communities with loveLife youth centres and NAFCI interventions compared with those in communities with no interventions.[9] It appeared that awareness or knowledge of youth interventions did not necessarily translate into engagement and/or behaviour change. However, a qualitative study on the NAFCI in the Greater Tzaneen subdistrict in Limpopo Province showed that adolescents used the NAFCI services at the clinic, especially contraception, STI and pregnancy services. Despite this, pregnancy and STI rates in the area did not decrease and HCT services were under-utilised.[10] A cross-sectional nationally representative household survey showed that men and women who participated in at least one loveLife programme were significantly less likely to be infected with HIV than those who did not.[11] Another cross-sectional populationbased household survey on 3 123 youth (aged 18 - 24 years) in four SA provinces reported that multimedia exposure and not face-toface programme exposure was found to be protective against HIV infection.[12] The Youth Friendly Services (YFS) programme, managed by loveLife between 1999 and 2006, was taken over by the DoH in 2006.

It was estimated that the YFS programme was implemented in 70% of primary healthcare facilities by 2012/13.[13] However, interviews conducted in 2011 with healthcare workers in eight healthcare centres in Agincourt, Mpumalanga Province, suggested that these services were lacking and fell below the national estimates.[13] An evaluation of 12 youth centres (under the loveLife programme, DoH centres and Youth and Adolescent Reproductive Health centres) was conducted nationally in 2001 among 1 399 youth aged 12 - 24 years and their parents. The survey showed that overall, while there was a fair degree of awareness of these centres, only 29% of youth visited the sites.[14] Interestingly, centres offering recreational activities were busier than those providing SRH services only. Many of these centres have since ceased to function owing to lack of funding.

Overall, the evidence is that while several youth programmes have been implemented to address SRH, youth still face barriers when accessing this care.

The implementation of a school-based SRH model is discussed

by Frolich et al.[15] in this issue of SAMJ. The school programme was provided by the Centre for the AIDS Programme of Research in South Africa (CAPRISA) mobile services. This model was developed for high-school students in 14 schools in KwaZulu-Natal Province and comprised in-school SRH components. It included information giving and counselling together with HCT and referral to in-school services or standard public health sector services if required.[15] The in-school services were provided by professional nurses from the study team and offered contraception including emergency contraception, HCT, syndromic management of STIs and pregnancy testing. In addition, referral was available for termination of pregnancy and HIV treatment and care. A counsellor was also available through a local NGO link who provided customised HCT incorporating counselling in relationships, negotiation around sex, high-risk sexual practices and assertive behaviour. These services were provided in the afternoon (12h00 - 16h00) and therefore could be accessed after the school day. The services were rotated through the schools. The model was designed with input from an extensive community consultation and uptake was high. The important finding that few referrals to out-of-school services were taken up, even though the local DoH had been consulted about the programme, highlights the reluctance to attend local DoH facilities for SRH care demonstrated by adolescent learners. This is supported by studies that have shown that healthcare workers lack adolescentfriendly training or restrict services to adolescents younger than 16 years,[4] and raises important concerns about whether these out-ofschool DoH- and NGO-driven services are acceptable, available and accessible, as it ultimately impacts upon service use by youth.

For long-term sustainability, the model implemented in the CAPRISA study would need to be adopted by the public sector, not only to provide the services but to ensure that the referral links with local facilities are youth friendly. Learners may lose interest and confidence in on-site services if they are unable or unwilling to attend standard services in their community. The model used in this study is aligned with the suggested model outlined in the ISHP, and the results suggest that the on-site approach is popular and acceptable to learners. However, the ISHP is also in the early stages of introduction, and though it is a good plan, it may be limited by resources in the public sector. As a follow-up to the CAPRISA study, we recommend that further research be undertaken to investigate how this on-site approach would be achieved if local public sector facilities could indeed spare staff to rotate through schools to provide services, and moreover provide

Table 1. Policies addressing youth SRH 1999

National Policy on HIV and AIDS for Learners and Educators in Public Schools and Students and Educators in Further Education and Training Institutions

2000

National HIV and AIDS Life Skills Education Programme

2003

National School Health Policy

2005

South African Children’s Act

2009

Revised HIV and AIDS Life Skills Education Programme

2012

Integrated School Health Policy

2013

Department of Health’s Integrated Strategy on HIV, STIs and TB, 2012 - 2016

SRH = sexual and reproductive health; STIs = sexually transmitted infections; TB = tuberculosis.

677

October 2014, Vol. 104, No. 10

EDITORIALS

services after school hours for referral. This could be based on the existing mobile clinic approach, as equipment and consumables would be required to provide basic SRH services.

Mags E Beksinska Maternal, Adolescent, and Child Health Research, Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of the Witwatersrand, Durban, South Africa, and Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, UK mbeksinska@matchresearch.co.za Lavanya Pillay Cecilia Milford Maternal, Adolescent, and Child Health Research, Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of the Witwatersrand, Durban, South Africa Jennifer A Smit Maternal, Adolescent, and Child Health Research, Department of Obstetrics and Gynaecology, Faculty of Health Sciences, University of the Witwatersrand, Durban, South Africa, and School of Pharmacy and Pharmacology, College of Health Sciences, University of KwaZulu-Natal, Durban Corresponding author: M Beksinska (mbeksinska@matchresearch.co.za) 1. Guttmacher Institute. Facts on the Sexual and Reproductive Health of Adolescent Women in the Developing World. New York: Guttmacher Institute, 2010. http://www.guttmacher.org/pubs/FBAdolescents-SRH.pdf (accessed 28 June 2014).

2. Shisana O, Rehle T, Simbayi LC, et al. South African National HIV Prevalence, Incidence and Behaviour Survey, 2012. Cape Town: HSRC Press, 2014:1-153.

3. Mchunu G, Peltzer K, Tutshana B, Seutlwadi L. Adolescent pregnancy and associated factors in South African youth. Afr Health Sci 2012;12(4):426-434. [http://dx.doi.org/10.4314/ahs.v12i4.5] 4. Holt K, Lince N, Hargey A, et al. Assessment of service availability and heath care workers’ opinions about young women’s sexual and reproductive health in Soweto, South Africa. Afr J Reprod Health 2012;16(2):283-294.

5. Department of Health and Department of Basic Education. Integrated School Health Policy 2012. http://www.education.gov.za/Programmes/HealthPromotion/IntegratedSchoolHealthProgramme/ tabid/870/Default.aspx on 09/07/2014 (accessed 9 July 2014).

6. Shung-King M. From ‘step-child of primary healthcare’ to priority programme: Lessons for the implementation of the National Integrated School Health Policy in South Africa. S Afr Med J 2013;103(12):895-898. [http://dx.doi.org/10.7196/SAMJ.7550] 7. Kumalo F, Panday S, Sithole S. The Department of Basic Education’s Draft Integrated Strategy on HIV and AIDS, 2012-2016. South Africa: Department of Basic Education, 2011. http://www.education.gov. za/LinkClick.aspx?fileticket=S1OOfnrAuLs%3d&tabid=869&mid=2451 (accessed 10 July 2014).

8. Panday S, Kumalo F, Dano A. Sexuality education – panacea for the prevention of HIV and AIDS amongst young people in schools? Presented at the 5th SA AIDS Conference, Durban, 9 June 2011. http://www.education.gov.za/LinkClick.aspx?fileticket=27cnozr3oVc%3D&tabid=93&mid=1722 (accessed 10 July 2014).

9. Pettifor AE, Kleinschmidt I, Levin J, et al. A community-based study to examine the effect of a youth HIV prevention intervention on young people aged 15-24 in South Africa: Results of the baseline survey.

Trop Med Int Health 2005;10(10):971-980. [http://dx.doi.org/10.1111/j.1365-3156.2005.01483.x] 10. Baloyi GO. The evaluation of the national adolescent-friendly clinic initiative (NAFCI) programme in greater Tzaneen sub-district, Limpopo Province, South Africa. Master’s dissertation. Pretoria: University of South Africa, 2006. http://uir.unisa.ac.za/bitstream/handle/10500/1640/dissertation. pdf?sequence=1 (accessed 8 July 2014).

11. Pettifor AE, Rees HV, Kleinschmidt I, et al. Young people’s sexual health in South Africa: HIV prevalence and sexual behaviours from a nationally representative household survey. AIDS 2005;19(14):1525-1534.

12. Peltzer K, Ramlagan S, Chirinda W, Mlambo G, Mchunu G. A community-based study to examine the effect of a youth HIV prevention programme in South Africa. Int J STD AIDS 2012;23(9):653-658. [http://dx.doi.org/10.1258/ijsa.2012.011457] 13. Geary RS, Gomez-Olive FX, Kahn K, Tollman S, Norris SA. Barriers to and facilitators of the provision of a youth-friendly health services programme in rural South Africa. BMC Health Serv Res 2014;14(259):1-8. [http://dx.doi.org/10.1186/1472-6963-14-259] 14. Erulkar AS, Beskinska M, Cebekhulu Q. An assessment of youth centres in South Africa, 2001. http:// pdf.usaid.gov/pdf_docs/PNACN848.pdf (accessed 27 July 2014).

15. Frolich JA, Mkhize N, Dellar RC, Mahlase G, Montague C, Abdool Karim Q. Meeting the sexual and reproductive health needs of high school students in South Africa: Experiences from rural KwaZuluNatal. S Afr Med J 2014;104(10):687-690. [http://dx.doi.org/10.7196/SAMJ.7841]

S Afr Med J 2014;104(10):676-678. DOI:10.7196/SAMJ.8809

Orphans, HIVE and HAND: Who are the watch-keepers?

Since 2004, substantial numbers of South African (SA) children have benefited from antiretroviral treatment. Untreated children are at risk of central nervous system (CNS) sequelae, with prevalence rates of 20 - 60%.[1,2] HIV-1 invades the developing CNS earlier and with greater severity than in adults, resulting in the condition known as HIV encephalopathy (HIVE).[1] In addition, patients on highly active antiretroviral therapy (HAART) may remain vulnerable to the effects of HIV on the brain, because the CNS may be a reservoir for persistent viral replication.[3] The concept of a ‘milder’ form of neurocognitive disturbance in HIV-infected children, akin to the adult condition of HAND (HIV-associated neurocognitive disorder), is recognised but has yet to be defined.[4] This ‘milder’ condition of HAND may have significant effects in functional terms on a child’s learning potential. Furthermore, early severe deprivation is often associated with neurocognitive delay and/ or cognitive impairment.[5,6] Facilitating optimal development of ‘heart’, mind and body is a priority among professionals caring for sick children.

In SA, children with developmental quotients (DQs) of ≥65 attend mainstream schools. Those with DQs between 35 and 50 may receive education at training centres. Children in the grey area with DQs of 51 - 64 may go onto a waiting list for a special-needs school. However, the trend now is for inclusive education, and the reality is that such learners remain in mainstream schooling with minimal remedial support. Two short case scenarios and a letter from an educator

678

highlight the limitations of this system in the context of children living with HIV. A, aged 10 years. A spent the early part of his life in St Joseph’s Home in Cape Town as an orphan, because no family member could be traced. When he was 1 year old, HIVE was diagnosed and he was enrolled on HAART. He had a mastoidectomy which has left him disfigured. When he was 25 months old, a developmental assessment showed that his gross motor development was at the level of 11 months, his fine motor development at 18 months, his language at 9 months and his personal/social development at 9 - 12 months. Repeated tests showed a similar pattern. It was recommended that he attend a LSEN (learner with special education needs) school, but we were informed that when he went for assessment, his ‘home’ mother at the orphanage was told he was too high-functioning to attend. He was therefore enrolled in a mainstream school in grade R in 2009 and proceeded to grade 1 in 2011. The attending developmental paediatrician wrote to the education district office in 2011 and recommended consideration for transfer to an LSEN school. This did not happen, and he repeated grade 1 in 2012. Apparently he receives ongoing teacher support after school in a class of 8 children. His DQ is 75, with severe weaknesses in his verbal score and with abstract tasks. Each year, his report shows outcome scores of 1 (‘not achieved’) despite which he gets promoted to the next grade. He is now 10 years old, cannot read and has rudimentary writing and numeracy skills. The health professionals and his caregiver are all concerned regarding his future. He appears to be happy and he gets on well with the other children at the orphanage,

October 2014, Vol. 104, No. 10

EDITORIALS

but what does the future hold for this child? What can he dream about achieving, and how can we help him to set achievable goals?

B, aged 12 years. B was abandoned by her mother and spent her early years in Nazareth House, Cape Town. HIVE was diagnosed and HAART commenced. Placement at a children’s home was secured. Her motor milestones were delayed and she only walked independently at 2 years, 7 months. She apparently repeated grade 1 three times and grade 2 twice. She underwent cognitive testing in 2011, which showed that her general intellectual functioning was borderline, motor co-ordination average, processing speed borderline, attention profoundly impaired, working memory average, visual spatial ability borderline, language low average, verbal memory low average, visual memory borderline, and executive functioning low average. Behaviour problems necessitated psychiatric referral.

She continues to struggle at school, and her caregiver and attending health professionals are extremely concerned. She has responded well to antiretrovirals (ARVs) and is virologically suppressed, but what chance does she have of living a dignified and fulfilling life when she cannot read and struggles with numeracy?

The two children described represent the tip of the iceberg. In our clinics we have at least another 150 about whom we are concerned. What about children in the rural areas? Such children will leave school at the age of 16 years and in all likelihood will never have the satisfaction of being employed. Educators, as reflected in the letter below from a caring teacher, are turning to health professionals for education plans.

‘I’ve got this little boy called ----. He came to my attention this year. He is doing grade 2 for the first time. He is not coping at all. He cannot read. He only writes when we copy from the chalk-board. He cannot listen to the instructions and answer correct questions. He just copy [sic] the questions again. He repeated grade 1 and progresses to the next grade. Our policy stated that child cannot stays [sic] in same grade for more than 2 years. Because of that policy he is going to be progressed [sic] to the next grade what [sic] is grade 3.’

This editorial seeks to create an awareness of this tragic problem.

How do we find ways of combining health and educational resources to educate and maximise the potential of children living with HIV? Roll-out of ARVs has helped, but these children still have a long and bumpy road to navigate. Their current circumstances fall far short of the realisation of their constitutional rights.

679

Kathie Walker Medical Officer, Neurology and Cardiology, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa, and G26 HIV/AIDS Service, Groote Schuur Hospital, Cape Town buley@iafrica.com Mandy Inglis Medical Officer, G26 HIV/AIDS Service, Groote Schuur Hospital, Cape Town, South Africa Gwen Norton Rebecca Sher Dayle Zieff Medical Officers, G26 HIV/AIDS Service, Groote Schuur Hospital, Cape Town, South Africa, Crossroads HIV/AIDS Service, Cape Town, and Mitchell’s Plain HIV/AIDS Service, Cape Town Taryn McCann Clinical Psychologist, HIV/TB Specialised Health Department, City of Cape Town, South Africa Paul Roux Director, G26 HIV/AIDS Service, Groote Schuur Hospital, Cape Town, South Africa 1. Van Rie A, Harrington PR, Dow A, Robertson K. Neurologic and neurodevelopmental manifestations of pediatric HIV/AIDS: A global perspective. Eur J Paediatr Neurol 2007;11(1):1-9. [http://dx.doi. org/10.1016/j.ejpn.2006.10.006] 2. Lobato MN, Caldwell MB, Ng P, Oxtoby MJ. Encephalopathy in children with perinatally acquired human immunodeficiency virus infection. Pediatric Spectrum of Disease Clinical Consortium. J Pediatr 1995;126(5):710-715. [http://dx.doi.org/10.1016/S0022-3476(95)70397-7] 3. Sonza S, Crowe S. Reservoirs for HIV infection and their persistence in the face of undetectable viral load. AIDS Patient Care STDS 2001;15(10):511-518. [http://dx.doi. org/10.1089/108729101753205676] 4. Martin SC, Wolters PM, Toledo-Tamula MA, et al. Cognitive functioning in school-aged children with vertically acquired HIV infection being treated with highly active antiretroviral therapy (HAART). Dev Neuropsychol 2006;30(2):633-657. [http://dx.doi.org/10.1207/ s15326942dn3002_1] 5. Rutter ML, Kreppner JM, O’Connor TG. English, Romanian Adoptees Study Team. Specificity and heterogeneity in children’s responses to profound institutional privation. Br J Psychiatry 2001;179(2):97-103. [http://dx.doi.org/10.1192/bjp.179.2.97] 6. Behen ME, Helder E, Rothermel R, et al. Incidence of specific absolute neurocognitive impairment in globally intact children with histories of early severe deprivation. Child Neuropsychol 2008;14(5):453469. [http://dx.doi.org/10.1080/09297040802244136]

S Afr Med J 2014;104(10):678-679. DOI:10.7196/SAMJ.8274

October 2014, Vol. 104, No. 10

RESEARCH

Monitoring of non-communicable diseases such as hypertension in South Africa: Challenges for the post-2015 global development agenda C Day,1 BSc Pharm, MMedSci; P Groenewald,2 MB ChB, MPH; R Laubscher,3 BComm; S Chaudhry,1 BSc MPH; N van Schaik,1 MB ChB; D Bradshaw,2 DPhil (Oxon) ealth Systems Trust, Durban, South Africa H Burden of Disease Research Unit, Medical Research Council, Cape Town, South Africa 3 Biostatistics Unit, Medical Research Council, Cape Town, South Africa 1 2

Corresponding author: Candy Day (candy.day@hst.org.za)

Background. Examining the non-communicable disease (NCD) profile for South Africa (SA) is crucial when developing health interventions that aim to reduce the burden of NCDs. Objective. To review NCD indicators in national data sources in order to describe the burden of NCDs in SA, using hypertension as an example.

Methods. Age, gender, district of death and underlying cause of death data were obtained for 2008 and 2009 mortality unit records from Statistics SA and adjusted using STATA 11. Data for raised blood pressure were obtained from four national household surveys: the South African Demographic and Health Survey 1998, the Study on Global Ageing and Adult Health 2007, and the National Income Dynamics Study 2008 and 2010.

Results. The proportion of years of life lost due to NCDs was highest in the metros and least-deprived districts, with all metros (especially Mangaung) showing high age-standardised mortality rates for ischaemic heart disease, cerebrovascular disease and hypertensive disease.

The prevalence of hypertension has increased since 1998. National household surveys showed a measured hypertension prevalence of over 40% in adults aged ≥25 years in 2010. Treatment coverage was 35.7%. Only 36.4% of hypertensive cases (on treatment) were controlled.

Conclusion. Further work is needed if NCD monitoring is to be enhanced. Priority targets for NCDs must be integrated into national health planning processes. Surveillance requires integration into national health information systems. Within primary healthcare, a larger focus on integrated chronic care is essential.

S Afr Med J 2014;104(9):680-687. DOI:10.7196/SAMJ.7868

The idea of universal health coverage (UHC) as a goal of health policy development has gained wide acceptance at both national and global levels since the publication of the World Health Report 2010.[1] UHC is now also being seen as a critical component of sustainable development and as such has been proposed as one of the key goals of the post-2015 development agenda that it is envisaged will extend the development challenges posed by the Millennium Development Goals.[2] Its aim is to ensure that all have access to needed healthcare of sufficient quality to be effective and that all have financial protection from the costs associated with using such health services. Reducing non-communicable diseases (NCDs) and their risk factors is one of the neglected priorities within this goal.

In March 2013, the World Health Assembly adopted the comprehensive global monitoring framework for NCDs[3] and urged member states to develop national targets and indicators. In August 2013, the South African (SA) national Department of Health (DoH) released its Strategic Plan for the Prevention and Control of Noncommunicable Diseases 2013-17,[4] setting out national goals and targets. Table 1 shows these targets, together with those of the World Health Assembly. Such a strategy was crucial, given that estimates had predicted that the burden of disease relating to NCDs would continue to rise in SA if left unchecked.[5,6] In order to identify health interventions that will focus on reducing the burden of NCDs, it is important to examine the burden of NCD profile for the country. This study aimed to do this by reviewing NCD indicators in national data sources in SA.

680

Methods

The burden of disease analysis was based on the unit records for 2008 and 2009 mortality data provided by Statistics SA. These included age, sex, district of death and underlying cause of death coded to the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10).

STATA 11 was used to adjust the data, firstly by redistributing deaths of unknown ages proportionally by age and gender across each of the known causes of death. Causes of death used as pseudonyms for AIDS were combined with the HIV deaths.

Deaths misclassified to ill-defined signs and symptoms and other ‘garbage codes’ (intermediate causes of death such as septicaemia; mechanisms of death such as cardiac arrest, which could be produced by a variety of different causes; partially specified causes such as cancer with unknown site of the disease; or risk factors such as hypertension) were proportionally redistributed to specified causes within each age and gender category. The ICD codes were aggregated according to the updated National Burden of Disease (NBD) list, which is a condensed list of conditions containing the most prevalent diseases across SA, including those of public health importance. The proportions of deaths and years of life lost (YLLs) due to the four broad cause groups were calculated for each of the 52 districts. YLLs are a measure of premature mortality based on the age at death and therefore highlight the causes of death that should be targeted for prevention. In line with the initial SA NBD study, the highest observed national life expectancy was selected as the standard against which YLLs are calculated.

October 2014, Vol. 104, No. 10

RESEARCH

Data for raised blood pressure are presented from four national household surveys: the South African Demographic and Health Survey (SADHS) 1998,[7] the Study on Global Ageing and Adult Health (SAGE) 2007,[8] and the National Income Dynamics Study (NiDS) 2008[9] (wave 1) and 2010[10] (wave 2). (Note: The third wave of the NiDS has been released, together with updates to the previous two waves, since this analysis was completed.)

Individuals were classified as hypertensive if their average systolic blood pressure was ≥140 mmHg or their diastolic blood pressure ≥90 mmHg, or if they used blood pressure medication. The data were checked for outlier values, which were excluded from the analysis.

Individuals without a valid blood pressure measurement who were not on blood pressure medication were omitted from the analysis. (A valid blood pressure measurement complies with the following set of rules: systolic 80 - 240 mmHg; diastolic 35 - 140 mmHg; systolic at least 15 units more than the corresponding diastolic; absolute difference between two systolic or diastolic measurements not more than 5 units.)

While the surveys had similar procedures for measuring hypertension, the sampling procedures were slightly different.

Triangulation of multiple data sources was therefore undertaken to better describe the burden of disease and effective treatment coverage of hypertension.

Table 1. Non-communicable disease prevention and control goals and targets set by the World Health Assembly and the South African Strategic Plan for the Prevention and Control of Non-communicable Diseases WHO, 66th World Health Assembly – a set of voluntary global targets for the prevention and control of NCDs: Global targets for 2025 and selected indicators Premature mortality from non-communicable disease arget: A 25% relative reduction in overall mortality from cardiovascular T diseases, cancer, diabetes, or chronic respiratory diseases Behavioural risk factors arget: At least a 10% relative reduction in the harmful use of alcohol, as T appropriate, within the national context Target: A 10% relative reduction in prevalence of insufficient physical activity Indicators: Prevalence of insufficiently physically active adolescents defined as <60 minutes of moderate- to vigorous-intensity activity daily ge-standardised prevalence of insufficiently physically active persons aged A ≥18 years (defined as <150 minutes of moderate-intensity activity per week, or equivalent) Target: A 30% relative reduction in mean population intake of salt/sodium arget: A 30% relative reduction in prevalence of current tobacco use in persons T aged ≥15 years Biological risk factors

Target: A 25% relative reduction in the prevalence of raised BP, or contain the prevalence of raised BP according to the national circumstances I ndicator: Age-standardised prevalence of raised BP among persons aged ≥18 years (defined as systolic BP ≥140 mmHg and/or diastolic BP ≥90 mmHg) Target: Halt the rise in diabetes and obesity

South African Strategic Plan for the Prevention and Control of Non-communicable Diseases: 2020 goals and targets 1. R educe by at least 25% the relative premature mortality (<60 years) from NCDs by 2020 2. Reduce by 20% tobacco use by 2020 3. R educe by 20% the per capita consumption of alcohol by 2020 4. R educe mean population intake of salt to <5 g per day by 2020 5. Reduce by 10% the percentage of people who are obese and/or overweight by 2020 6. R educe the prevalence of people with raised BP by 20% by 2020 (through lifestyle and medication) 7. I ncrease the prevalence of physical activity (defined as 150 minutes of moderate-intensity physical activity per week, or equivalent) by 10% 8. Every woman with sexually transmitted diseases to be screened for cervical cancer every 5 years, otherwise every woman to have three screens in a lifetime (and as per policy for women who are HIV-positive) 9. Increase the percentage of people controlled for hypertension, diabetes and asthma by 30% by 2020 in sentinel sites 10. Increase the number of people screened and treated for mental disorders by 30% by 2030 [sic]

Indicators: Prevalence of overweight and obesity in adolescents Age-standardised prevalence of overweight and obesity in persons aged ≥ 18 years (defined as BMI ≥25 for overweight and BMI ≥30 for obesity) National systems response Target: At least 50% of eligible people receive drug therapy and counselling (including glycaemic control) to prevent heart attacks and strokes Indicator: Proportion of eligible persons (defined as aged ≥40 years with a 10-year cardiovascular risk ≥30%, including those with existing cardiovascular disease) receiving drug therapy and counselling (including glycaemic control) to prevent heart attacks and strokes arget: An 80% availability of the affordable basic technologies and essential T medicines, including generics, required to treat major non-communicable diseases in both public and private facilities WHO = World Health Organization; NCDs = non-communicable diseases; BP = blood pressure; BMI = body mass index (kg/m²).

681

October 2014, Vol. 104, No. 10

RESEARCH

Results

The burden of disease analysis shows that NCDs have become the largest broad cause of YLLs in South Africa (32.0% of YLLs in 2009). The percentage of YLLs per district by broad cause group is shown in

Fig. 1, highlighting substantial differences in the burden due to NCDs relative to that caused by injuries, HIV, tuberculosis, communicable, maternal, perinatal and nutrition-related diseases. The percentage of YLLs due to NCDs tends to be highest

in the metros and least-deprived districts.

Individual causes of death due to NCDs feature strongly in the ten leading causes of mortality. All metros show high agestandardised mortality rates for ischaemic heart disease, cerebrovascular disease and

Fig. 1. Percentage of YLLs by broad cause group, by district, 2009. (YLLs = years of life lost; NCD = non-communicable disease; TB = tuberculosis.)

682

October 2014, Vol. 104, No. 10

RESEARCH Metro Buffalo City

Cape Town

Ekurhuleni

eThekwini

Johannesburg

Mangaung

N Mandela Bay

Tshwane

Rank 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12

Leading cause Tuberculosis Cerebrovascular disease Hypertensive heart disease HIV/AIDS Ischaemic heart disease Lower respiratory infection COPD Oesophagus Fires, hot substances Diarrhoeal disease Interpersonal violence Diabetes mellitus Ischaemic heart disease Tuberculosis Hypertensive heart disease Cerebrovascular disease HIV/AIDS Trachea/bronchi/lung Interpersonal violence COPD Lower respiratory infection Road injuries Diabetes mellitus Fires, hot substances Lower respiratory infection Tuberculosis Cerebrovascular disease Ischaemic heart disease Hypertensive heart disease HIV/AIDS Diarrhoeal disease COPD Diabetes mellitus Fires, hot substances Meningitis/encephalitis Nephritis/nephrosis Tuberculosis Ischaemic heart disease Cerebrovascular disease Lower respiratory infection Diarrhoeal disease HIV/AIDS Hypertensive heart disease Interpersonal violence Diabetes mellitus Nephritis/nephrosis Road injuries Meningitis/encephalitis Lower respiratory infection Tuberculosis Ischaemic heart disease Cerebrovascular disease HIV/AIDS Hypertensive heart disease Diarrhoeal disease COPD Fires, hot substances Nephritis/nephrosis Septicaemia Diabetes mellitus Tuberculosis Lower respiratory infection Hypertensive heart disease Cerebrovascular disease Diarrhoeal disease HIV/AIDS Ischaemic heart disease Nephritis/nephrosis COPD Diabetes mellitus Septicaemia Fires, hot substances Tuberculosis Hypertensive heart disease Cerebrovascular disease HIV/AIDS Ischaemic heart disease Lower respiratory infection Interpersonal violence Diabetes mellitus Asthma Diarrhoeal disease Trachea/bronchi/lung COPD Hypertensive heart disease Ischaemic heart disease Lower respiratory infection Tuberculosis Cerebrovascular disease HIV/AIDS Road injuries Diarrhoeal disease Diabetes mellitus COPD Nephritis/nephrosis Cardiomyopathy

Broad cause group of leading causes Communicable, maternal, perinatal and nutrition HIV and TB Injuries NCDs

319.0 135.7 118.3 105.0 98.5 96.4 73.6 60.1 58.6 55.0 46.1 44.9 126.1 87.5 75.5 72.1 64.9 45.5 39.5 34.2 33.0 22.2 21.7 19.1 175.8 155.1 95.2 93.2 80.5 78.8 77.3 38.2 33.6 32.9 32.0 28.7 231.5 143.6 121.8 116.2 89.1 86.6 79.6 44.4 40.3 37.2 33.0 26.3 116.7 112.0 88.5 83.0 79.1 75.6 48.1 37.5 33.0 32.9 30.5 30.3 361.2 304.6 161.8 148.3 138.0 119.9 104.9 46.9 44.7 44.0 41.7 40.9 239.6 129.8 109.7 100.6 99.0 71.4 55.3 45.5 43.1 39.3 38.8 36.5 128.1 112.8 109.8 102.0 94.8 79.5 60.7 57.6 35.9 31.6 30.8 27.5 0

50

100

150 200 250 Deaths (/100 000)

300

350

400

Fig. 2. Leading age-standardised mortality rates (deaths/100 000 population) by metro, highlighting NCD causes, 2009. (NCD = noncommunicable disease; COPD = chronic obstructive pulmonary disease; TB = tuberculosis.)

683

October 2014, Vol. 104, No. 10

RESEARCH

Fig. 3. Hypertension indicators based on four surveys, by gender and age group, 1998 - 2010.

684

October 2014, Vol. 104, No. 10

RESEARCH

Table 2. Main chronic NCD indicators in the DHIS, SA Existing data based on NIDS 2010 Group

Indicator

Chronic care

Asthma detection rate, %

2008/09

2009/10

2010/11

2011/12

2012/13

Status of indicator in NIDS 2013

0.1

0.2

0.1

Discontinued

Asthma <18 years rate, %

15.5

16.9

18.2

Discontinued

Diabetes high-risk cases incidence rate (annualised), /1 000

2.3

2.8

1.8

NIDS 2013 – changed to ‘Diabetes incidence (annualised)’

Diabetes mellitus caseload, %

3.1

3.2

2.5

1.7

1.3

Discontinued

Diabetes mellitus detection rate, %

0.1

0.1

0.1

0.1

0.1

NIDS 2013 (split into <18 and ≥18 years) and changed to /1 000

Epilepsy detection rate, %

0.1

0.1

0.1

Discontinued

Epilepsy <18 years rate, %

18.0

17.2

17.2

Discontinued

9.0

6.4

5.1

Discontinued

Hypertension caseload, %

12.1

12.3

Hypertension detection rate, %

0.3

0.3

Hypertension high-risk cases incidence rate (annualised), /1 000

0.4

0.3

0.2

Discontinued

7.6

7.6

4.9

NIDS 2013 – changed to ‘Hypertension incidence (annualised)’*

Eye care

Cataract surgery rate (annualised), /million

231.5

387.6

546.9

729.8

553.2

NIDS 2013

Mental health

Mental health caseload, %

0.3

0.3

0.9

1.3

1.4

NIDS 2013 – additional indicators added relating to mental health admissions

Mental health visits ≥18 years rate, %

94.7

94.0

94.8

95.7

95.6

NIDS 2013

Cervical cancer screening coverage (annualised), %

46.5

47.6

52.2

55.0

55.4

NIDS 2013

Reproductive health

NCD = non-communicable disease; DHIS = District Health Information System; SA = South Africa; NIDS = National Indicator Data Set. * The NIDS 2013 proposes to measure hypertension incidence (annualised), which includes newly diagnosed hypertension clients (of all ages) initiated on treatment per 1 000 population aged ≥40 years.

hypertensive disease (Fig. 2), although the overall age-standardised mortality for NCDs in Mangaung (1 082.2/100 000 population) is 1.6 times higher than in Cape Town (676.0).

Extensive routine information systems exist for key infectious diseases as well as maternal and child health, but minimal information is available on NCDs. Chronic disease rates collected by the District Health Information System (DHIS) are difficult to interpret in terms of disease burden or service coverage.[11] Many indicators are not collected by all provinces, and most indicators have either been discontinued or altered between the 2010 and 2013 National Indicator Data Sets. Table 2 shows the currently available chronic disease indicators at national level.

Fig. 3 shows hypertension indicators based on four surveys: SADHS, SAGE, NiDS 2008 and NiDS 2010. The number of survey respondents (aged ≥15 years) was 13 826 for SADHS 1998, 4 227 for SAGE 2007, 16 878 for NiDS 2008 and 21 955 for NiDS 2010. National household surveys showed a measured hypertension prevalence of over 40% in adults aged ≥25 years in 2010. Selfreported prevalence was much lower, indicating that most cases were not diagnosed. Treatment coverage was very low (35.7%), and only 36.4% of those on treatment were controlled. Results show that the prevalence of hypertension has increased since 1998, and that it increases with advancing age (both genders, all surveys), with high levels of hypertension (typically between 50% and 75%) among individuals aged ≥45 years in all surveys. In general, the prevalence among young males is higher than that among young females, while it is higher among females in the older age categories. The SAGE 2007

685

generally reports higher prevalences than the NiDS 2008 per gender and age category. In an analysis of the SAGE data for all six countries, SA had the highest hypertension prevalence rate of 77.9% in people aged ≥50 years.[12] Fig. 4 outlines the number of adults with hypertension, the num­ ber on treatment and the number controlled on treatment based on the three most recent surveys. There are about 8.2 million people aged ≥15 years with hypertension in SA, of whom about 2.7 million are on treatment (and about 0.9 million controlled on treatment).

The estimated diagnosed cases of hypertension reported in the South African Health Review 2011 (based on the total population and disease incidence rates extrapolated from the private sector risk equalisation fund study) was 3.3 million (with 2.1 million on treatment).[13] Similarly, the Statistics SA General Household Survey 2010 indicates that 3.2 million adults aged ≥25 years have selfreported hypertension.[14] Multiple sources therefore confirm the huge number of people with hypertension who are not diagnosed and hence are untreated, and the substantial number on treatment who are not controlled.

Discussion

Burden of disease analysis is useful for monitoring the ultimate impact of NCDs. In 2009, YLLs due to NCDs surpassed those from communicable and related causes. NCDs such as cerebrovascular, hypertensive and ischaemic heart disease are in the leading ten agestandardised causes of death in all metros. Improved quality and completeness of death registration are needed for reliable results.

October 2014, Vol. 104, No. 10

RESEARCH

Fig. 4. Estimated numbers with hypertension, on treatment and controlled on treatment, based on three surveys, by gender and age group, 2007 - 2010.

(M = million.)

The DHIS has potential to monitor health service delivery for NCDs, but late adoption of well-formulated indicators has limited its utility so far.

Surveys provide limited geographical disaggregation and trend analysis, yet they address some monitoring gaps and are better suited to understanding the complex interplay of risk factors, demographics, equity, service availability and quality that are components of achieving UHC. The South African National Health and Nutrition Examination Survey[15] is expected to provide rich data for evaluation of NCDs. The reported prevalence of hypertension of 10.2% for participants aged ≥15 years is substantially lower than expected,

686

but cannot be directly compared with other sources because it only measures high blood pressure (systolic ≥140 mmHg and diastolic ≥90 mmHg) and excludes patients on medication and controlled. There is a need to standardise the definition of hypertension indicators in terms of the age categories included (World Health Organization ≥18 years, SA not specified but ≥15 years usually reported) and whether controlled hypertensives are included (hypertension prevalence) or not (raised systolic and/or diastolic pressure prevalence), so as to ensure uniformity across all current monitoring frameworks.

More work is needed to refine NCD monitoring in SA, to enable the ten goals of the National Strategic Plan to be assessed. The priority

October 2014, Vol. 104, No. 10

RESEARCH

targets for NCDs need to be integrated into national health planning processes, and surveillance requires integration into national health information systems. Finally, a greater focus on integrated chronic care within primary healthcare is needed at all levels to meet the longterm requirements for the effective management of NCDs. References 1. World Health Organization. Health Systems Financing: The Path to Universal Coverage. The World Health Report 2010. Geneva: WHO, 2010. www.who.int/whr/2010/en/ (accessed 22 November 2010).

2. Thematic Group on Health for All. Health in the Framework of Sustainable Development. Technical Report for the Post-2015 Development Agenda. Paris: Sustainable Development Solutions Network (SDSN), 2014.

3. World Health Organization. Draft Comprehensive Global Monitoring Framework and Targets for the Prevention and Control of Noncommunicable Diseases A66/8. Geneva: WHO, 2013. http://apps.who. int/gb/ebwha/pdf_files/WHA66/A66_8-en.pdf (accessed 8 May 2013).

4. National Department of Health. Strategic Plan for the Prevention and Control of Non-Communicable Diseases 2013-17. Pretoria: NDoH, 2013.

5. Abegunde DO, Mathers CD, Adam T, Ortegon M, Strong K. The burden and costs of chronic diseases in low-income and middle-income countries. Lancet 2007;370(9603):1929-1938. [http://dx.doi. org/10.1016/S0140-6736(07)61696-1]

6. Mayosi BM, Flisher AJ, Lalloo UG, Sitas F, Tollman SM, Bradshaw D. The burden of non-communicable diseases in South Africa. Lancet 2009;374(9693):934-947. [http://dx.doi.org/10.1016/S0140-6736(09)61087-4] 7. Department of Health, Medical Research Council, and Macro International. South African Demographic and Health Survey 1998. Full Report. Pretoria: National Department of Health, 2002.

8. Kowal P, Chatterji S, Naidoo N, et al. Data resource profile: The World Health Organization Study on global AGEing and adult health (SAGE). Int J Epidemiol 2012;41(6):1639-1649. [http://dx.doi.org/ 10.1093/ije/dys210] 9. Southern Africa Labour and Development Research Unit. National Income Dynamics Study 2008, Wave 1 [dataset]. Version 4.1 ed. Cape Town: DataFirst, 2012.

10. Southern Africa Labour and Development Research Unit. National Income Dynamics Study 2010-11, Wave 2 [dataset]. Version 1 ed. Cape Town: DataFirst, 2012.

11. Massyn N, Day C, Haynes R, Barron P, English R, Padarath A. District Health Barometer 2011/12.

Durban: Health Systems Trust, 2013.

12. Lloyd-Sherlock P, Beard J, Minicuci N, Ebrahim S, Chatterji S. Hypertension among older adults in low- and middle-income countries: Prevalence, awareness and control. Int J Epidemiol 2014;43(1):11628. [http://dx.doi.org/10.1093/ije/dyt215] 13. Day C, Gray A, Budgell E. Health and related indicators. In: Padarath A, English R, eds. South African Health Review 2011. Durban: Health Systems Trust, 2011.

14. General Household Survey 2010. Statistical Release P0318 (Revised version). Pretoria: Statistics South Africa, 2011.

15. Shisana O, Labadarios D, Rehle T, et al. South African National Health and Nutrition Examination Survey (SANHANES-1). Cape Town: HSRC Press, 2013.

Accepted 2 April 2014.

Meeting the sexual and reproductive health needs of high-school students in South Africa: Experiences from rural KwaZulu-Natal J A Frohlich,1 DCur; N Mkhize,1 RN; R C Dellar,1 MBiochem; G Mahlase,2 BCur, BSocSc Hons; C T Montague,1 MBA, PhD; Q Abdool Karim,3 PhD entre for the AIDS Programme of Research in South Africa (CAPRISA), Nelson R Mandela School of Medicine, C College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa 2 Zimnandi Zonke, 69 West Street, Pietermaritzburg, South Africa 3 Mailman School of Public Health, Department of Epidemiology, Columbia University, New York, USA 1

Corresponding author: Q Abdool Karim (abdoolq2@ukzn.ac.za) Background. Adolescents in South Africa (SA) have a huge unmet need for sexual and reproductive health (SRH) services. Integrating such services into schools may overcome many of the current barriers to access.

Objectives. We describe an SRH service model developed for high-school students and its implementation in 14 high schools in rural SA. Methods. Following consultation with community and other key stakeholders about the demand for and acceptability of adolescenttargeted SRH services, a three-tier school-based model was developed that included: (i) in-school group SRH information and awareness sessions; (ii) in-school individual SRH counselling and customised HIV counselling and testing (CCT); and (iii) referrals to in-school fixed, in-school mobile or public sector primary SRH clinics.

Results. From October 2011 to June 2012, 70 consultative meetings were held. There was overwhelming support for the pilot founded on concerns about the high HIV prevalence and teenage pregnancy rates among adolescents in the community. SRH information was provided to 8 867 high-school students, 4 171 (47.0%) of whom accessed on-site CCT services for HIV. The gender-specific prevalence of HIV in these students was 3.3% (64/1 962) and 1.1% (24/2 209) for females and males, respectively. Two hundred and thirty-nine students (5.7%) were referred for clinical services at in-school fixed, in-school mobile or public sector primary SRH clinics.

Conclusions. The SRH service provision pilot was acceptable in the community and seems feasible for scale-up. Further work is required to understand inter-school variability in uptake, identify additional service needs of students, and characterise SRH demand dynamics.

S Afr Med J 2014;104(9):687-690. DOI:10.7196/SAMJ.7841

Both globally and within South Africa (SA), the Vulindlela subdistrict in KwaZulu-Natal Province is at the epicentre of the HIV pandemic.[1,2] In the context of global decreases in HIV prevalence, high infection rates in adolescent girls are fuelling a growing epidemic in this rural community.[3] Crucially, adolescenttargeted HIV prevention interventions may represent an efficient way to improve predicted disease trajectories.[3,4]

687

Associations of high HIV rates with high incidences of sexually transmitted infections (STIs), high rates of unplanned teenage pregnancy and poor educational and economic outcomes are apparent in Vulindlela.[5,6] Given that age of sexual debut is considered an important covariate in these associations, adolescence is recognised as a critical period for sexual and reproductive health (SRH) beyond HIV prevention.[7,8] However, despite the obvious need for SRH facilities and a supportive legal framework,[9] adolescent-focused

October 2014, Vol. 104, No. 10

RESEARCH

services are scarce[10] and young people face a number of barriers to current services.[11-13] The purpose of this pilot study was to develop a framework for the introduction of SRH services for adolescents into schools, namely the Centre for the AIDS Programme of Research in South Africa (CAPRISA) SRH pilot (CSRHP), with the aim of improving adolescent SRH by identifying barriers to services, surveying the current state of SRH, and assessing how adolescents respond to specific forms of SRH interventions. In this paper, we describe the formative research and community consultation processes leading to the packaging, delivery, uptake and acceptability of CSHRP.

Methods

Vulindlela demographics and enrolment

The rural subdistrict of Vulindlela has limited infrastructure and few employment opportunities and is characterised by high levels of poverty. Health services are provided by seven public sector primary healthcare (PHC) clinics; the closest referral hospitals are approximately 30 km away. There are 42 high schools in the subdistrict, and on the basis of enrolment numbers and the matriculation examination pass rate in 2009, 14 schools were selected for implementation of the CSRHP. These schools had a population of 6 415 students (3 181 males, 3 234 females) in the target grades 9 - 11, with an age range of 12 - 28 years.

Community mobilisation and consultation on SRH service provision

The SRH service provision was piloted following several consultative meetings. The provincial Department of Education (DoE) and Department of Health (DoH) as well as the school governing bodies and school personnel were consulted in order to form key partnerships to review proposed implementation plans.

To determine acceptability of CSRHP, consultations were held with key stakeholders in the community. At these meetings information on the burden of HIV/AIDS, the risk groups for HIV acquisition, the drivers of the epidemic, community needs and potential concerns were discussed. The core elements of the engagement process were to build mutual respect and community ownership of the project.

Model of SRH services and assessment

A three-tier adolescent-tailored SRH service was piloted incrementally from October 2011 to June 2012 (Table 1). The uptake of SRH services was recorded and referrals to PHC clinics tracked to assess demand for CSRHP provisions and linkage of care. At the point of departure from customised HIV counselling and testing (CCT), those students tested for HIV were asked to give a reason for testing to assess risk behaviour.

Data analysis

Differences in HIV prevalence between female and male students were explored by Ď&#x2021;2 tests, and where appropriate odds ratios were calculated. These analyses were performed using LaMorteâ&#x20AC;&#x2122;s epidemiology/biostatistics tool.[14]

Results

Between October and December 2011, 14 consultative meetings were held between CAPRISA and the provincial DoH (n=3), the provincial DoH (n=2) and PHC managers (n=9) on the roles and responsibilities in the proposed plans for CSRHP. A further 56 consultative meetings with a broad range of stakeholders were held, including the traditional council of the six school wards (n=6), the traditional council health committee (n=1), student representative council and school governing bodies (n=12), principals and educators (n=14), school research support groups (n=14), and the CAPRISA research support group (n=1). Targeted group meetings were held with female (n=8) and male (n=4) students.

Students self-identified major barriers to current SRH services as discomfort in communication with adults, lack of adolescent-specific services, cost implications of travel to clinics, incompatibility of school and clinic opening hours, and concerns about confidentiality, specifically with regard to personal connections to clinic staff. The community was concerned about the high rates of intergenerational relationships, teenage pregnancy and HIV in adolescents, and were supportive of improving access to contraception and provision of STI treatment.

A total of 8 867 students across the 14 schools were exposed to at least two sessions of the tier 1 in-school group SRH information and awareness sessions over a 6-month period from January 2012.

Table 1. CSRHP service provisions Tier 1: In-school group SRH information and awareness sessions Nurse-driven, short in-school group sessions providing general information on HIV, STIs, CCT, sexuality, wellness, availability of the SRH services and referral procedures were held once a quarter. Leaflets promoting the availability of the SRH service and the number of a dedicated information helpline were distributed at the schools.

Tier 2: In-school individual SRH counselling and CCT Individual counselling services were provided 6-monthly in partnership with a local NGO and were delivered between 12h00 and 16h00, giving opportunities to attend both in and out of school hours. The counsellors were trained in adolescent engagement and CCT, which expands on standard HIV counselling to include collaborative discussions on relationships, negotiating sex, assertive behaviour and high-risk sexual practices.

Tier 3: Referrals to in-school fixed, in-school mobile or public sector primary SRH clinics Students could access SRH services following referrals from the CCT sessions or could self-refer. Referrals were made either to an in-school fixed or mobile SRH service or to a local public sector primary healthcare clinic. In-school services were professional nurse driven and typically equipped for: screening and treatment of common STIs; male and female condom provision; counselling, including CCT; contraception, including emergency contraception; pregnancy testing; screening for pregnancies; and providing referrals and information on issues requiring further management, including safe termination of pregnancy and HIV treatment. Students were seen individually from 12h00 to 16h00 and services were rotated across the 14 schools.

CSRHP = Centre for the AIDS Programme of Research in South Africa sexual and reproductive health pilot; SRH = sexual and reproductive health; STIs = sexually transmitted infections; CCT = customised counselling and testing; NGO = non-governmental organisation.

688

October 2014, Vol. 104, No. 10

RESEARCH

Table 2. Age- and gender-specific HIV prevalence in students accessing HIV CCT Age group (years)

Total n/N (%)

Females n/N (%)

Males n/N (%)

OR

95% CI

p-value

≤15

26/1 367 (1.9)

23/701 (3.2)

3/666 (0.4)

7.28

2.18 - 24.37

<0.001

16 - 17

22/816 (2.6)

17/439 (3.8)

5/377 (1.3)

2.92

1.07 - 7.99

0.029

18 - 19

16/432 (3.7)

12/214 (5.6)

4/218 (1.8)

3.06

0.97 - 9.62

0.046

≥20

7/180 (3.8)

7/96 (7.2)

0/84 (0.0)

N/A

N/A

0.015

Total

71/2 795 (2.5)

59/1 450 (4.0)

12/1 345 (0.8)

4.56

2 795

<0.001

CCT = customised HIV counselling and testing; OR = odds ratio; CI = confidence interval.

300

Female Male

250 200 150 100 50

Contraception

Pregnancy

TB treatment

HIV treatment

STI treatment

0 Total

Students referred to tier 3 services, n

There was a steady increase in the uptake of tier 2 in-school individual SRH counselling and CCT throughout the pilot, with a total of 2 795 students (44.0%) attending these sessions, of whom 1 450 (52.0%) were female and 1 345 (48.0%) male; however, there was considerable variability between schools, with uptake ranging from 19% to 96%.

The main reasons for engagement with HIV CCT were self-reported as engaging in unprotected sex, concerns surrounding caring for HIV-positive household members, and experience of some form of sexual abuse. In the former case, unprotected sex was typically self-reported to be initiated for one of three reasons: (i) the perception that medical male circum­ cision confers complete protection against HIV infection; (ii) unplanned sex; and (iii) refusal to use barrier contraceptives.

Seventy-one students (2.5%) tested HIVpositive and were referred from tier 2 services for clinical tier 3 services; of these 59 (83.1%) were female and 12 (16.9%) male (Table 2). Overall, female students were at 4.6-fold higher risk than male students of being HIV-positive (p<0.001).

The greatest differences between male and female student HIV prevalence were observed in the youngest age group of <15 years (p<0.001), with relatively less significant differences between females and male students with increasing age thereafter.

Two hundred and thirty-nine students (5.7%), of whom 214 (89.5%) were female and 25 (10.5%) male, were referred to clinical tier 3 SRH services for reasons other than positive HIV serostatus. Of the students referred, 97 (40.6%) were treated for STIs, of whom 76 (78.4%) were female and 21 (21.6%) male; 9 (3.8%) were diagnosed with symptoms of pulmonary tuberculosis and referred to the local PHC clinic; 100 (41.8%) were counselled and initiated on contraception; and 33 (13.8%) tested positive for a pregnancy

Reasons for referral Fig. 1. Gender disparity in referrals from tier 2 to tier 3 services. (STI = sexually transmitted infection; TB = tuberculosis.)

and were referred for antenatal care.

Gender disparity in reasons for tier 2 to tier 3 referral is shown in Fig. 1. None of the students requested emergency contraception. All students attending the tier 2 services were provided with male and/or female condoms.

The uptake of referrals to tier 3 services was tracked (data not shown). Uptake varied considerably by service point type (in-school fixed, in-school mobile or public sector primary SRH clinics). Critically, <10% of students referred to non-school-based and non-adolescent-targeted PHC clinics were registered as attending their referral appointments.

Discussion

Community consultations were critical in the development of the CSRHP, not only for the formation of local partnerships central to its implementation and in the assessment of barriers to current services,

689

October 2014, Vol. 104, No. 10

but also in acknowledging that broader community factors beyond the individual are essential targets in any behaviour change intervention.

HIV, pregnancy and STI prevalence rates among students accessing CSRHP services confirmed previous reports that the majority of adolescents in this district are sexually active and reflected community concerns regarding their requirement for tailored services.[5] The incidence rates observed in the pilot clarified the SRH needs of adolescents in the community and will help to guide future policy decisions.

Particularly striking is the disparity of HIV infection and STI rates between the genders, highlighting the urgent need for femaletargeted interventions. Further, self-reported motivations for HIV testing included several misconceptions that highlight the continued need for SRH education in schools.

One of the central aims of the CSRHP was to evaluate how best to implement

RESEARCH

evidence-based prevention interventions, such as CCT counselling.

The pilot demonstrated that brief in-class information sessions facilitated student uptake of individual SRH and CCT counselling and that it was feasible to provide CCT in schools. The fact that <10% of referrals from adolescent-tailored PHC clinics were fulfilled highlights the greater acceptability of the programme to students who are otherwise unwilling to attend primary healthcare clinics. However, these data also suggest that linkage of care needs to be strengthened in order to offer complete coverage for SRH needs.

There was considerable variation in the uptake of services at individual levels between schools, and delineating the causes of such school-level variation will no doubt be critical in optimising future implementation strategies. In some schools, limited infrastructure was a barrier to service provision, particularly in the case of maintaining confidentiality for HIV-positive students.

For this, ease of access, and probably multiple other complex reasons, in general the in-school mobile services were preferred, although it was noted that different students favoured different service points. These data highlight the need for variety in SRH service provision; assessing user patterns of access to care is critical in determining the correct balance of services. Further work is needed to identify the frequency of SRH service provision and demand creation necessary to ensure sustainability of any successes. Moreover, the CSRHP indicates that while school-based SRH service provision is desperately required and in principle feasible, considerable evidence-based work remains to maximise the benefits of any investments.

Acknowledgements. We thank all our field staff for their contributions to the working of the CSRHP. We are also extremely grateful to those learners who engaged with the programme, and the community for their ongoing support and cooperation.

690

Funding. This publication was supported by the US Centers for Disease Control and Prevention (CDC) under the terms of 5U2GPS001350. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the CDC. References 1. Shisana O, Stoker D, Simbayi LC, et al. South African national household survey of HIV/AIDS prevalence, behavioural risks and mass media impact – detailed methodology and response rate results.

S Afr Med J 2004;94(4):283-288.

2. Rehle T, Shisana O, Pillay V, Zuma K, Puren A, Parker W. National HIV incidence measures – new insights into the South African epidemic. S Afr Med J 2007;97(3):194-199.

3. Karim QA, Kharsany AB, Frohlich JA, et al. Stabilizing HIV prevalence masks high HIV incidence rates amongst rural and urban women in KwaZulu-Natal, South Africa. Int J Epidemiol 2011;40(4):922-930. [http://dx.doi.org/10.1093/ije/dyq176] 4. Abdool Karim Q, Kharsany AB, Frohlich JA, et al. HIV incidence in young girls in KwaZulu-Natal, South Africa – public health imperative for their inclusion in HIV biomedical intervention trials. AIDS Behav 2012;16(7):1870-1876. [http://dx.doi.org/10.1007/s10461-012-0209-y] 5. Pettifor AE, Rees HV, Kleinschmidt I, et al. Young people’s sexual health in South Africa: HIV prevalence and sexual behaviors from a nationally representative household survey. AIDS 2005;19(14):1525-1534. [http://dx.doi.org/10.1097/01.aids.0000183129.16830.06] 6. Jukes M, Simmons S, Bundy D. Education and vulnerability: The role of schools in protecting young women and girls from HIV in southern Africa. AIDS 2008;22(Suppl 4):S41-S56. [http://dx.doi. org/10.1097/01.aids.0000341776.71253.04] 7. Sawyer SM, Afifi RA, Bearinger LH et al. Adolescence: A foundation for future health. Lancet 2012;379(9826):1630-1640. [http://dx.doi.org/10.1016/S0140-6736(12)60072-5] 8. Bearinger LH, Sieving RE, Ferguson J, Sharma V. Global perspectives on the sexual and reproductive health of adolescents: Patterns, prevention, and potential. Lancet 2007;369(9568):1220-1231. [http:// dx.doi.org/10.1016/S0140-6736(07)60367-5] 9. Republic of South Africa. Children’s Act 38 of 2005. http://wwwinfogovza/view/ DownloadFileAction?id=67892 (accessed 19 September 2013).

10. Maharaj P, Munthree C. The quality of integrated reproductive health services: perspectives of clients in KwaZulu-Natal, South Africa. Curationis 2005;28(1):52-58. [http://dx.doi.org/10.4102/curationis. v28i1.922] 11. Alli F, Maharaj P, Vawda MY. Interpersonal relations between health care workers and young clients: Barriers to accessing sexual and reproductive health care. J Community Health 2013;38(1):150-155. [http://dx.doi.org/10.1007/s10900-012-9595-3] 12. Tylee A, Haller DM, Graham T, Churchill R, Sanci LA. Youth-friendly primary-care services: How are we doing and what more needs to be done? Lancet 2007;369(9572):1565-1573. [http://dx.doi. org/10.1016/S0140-6736(07)60371-7] 13. World Health Organization. Promoting Adolescent Sexual and Reproductive Health Through Schools in Low Income Countries: An Information Brief. Geneva: WHO, 2008. http://whqlibdoc.who.int/ hq/2009/WHO_FCH_CAH_ADH_09.03_eng.pdf (accessed 20 September 2013).

14. LaMorte F. Epidemiology/Biostatistics Tools. medlib.bu.edu/busm/LaMorte.xls (accessed 4 Feburary 2014).

Accepted 16 May 2014.

October 2014, Vol. 104, No. 10

RESEARCH

Comparability of total cardiovascular disease risk estimates using laboratory and non-laboratory based assessments in urban-dwelling South Africans: The CRIBSA study N Peer,1 MB ChB, MBA, MPH, PhD; C Lombard,2 MSc, PhD; K Steyn,3 NED, MSc, MD; T Gaziano,4 MSc, MD; N Levitt,3,5 MB ChB, MD, FCP (SA) on-communicable Diseases Research Unit, Medical Research Council, Durban, South Africa N Biostatistics Unit, Medical Research Council, Cape Town, South Africa 3 Chronic Disease Initiative for Africa, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 4 Division of Cardiovascular Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, USA 5 Division of Diabetic Medicine and Endocrinology, Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 1 2

Corresponding author: N Peer (nasheeta.peer@mrc.ac.za)

Objectives. To establish the prevalence and determinants of the 10-year risk of a cardiovascular disease (CVD) event in 25 - 74-year-old black Africans in Cape Town, South Africa, using Framingham laboratory- and non-laboratory-based and National Health and Nutrition Examination Survey (NHANES) I non-laboratory-based equations.

Methods. CVD risk factors were determined by questionnaires, clinical measurements and biochemical analyses. Survey logistic regression analyses assessed the sociodemographic determinants of CVD risk ≥20%.

Results. There were 1 025 participants, 369 men and 656 women. Mean 10-year risk for a CVD event by Framingham laboratory- and non-laboratory-based and NHANES I non-laboratory-based equations for men was 9.0% (95% confidence interval 7.7 - 10.3), 11.1% (9.6 - 12.6) and 9.0% (7.6 - 10.3), and for women 5.4% (4.7 - 6.1), 6.8% (5.9 - 7.7) and 8.7% (7.6 - 9.8). Correlations between laboratory- and non-laboratory-based scores were high (0.915 - 0.963). The prevalence of laboratory-based CVD risk ≥20% was 13.0% in men and 6.1% in women. In the logistic model for men, ≤7 years of education (odds ratio 3.09; 95% CI 1.67 - 5.71) and being unemployed (3.44; 1.21 - 9.81) compared with employed were associated with laboratory-based high risk. In women, high risk was associated with ≤7 years of education (4.20; 1.96 - 9.01), living in formal v. informal housing (2.74; 1.24 - 6.06) and being poor (middle v. lowest tertile 0.29; 0.13 - 0.66). In the Framingham non-laboratory-based logistic models there were no changes in the direction or significance of the variables except for housing, which was no longer significant in women.

Conclusions. Comparability of laboratory- and non-laboratory-based CVD risk estimates illustrates the utility of the latter in resourceconstrained settings.

S Afr Med J 2014;104(10):691-696. DOI:10.7196/SAMJ.8125

Treatment of cardiovascular disease (CVD) risk factors has tradi­ tionally been based on the presence or absence of a single CVD risk factor, such as hypertension, hyperlipidaemia or diabetes, without considering the continuous relationship between blood pressure (BP), blood glucose, blood cholesterol and cardiovascular risk.[1] While this approach appears straightforward, it may result in committing some individuals with only a small cardiovascular risk to years of unnecessary treatment or, conversely, neglecting to treat individuals with an overall higher risk.[1,2] This is because a combination of several slightly elevated risk factors may result in a much higher total risk than a single, more strikingly raised factor.[3,4] Moreover, single risk factor approaches are neither cost-effective nor affordable for poorer individuals and in developing regions with limited resources.[2] Given the enormous burden of CVD and the high costs of management, it is therefore essential to prioritise cost-effective approaches that target high-risk individuals.

Adoption of the multifactorial CVD risk assessment approach to identify high-risk individuals who need interventions is widely advocated, with the initiation of therapy based on the predicted absolute cardiovascular risk of the individual.[1] The total CVD risk assessment approach is particularly recommended as a cost-effective

691

strategy in developing regions with scarce resources. Effective CVD prevention therefore warrants a paradigm shift from the treatment of single risk factors in isolation, to the management of total CVD risk with an improvement in the profile of all risk factors that will lead to the development of CVD. Several computerised methods for estimating total cardiovascular risk have been developed. The first, best known and most frequently used risk estimation system was developed by the Framingham Heart Study researchers in the USA.[3,4] This score has been validated across different populations, modified for use in several countries and recommended by numerous international guideline committees for CVD prevention.

In South Africa (SA), the South African Heart Association and the Lipid and Atherosclerosis Society of Southern Africa,[5] as well as the Southern African Hypertension Society in conjunction with the National Department of Health (DoH),[6] have adopted a cardiovascular risk stratification approach for the management of CVD risk factors. Given the lack of prospective data in the African setting and the absence of locally validated total CVD risk assessment tools, and in view of the fact that the Framingham risk scores have been validated in white and black populations and are transportable to other culturally diverse populations, this approach has been considered appropriate for local use.[5]

October 2014, Vol. 103, No. 10

RESEARCH

Most scoring systems require expensive laboratory tests; however, recent advances include the development of models that use simple office-based predictors easily obtained in primary care and do not require laboratory testing. The body mass index (BMI) has replaced total cholesterol (TC) and high-density lipoprotein (HDL) cholesterol in these models. Considering the increasing burden of CVD and the need for cost-effective use of limited resources in the developing world, the introduction of non-laboratory-based tools in this milieu is highly relevant. The use of non-laboratory-based total CVD risk assessment has the potential to improve worldwide utility of the risk scores and enhance targeted CVD prevention efforts,[3,4] particularly in resource-constrained settings such as SA, where widespread laboratory availability is problematic and not economically feasible.

This study aimed to determine the 10-year risk of developing a CVD event in the black population of Cape Town using the Framingham laboratory- and non-laboratory-based equations. Additionally, the non-laboratory-based score developed using the National Health and Nutrition Examination Survey (NHANES) I population data in the USA was used to calculate total CVD risk. This equation was found to be highly correlated with commonly used laboratory scores in SA populations.[7] The sociodemographic determinants associated with high-risk scores (≥20%) were also ascertained.

Methods

Study population and sampling procedure

A sample of 25 - 74-year-old men and women in the predominantly black residential areas of Langa, Guguletu, Crossroads, Nyanga and Khayelitsha in Cape Town participated in this cross-sectional study in 2008/09. The sampling procedure for the current study included a three-stage cluster sampling and has been described in detail elsewhere.[8] The prespecified age and gender quotas included disproportionate sampling across age groups to ensure at least 50 men and women in each gender category. Among other criteria, individuals on tuberculosis or antiretroviral therapy or who had received cancer treatment within the past year were excluded.

Additionally, participants with a self-reported history of ischaemic heart disease (IHD) or stroke were excluded for this analysis.

Data collection

Data collected by administered questionnaires included socio­ demographic characteristics, medical history and self-reported tobacco use (World Health Organization (WHO) STEP-wise surveillance questionnaire).[9] Assets defining wealth were recorded and included ownership of consumer items such as a radio, television, telephone, refrigerator, personal computer, washing machine, motor vehicle, bicycle and electricity, and the source of drinking water and toilet facilities.

Height and weight were measured using standardised techniques.

Three BP measurements were taken at 2-minute intervals and the average of the second and third measurements was used in the analyses.

Blood samples for lipid and glucose estimations were drawn following an overnight fast of 10 hours. A standard oral glucose tolerance test was then administered and blood samples taken 120 minutes later.[10] Blood samples were kept on ice and transported to the laboratory within 6 hours to be centrifuged, aliquoted and stored at –80° until the assays were performed.

Definitions

Diabetes was diagnosed according to the 1998 WHO criteria,[10] the use of hypoglycaemic agents or the subject having being told they were diabetic by a doctor/nurse. Hypertension was defined

692

as BP ≥140/90 mmHg or using antihypertensive agents. BMI was computed as kg/m2. Smoking status was defined as currently smoking daily or occasionally.

The absolute risk of having a CVD event, defined as IHD, stroke, transient ischaemic attack or heart failure, within 10 years was calculated using the Framingham[11] and NHANES I equations.[12] A score ≥20% was considered to indicate high risk and 10 - 19.99% to indicate moderate risk.

Statistical analysis

Data analyses were done using STATA 12. Descriptive statistics, including crude prevalence, were calculated using the weights based on the sample design and adjusted for the realised sample. A principal component analysis of the pooled data, based on the assets that defined wealth, was used to develop an asset index[13] and categories of relative wealth were created using tertiles. The first component of the principal component analysis placed the highest loading on having a toilet and a tap inside the house and explained 31.0% of the variation. The second component seemed to measure the ownership of luxury items such as a car and a personal computer and explained 12.2% of the variation. All variables, except bicycle and telephone, had approximately equal loadings.

The equations for calculating the 10-year risk of developing a CVD event are gender-specific and include the variables of age, diabetes status, smoking status, treated and untreated systolic BP, TC and HDL cholesterol levels for the laboratory-based equations. BMI replaced lipids in the non-laboratory-based equations.[11,12] Concordance correlation coefficients determined the correlations of the mean scores calculated by the laboratory-based equations with the two non-laboratory based equations. The McNemar test compared the frequencies of estimated high risk calculated using the laboratorybased equations with the two non-laboratory based equations.

The univariate analyses are presented as mean or percentage values with 95% confidence intervals (CIs). The unadjusted survey-based odds ratio (OR) and 95% CI for the associations of the sociodemographic variables with total CVD risk ≥20% were calculated. On account of the high level of correlation between the risk scores, only the associations for the Framingham laboratorybased CVD risk scores are presented in men and women. Survey multiple logistic regression analyses determined the independent associations of the sociodemographic variables with estimated total CVD risk ≥20%. The same sociodemographic variables were inclu­ ded in the unadjusted and adjusted analyses. p-values are presented for the adjusted analyses.

The University of Cape Town’s Research and Ethics Committee approved the study. All participants signed informed consent.

Results

The realised study sample comprised 1 099 participants, 1 025 of whom (369 men and 656 women) were included in this analysis.

Seventy-four participants with a self-reported history of IHD or stroke were excluded. The overall response rate was 86%, the non-responders, i.e. the selected people who the study team were unsuccessful in contacting, totalling 187 (79 men).

The overall mean 10-year risk for a CVD event estimated using the laboratory-based scores was low at 7.1% and significantly higher in men than in women (9.0% v. 5.4%; p<0.001) (Table 1).

The non-laboratory-based mean scores were comparable to these laboratory-based estimates (Table 1 and Fig. 1). The concordance correlations between the Framingham laboratory and non-laboratory risk scores were very high at 0.936 for men and 0.924 for women. The concordance correlations between the Framingham laboratory-based

October 2014, Vol. 103, No. 10

RESEARCH

Table 1. Total CVD risk estimates using laboratory- and non-laboratory-based equations in men and women Men (N=369) n

%

95% CI

Women (N=656) n

%

Total (N=1 025)

95% CI

n

%

95% CI

Framingham CVD risk using lipid profiles Mean

9.0

7.7 - 10.3

5.4

4.7 - 6.1

7.1

6.4 - 7.9

Moderate risk (10 - 19.99%)

57

12.2

9.2 - 16.0

71

8.3

6.3 - 10.9

128

10.2

8.3 - 12.4

High risk (≥20%)*

67

13.0

9.9 - 17.0

55

6.1

4.6 - 8.0

122

9.4

7.6 - 11.6

11.1

9.6 - 12.6

6.8

5.9 - 7.7

8.8

7.9 - 9.7

Framingham CVD risk using BMI Mean Moderate risk (10 - 19.99%)

71

16.2

12.6 - 20.7

83

10.3

8.2 - 12.8

154

13.1

11.0 - 15.5

High risk (≥20%)*

87

17.4

13.8 - 21.8

74

8.4

6.4 - 10.9

161

12.7

10.6 - 15.2

9.0

7.6 - 10.3

8.7

7.6 - 9.8

8.8

7.9 - 9.8

CVD risk using BMI (NHANES I) Mean Moderate risk (10 - 19.99%)

64

14.5

10.9 - 19.0

84

10.1

8.0 - 12.7

148

12.2

10.1 - 14.6

High risk (≥20%)†

65

12.2

9.3 - 15.7

121

14.0

11.4 - 17.0

186

13.1

11.1 - 15.5

80

NHANES non-laboratory based risk scores 0 20 40 60 80

80

NHANES non-laboratory based risk scores 0 20 40 60 80

Framingham non-laboratory based risk scores 0 20 40 60 80

and NHANES I risk scores were 0.950 and 0.786 in men and women, respectively.

The prevalence of estimated high total CVD risk (≥20%) according to the laboratory-based scores was 13.0% in men and 6.1% in women (p<0.001) (Table 1).

In men, the frequencies of estimated high risk were significantly different between the laboratory-based and the Framingham non-laboratory-based scores (p<0.001) but were similar between the former and the NHANES I non-laboratory scores (p=0.695).

Taking the laboratory-based scores as the gold standard, the sensitivity was 97.0% and 79.1%, respectively, and the specificity 92.7% and 96.0%, respectively. In women, the frequencies of estimated high risk were significantly different for both comparisons (p<0.001). The sensitivity of 98.2% and 100%, respectively, was very high. The specificity for the comparison of estimated high risk between the two Framingham equations was 96.7% and that between the laboratory-based and the NHANES I nonlaboratory scores 89.0%.

The prevalences of the individual CVD risk factors were similar in men and women for hypertension (p=0.985), diabetes (p=0.071) and HDL cholesterol:TC <20% (p=0.170) (Fig. 2). Men and women differed in smoking prevalence, which was significantly higher in men than in women (58.4% v. 9.8%; p<0.001). Overweight and obesity was significantly higher in women (82.0%) than in men (29.2%) (p<0.001).

As shown in Table 2, the adjusted odds for estimated high CVD risk by the Framingham laboratory-based scores were significantly associated with ≤7 years of education (p<0.001)

Framingham non-laboratory based risk scores 0 20 40 60 80

CVD = cardiovascular disease; CI = confidence interval; BMI = body mass index; NHANES = National Health and Nutrition Examination Survey.

Non-laboratory CVD risk scores used BMI instead of lipids. Men compared with women: *p<0.001; †p=0.390.

Men

0

20 40 60 Framingham laboratory-based risk scores Women

0

20 40 60 Framingham laboratory-based risk scores

Men

0

20 40 60 80 Framingham laboratory-based risk scores Women

0

20 40 60 Framingham laboratory-based risk scores

80

Fig. 1. Scatterplots of the Framingham laboratory-based total CVD risk scores with the Framingham and NHANES non-laboratory-based CVD risk scores (CVD = cardiovascular disease; NHANES = National Health and Nutrition Examination Survey).

and unemployment (p=0.021) in men. The significant adjusted odds for estimated high CVD risk by the laboratory-based scores in women were ≤7 years of education (p<0.001), better-quality housing (p=0.044) and being in the poorest wealth tertile (p=0.013). The work category with pensioners was associated with high CVD risk for both men and women because of the link with age, which is a function of the risk equation.

693

October 2014, Vol. 103, No. 10

In the Framingham non-laboratory-based logistic models, com­ pared with the lab­ oratory-based analyses, there were no changes in the direction or significance of the variables except for housing, which was no longer significant in women (p=0.231).

In the NHANES I logistic models, unlike the Framingham laboratory-based analyses, better housing (p=0.044) was associated with an estimated high CVD risk in men, while

RESEARCH

in women housing (p=0.133) and wealth (p=0.094) were no longer significant.

Discussion

The CRIBSA study, which is among the first to determine the 10-year risk of developing a CVD event in an urban African population in SA, found a modest prevalence of high risk (≥20%) in men and a low to moderate prevalence in women. This suggests that for cost-effective management, a relatively smaller proportion of participants require treatment compared with those with prevalent individual risk factors. For example, while only 13.0% of men and 6.1% of women would require interventions according to the Framingham laboratory-based high-risk estimates, hypertension prevalence was high at 35%. This is especially relevant in view of the potential burden that may be imposed on healthcare services if all individuals with only high BP were treated with medication.

Basing treatment decisions on a total CVD risk assessment approach enables individuals who would benefit the most from treatment to be identified and also results in optimal and cost-effective management, as shown

by Gaziano et al.[14] in an analysis of the SA hypertension guidelines.

The data confirm that the use of nonlaboratory scores in clinical practice may be a feasible alternative in our setting. There was a high correlation between the mean laboratory-based and non-laboratorybased scores, and a high proportion of participants identified as at high risk on the laboratory-based estimates were also identified by the non-laboratory estimates.

Gaziano et al.[7] also reported high correlations between laboratory- and non-

laboratory-based scores in SA populations.

Eliminating the need for costly laboratory measurements will enhance accessibility and utility of the total CVD risk assessment tool[4] and is particularly relevant in lowresource settings such as SA that face a high burden of multiple diseases.

Estimated high CVD risk by Framingham laboratory- and non-laboratory-based scores was found to be significantly related to unemployment in men, poverty in women and lower education levels in both. These are vulnerable groups that are likely to be less aware of the risks of CVD and may have difficulty in accessing healthcare because of financial constraints. There is therefore a pressing need to increase awareness of CVD among these individuals. Additionally, they should be targeted for screening and prevention of CVD and its risk factors, and their access to healthcare, if compromised, should be facilitated.

In view of the association of high CVD risk with poverty or lower socioeconomic status as defined by education level and asset index or wealth tertiles, the relation between better-quality housing and estimated high risk by the Framingham laboratory-based scores in women and the NHANES I scores in men was unexpected.

That wealth, education and housing quality may not be well correlated possibly accounts for these findings, underscoring the fact that socioeconomic dynamics are complex and further research in this area is needed.

Despite the high prevalence of CVD risk factors in both men and women, the two-fold greater predicted high risk of Framinghambased CVD in men compared with women is a function of the equations, which allocate

90

greater weight to men. In women, while high scores identify those at high risk, lower scores do not sufficiently ensure that individual women are at low risk.

It is difficult for women aged <75 years, even with several markedly eleva­ted risk factors, to be classified as at high risk.[15] Factors beyond the risk scores therefore need to be considered when determining therapy in women. These models do not incorporate all CVD risk factors, particularly physical activity and stress.

They also do not consider the duration of exposure to a risk factor, or include relevant family history.[15] In addition, for CVD risk management in women, medical and lifestyle history, markers of preclinical disease and other conditions need to be considered when determining the intensity of preventive therapy. Recommendations also include a lower cut-point for defining high risk in women as ≥10% 10-year risk for all CVD compared with the traditionally ≥20% 10-year risk estimate utilised.[15] The prevalence of high risk in women would then be 14.4%, 18.7% and 24.1% by the laboratory-based and non-laboratorybased Framingham and NHANES 1 scores, respectively.

Nevertheless, while there are some recognised limitations, 10-year risk esti­ mations represent an improvement over clinical judgement alone for appropriate risk stratification. Considering that a systematic approach to total CVD risk estimation seems to result in better risk factor control,[4] the weaknesses of the CVD risk prediction models should not defer the control of the major risk factors through this cost-effective approach.[2] Total CVD risk assessment is likely to remain an important therapeutic component for individuals and populations.

80

Study limitations

70 60 50 %

Men Women

40

Total

30 20

Limitations of the study included the low sample realisation in men (64%), which necessitated higher sampling weights and a loss of precision. The application in this study of risk estimation tools developed primarily in populations of European origin in wealthy regions with different incidences of CVD events to our population is another limitation.

Conclusion

10 0 Current smoking

Hypertension

Diabetes

HDLC:TC <20%

BMI ≥25 kg/m2

Fig. 2. Prevalence of cardiovascular disease risk score components presented according to gender.

(Hypertension = blood pressure ≥140/90 mmHg or on hypertension treatment; diabetes = raised fasting glucose ≥7.0 mmol/l, 2-hour glucose ≥11.1 mmol/l or known diabetes; HDLC = high-density lipoprotein cholesterol; TC = total cholesterol; BMI = body mass index.)

694

October 2014, Vol. 103, No. 10

Despite the high prevalence of many individual CVD risk factors, the estimates of a ≥20% 10-year risk for a CVD event in the black population of Cape Town were moderate in men and low to moderate in women, depending on the equation used.

This implies that for optimal cost-effective

0.065 0.18 - 1.05 0.44 0.47 - 1.74 0.91 7.1 205 0.105 0.85 - 5.14 0.89 - 3.59 124 3rd (richest)

15.4

1.78

2.10

0.69 - 3.25 1.00

1.49 0.87 - 3.33 1.70

1.00

108 2nd

14.8

137 1st (poorest)

9.3

management of CVD in this population, fewer individuals require medical intervention compared with those with raised single risk factors. The comparability of the Framingham laboratory- and non-laboratorybased CVD risk estimates illustrates the utility of the latter in this resource-limited setting and could further optimise costeffective strategies. In view of the fact that in this study high CVD risk was associated with unemployed men, the poorest women and less-educated adults, CVD management needs to target these vulnerable groups. Future research will be required to determine whether the total CVD risk approach results in improved health outcomes and benefits for the healthcare system in SA.

October 2014, Vol. 103, No. 10

CVD = cardiovascular disease; OR = odds ratio; CI – confidence interval. *Pensioners, homemakers, students and those receiving disability grants.

Bold font denotes significant findings with p<0.050

1.00

3.8 241

1.00 7.8 210

0.310

10.7 0.270

0.47 - 3.06 1.21 0.92 - 3.84 1.88 15.9 79 Built formal unit (private)

Asset index

0.98 - 4.09 2.01 1.21 - 4.42 2.32 108 Council/core house/hostel

18.9

0.693

131

0.47

0.24 - 0.95

0.29

0.13 - 0.66

0.003

0.013

0.013 1.24 - 6.06 2.74 1.44 - 5.71

0.78 - 3.24 1.59 0.83 - 3.32 1.66 6.5 250

0.136 1.00 1.00 9.1 182 Informal shack/other

House

0.021 1.21 - 9.81

7.22 - 67.66 22.10

3.44 1.21 - 8.56

9.33 - 80.14 27.4

3.22

54 Other*

47.7

227 Unemployed

9.7

1.00 3.2 88 Employed

Work

695

0.056

4.0 275

2.87

0.201

0.044 1.00

25.1 126

1.00

0.844

<0.001 3.22 - 29.00

0.36 - 3.54 1.12

9.66 4.74 - 36.73

0.38 - 3.68 2.9 397

1.18

2.5 133 1.00

1.29

1.00

0.83 - 3.24 1.64

1.00

242 ≥50

9.6 127 <50

14.9

2.07 - 6.55 3.69 23.0 142 ≤7

% of life spent in the city

<0.001

7.5 355 0.58 - 2.86

0.529

<0.001 1.67 - 5.71 3.09

1.00 1.00 7.5 227 >7

13.0 369 Education (years)

CVD risk ≥20%

<0.001

4.6 301

1.00

0.90 - 3.17

14.3 240

1.69

1.00

13.20

<0.001

1.64

1.00

1.00

0.74 - 3.62

0.220

<0.001 1.96 - 9.01 3.65 - 12.36 2.4 416

6.7

1.00 6.1 656

95% CI OR % N

Unadjusted

4.20

1.00

95% CI OR OR % N 95% CI OR

Adjusted

p-value

Unadjusted

95% CI

Women Men

Table 2. Prevalence and unadjusted and adjusted associations of sociodemographic factors with high total CVD risk (≥20% on laboratory-based estimates) in men and women

Adjusted

p-value

RESEARCH

Acknowledgements. We thank the participants, fieldworkers, Medical Research Council research nurse fieldworkers Debbie Jonathan and Theresa Gogela, fieldwork co-ordinator Erica April, study manager Serena van Haght, statisticians Nomonde Gwebushe, Rebecca Shanmugam and Ria Laubscher, and Dr Kirsty Bobrow.

We thank the City of Cape Town for provision of the aerial maps.

Conflict of interest. NL has received honoraria from Novartis for serving on the steering committee for the Navigator Trial and travel support from Novo Nordisk, Eli Lilly Laboratories and Sanofi Aventis. All other authors report no potential conflicts of interest, including specific financial interests, relevant to the subject of this manuscript.

Funding. This work was supported by an unrestricted grant from Servier Laboratories (South Africa), the Medical Research Council of South Africa, the Initiative for Cardiovascular Health Research in Developing Countries (IC Health) Foundation Council, and Brigham and Women’s Hospital, Harvard University. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

RESEARCH

References 1. Ker JA, Oosthuizen H, Rheeder P. Decision-making using absolute cardiovascular risk reduction and incremental cost-effectiveness ratios: A case study. Cardiovasc J Afr 2008;19(2):97-101.

2. Mendis S. The contribution of the Framingham Heart Study to the prevention of cardiovascular disease: A global perspective. Prog Cardiovasc Dis 2010;53(1):10-14. [http://dx.doi.org/10.1016/j. pcad.2010.01.001] 3. Bitton A, Gaziano TA. The Framingham Heart Study’s impact on global risk assessment. Prog Cardiovasc Dis 2010;53(1):68-78. [http://dx.doi.org/10.1016/j.pcad.2010.04.001] 4. Cooney MT, Dudina A, D’Agostino R, Graham IM. Cardiovascular risk-estimation systems in primary prevention: Do they differ? Do they make a difference? Can we see the future? Circulation 2010;122(3):300-310. [http://dx.doi.org/10.1161/CIRCULATIONAHA.109.852756] 5. Klug E. South African dyslipidaemia guideline consensus statement. S Afr Med J 2012;102(3):178-187.

6. Seedat YK, Croasdale MA, Milne FJ, et al. South African hypertension guideline 2006. S Afr Med J 2006;96(4):337-362.

7. Gaziano TA, Pandya A, Steyn K, et al. Comparative assessment of absolute cardiovascular disease risk characterization from non-laboratory-based risk assessment in South African populations. BMC Med 2013;11(1):1-11. [http://dx.doi.org/10.1186/1741-7015-11-170] 8. Peer N, Steyn K, Lombard C, Lambert EV, Vythilingum B, Levitt NS. Rising diabetes prevalence among urbandwelling black South Africans. PloS One 2012;7(9):e43336. [http://dx.doi.org/10.1371/journal.pone.0043336] 9. Bonita R, deCourten M, Dwyer T, Jamrozik K, Winkelmann R. Surveillance of Risk Factors for Noncommunicable Diseases: The WHO STEPwise approach. Geneva: World Health Organization, 2001.

10. World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications: Report of a WHO Consultation. Geneva: World Health Organization, 1999.

11. D’Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: The Framingham Heart Study. Circulation 2008;117(6):743-753. [http://dx.doi.org/10.1161/ CIRCULATIONAHA.107.699579] 12. Gaziano TA, Young CR, Fitzmaurice G, Atwood S, Gaziano JM. Laboratory-based versus nonlaboratory-based method for assessment of cardiovascular disease risk: The NHANES I Follow-up Study cohort. Lancet 2008;371(9616):923-931. [http://dx.doi.org/10.1016/S0140-6736(08)60418-3] 13. Filmer D, Pritchett LH. Estimating wealth effects without expenditure data – or tears: An application to educational enrollments in states of India. Demography 2001;38(1):115-132.

14. Gaziano TA, Steyn K, Cohen DJ, Weinstein MC, Opie LH. Cost-effectiveness analysis of hypertension guidelines in South Africa: Absolute risk versus blood pressure level. Circulation 2005;112(23):35693576. [http://dx.doi.org/10.1161/CIRCULATIONAHA.105.535922] 15. Mosca L, Benjamin EJ, Berra K, et al. Effectiveness-based guidelines for the prevention of cardiovascular disease in women – 2011 update: A guideline from the American Heart Association.

Circulation 2011;123(11):1243-1262. [http://dx.doi.org/10.1161/CIR.0b013e31820faaf8]

Accepted 2 June 2014.

Detecting virological failure in HIVinfected Tanzanian children E M Mgelea,1 MD, MMed; R Kisenge,1 MD, MMed, PhD; S Aboud,2 MD, PhD 1 2

Department of Paediatrics and Child Health, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania Department of Microbiology and Immunology, Muhimbili University of Health and Allied Sciences, Dar es Salaam, Tanzania

Corresponding author: E M Mgelea (drmgelea@gmail.com)

Background. The performance of clinical and immunological criteria to predict virological failure in HIV-infected children receiving antiretroviral therapy (ART) is not well documented.

Objective. To determine the validity of clinical and immunological monitoring in detecting virological failure in children on ART. Methods. A total of 218 children were included in the study. All were from care and treatment clinics in Dar es Salaam, Tanzania. Their mean age was 10.6 years, 122 (56.0%) were males, and the mean time on ART was 40.9 months. The study was conducted from August 2011 to March 2012. Data on sociodemographic and clinical characteristics and immunological and virological failure were based on World Health Organization definitions. Blood samples were collected for CD4+ T-cell count and viral load tests.

Results. Of 217 children with available viral load results, 124 (57.1%) had virological failure (>400 copies/mL), 25.0% immunological failure and 11.5% clinical failure. The sensitivity, specificity, positive predictive value and negative predictive value of clinical criteria were 12.9%, 90.3%, 64.0% and 43.8%, respectively, those for immunological criteria 22.6%, 73.1%, 53.3% and 41.4%, and those for the combination of clinical and immunological monitoring 25.8%, 69.9%, 53.3% and 41.4%. Children who received nevirapine (NVP)-based regimens were two times more likely (odds ratio 2.0; 95% confidence interval 1.20 - 3.64) to have virological failure than those on efavirenz and protease inhibitor-based regimens.

Conclusions. The study demonstrated poor performance of currently recommended clinical and immunological criteria for monitoring HIV-infected children on ART. Moreover, children on NVP-based regimens had a higher risk of developing virological failure than those on other regimens.

S Afr Med J 2014;104(10):696-699. DOI:10.7196/SAMJ.7807

Globally, it is estimated that 3.4 million children under the age of 15 years are living with HIV and AIDS, the majority residing in sub-Saharan Africa and southern and southeastern Asia. [1] In Tanzania, the exact number infected with HIV is unknown. However, 130 000 - 160 000 children are eligible for antiretroviral therapy (ART).[2] The use of ART in Tanzania increased from <1% of those meeting eligibility criteria in 2004 to 26% in 2012.[3] The World Health Organization (WHO) advocates a public health approach to ART, recognising the potential role of plasma HIV-1 RNA testing but recommending clinical and immuno­logical monitoring in

696

resource-constrained countries such as Tanzania.[4,5] It has been shown that there are challenges related to the use of clinical and immunological parameters to detect virological failure in adults receiving ART. The delay in recognition may result in increased acquisition of HIV drug-resistant mutations as well as increased morbidity and mortality.[6] However, there may be no clear benefit to routine measurement of viral load to ascertain virological failure in adults.[7] Data on clinical and immunological monitoring to detect virological failure in children are limited. Where methods for detecting virological failure are available, they are not affordable. The aim of the current study was therefore to determine the validity of clinical and immunological monitoring in detecting virological failure among Tanzanian HIV-infected children on ART.

October 2014, Vol. 103, No. 10

RESEARCH

Methods

Study design and population

A cross-sectional, health facility-based study was conducted from August 2011 to March 2012. A total of 218 HIV-infected children on ART were included. All were from care and treatment clinics in Dar es Salaam, the sites involved being Muhimbili National Hospital, Temeke, Amana, Mwananyamala, Infection Disease Control (IDC) and Sinza. The mean age of the children was 10.6 years (range 1 16), and 122 (56.0%) were males. The mean duration of time on ART was 40.9 months. The cohort group involved those who had been receiving ART for ≥6 months. Ethical approval was obtained from the Senate Research and Publications Committee of Muhimbili University of Health and Allied Sciences, Dar es Salaam. Written informed consent was obtained from the parents/guardians.

Sociodemographic and clinical characteristics including start date of ART, type of ART regimen, WHO HIV disease stage and incidence of opportunistic infections were recorded. Clinical failure was defined as new or recurrence of WHO HIV disease stage III or IV events after ≥6 months of ART.[2] Immunological failure was defined as a CD4+ count below baseline after at least 6 months of ART or a drop in the CD4+ count to <30% of the peak level. To confirm the clinical and/or immunological failures, virological failure was defined as a viral load >400 copies/mL in children receiving ART for ≥6 months.

CD4+ counts and HIV viral loads

Blood samples were collected for determination of CD4+ T-cell counts (FACSCalibur system, Becton Dickinson, USA) and viral load tests (Roche Cobas Amplicor HIV-1 RNA monitor version 1.5 assay, Roche Diagnostics, USA). The assay detection limit using standard protocol testing was 400 - 750 000 copies/mL, and a viral load <400 copies/mL indicated good response to ART. Testing was performed at the Department of Microbiology and Immunology laboratory, Muhimbili University of Health and Allied Sciences, Dar es Salaam.

Statistical analysis

Data were analysed using the Statistical Package for Social Scientists (SPSS) version 17.0, and sensitivity, specificity and predictive values of clinical and immunological criteria were calculated. Viral load was used as a reference method. The χ2 test was used to assess association between virological failure and clinical and immunological failures, opportunistic infections, ART regimen and WHO HIV disease stage.

A p-value of <0.05 was considered statistically significant. Logistic regression analysis was performed to determine the predictors associated with virological failure. Odds ratios (ORs) and 95% confidence intervals (CIs) are presented as the risk estimator.

Results

A total of 218 children on ART were included in the study. Of these, 122 (56.0%) were males. The largest age group was 11 - 15-yearolds (80 children, 36.7%). The mean age for the group as a whole was 10.6 years (range 1 - 16), and the mean duration of time on ART was 40.9 months. One hundred and fifty-three (70.2%) and 53 (23.4%) children were in WHO HIV disease stages III and IV, respectively (Table 1). One hundred and forty-seven (67.4%) were on nevirapine (NVP)-based regimens. Eighty-five (39.0%) had a history of opportunistic infections while on ART. Pulmonary tuberculosis was the most common opportunistic infection reported.

The median viral load was log 3.0. Twenty-five (11.5%) and 54 (25.0%) children had clinical and immunological failures, respectively, and 60 (27.5%) had both clinical and immunological failures. The

697

Table 1. Baseline sociodemographic, clinical and immuno­ logical characteristics of the study population (N=218) Characteristics

n (%)

Age (years) 1-5

34 (15.6)

6 - 10

66 (29.8)

11 - 15

80 (36.7)

≥16

38 (17.4)

Gender Male

122 (56.0)

Female

96 (44.0)

WHO HIV disease stage I

1 (0.5)

II

11 (5.0)

III

153 (70.2)

IV

53 (24.3)

ART regimen NVP, NRTI

147 (67.4)

EFV, NRTI

59 (27.1)

PI, NRTI

11 (5.0)

NRTI

1 (0.5)

Duration of time on ART (months) 6 - 30

95 (43.6)

31 - 55

63 (28.9)

56 - 79

38 (17.4)

≥80

22 (10.1)

Opportunistic infection

85 (39.0)

Pulmonary tuberculosis

35 (16.1)

Recurrent pneumonia

23 (10.6)

Skin and mucosal lesion

8 (3.7)

Chronic ear discharge

7 (3.2)

CNS HIV-related manifestations

7 (3.2)

HIV-related malignancy

5 (2.3)

CD4+% 0 - 15

9 (4.1)

16 - 25

20 (9.2)

≥26

5 (2.3)

CD4+ count (/µl) 0 - 200

59 (27.1)

201 - 350

31 (14.2)

351 - 500

42 (19.3)

≥501

52 (23.1)

WHO = World Health Organization; ART = antiretroviral therapy; NVP = nevirapine; NRTI = nucleoside reverse transcriptase inhibitors; EFV = efavirenz; PI = protease inhibitor; CNS = central nervous system.

sensitivity, specificity, positive predictive value (PPV) and negative predictive value of clinical, immunological and combined monitoring are summarised in Table 2. Immunological monitoring had a higher sensitivity (22.6% v. 12.9%) but lower specificity (73.1% v. 90.3%) than clinical criteria. Combined clinical and immunological criteria

October 2014, Vol. 103, No. 10

RESEARCH

Table 2. Performance characteristics of clinical, immunological and combined criteria in predicting virological failure in HIVinfected children on ART (N=217­) Criteria

Sensitivity (%)

Specificity (%)

PPV (%)

NPV (%)

Clinical (n=25)

12.9

90.3

64.0

43.8

Immunological (n=54)

22.6

73.1

52.8

41.5

Combined clinical and immunological (n=60)

25.8

69.6

53.3

41.4

ART = antiretroviral therapy; PPV = positive predictive value; NPV = negative predictive value.

Table 3. Predictors of virological failure among children on ART for ≥6 months Univariate analysis

Multivariate analysis

Predictor

OR (95% CI)

p-value

OR (95% CI)

p-value

Age (<59 mo. v. ≥60 mo.)

1.05 (0.46 - 2.44)

0.90

0.73 (0.38 - 1.37)

0.30

Duration on ART (6 mo. v. ≥7 mo.)

1.40 (0.50 - 3.97)

0.5

1.40 (0.40 - 4.02)

0.50

ART regimen (NVP-based v. other regimens)

1.80 (0.99 - 3.10)

0.05

2.0 (1.20 - 3.64)

0.03

WHO HIV disease stage (IV v. I - III)

1.03 (0.40 - 2.46)

0.9

1.03 (0.40 - 2.52)

0.90

OIs v. no history of OIs

1.05 (0.60 - 1.80)

0.87

0.93 (0.50 - 1.60)

0.75

CD4+ count <350 cells/µl or CD4+% >25%

0.67 (0.12 - 4.06)

0.67

1.78 (0.21 - 15.50)

0.60

OR = odds ratio; CI = confidence interval; ART = antiretroviral therapy; NVP = nevirapine; WHO = World Health Organization; OIs = opportunistic infections.

had higher sensitivity but lower specificity in detecting virological failure (Table 2).

To assess the association of certain immunological and clinical variables with virological failure in this cohort, we performed univariate and multivariate analysis. The use of NVP was a predictor for virological failure (Table 3), showing a two times higher risk than other regimens (OR 2.0; 95% CI 1.20 - 3.64; p=0.03).

Discussion

Proper monitoring of children on ART is key to preventing emergence of HIV drug resistance, but it can be challenging in resource-limited settings. In this study, we showed that the proportion of children on ART with virological failure was highest, followed by immunological and clinical failure. Clinical and immunological criteria showed poor sensitivity and specificity for detection of virological failure in children on ART, and all the children had a detectable viral load despite being on ART for ≥6 months (the defined period for viral suppression to an undetectable level). NVP-based regimens were independent significant predictors of virological failure in children on ART. The rate of virological failure in this study was high (57%) compared with those reported in previous studies: 20% in Thailand,[8] 26% in Uganda,[9] 32% in the Kilimanjaro region, Tanzania,[10] and 50% in Cote d’Ivoire.[11] The differences observed between the current and previous studies could be explained by the different viral load cut-off points used, e.g. >1 000 copies/mL to indicate virological failure was used in the Thailand study. The Uganda study was a prospective cohort study as opposed to our cross-sectional study, which could have resulted in closer medical attention and monitoring of participants. However, the participants in the two studies were of similar ages.

Some of reasons for the low sensitivity of immunological criteria for virological failure in HIV-infected children on ART have been found to be opportunistic infections, individual variation, and evidence that HIV-specific CD4+ T cells increase when the viral load increases.[12] Immunological criteria were two times more sensitive

698

than clinical criteria in the current and previous studies, supporting the concept that immunological failure occurs earlier than clinical failure.[13] When a combination of clinical and immunological criteria was used, the sensitivity and specificity to predict virological failure were 25.8% and 69.9%, respectively. The combination of clinical and immunological criteria therefore had higher sensitivity but relatively low specificity in predicting virological failure, i.e. the combination of the two criteria offers a better chance of predicting virological failure than a single criterion, but at the expense of lower specificity.

Our findings are in agreement with those of previous studies conducted elsewhere. In a prospective cohort study of children aged <16 years in South Africa by Davies et al.,[14] the sensitivity of immunological criteria was 10.0%, with a PPV of 42.0%, and immunological criteria were therefore unable to identify children on ART who were failing virologically. A study to determine the performance of combined clinical and immunological criteria by Lynen et al.[15] showed that combining clinical and immunological criteria resulted in sensitivity of 29 - 33%, which is comparable to the current study findings. A recent study from Thailand by Bunupuradah et al.[16] examining the accuracy of immunological failure in predicting virological failure in HIV-infected children on first-line ART showed that immunological failure had a sensitivity of 20.4% and specificity of 93.9% in predicting the virological failure, comparable to our study.

Our study and previous studies from Uganda and Thailand,[8,9] showed that children on NVP-based regimens were more likely to have virological failure than those on efavirenz and protease inhibitor-based regimens. In the current study, more than two-thirds of the children received NVP-based regimens. There is evidence that use of single-dose NVP prophylaxis during labour leads to selection of NVP-resistant strains.[17] Pre-exposure of children to NVP via their mothers as part of prevention of mother-to-child transmission of HIV may have predisposed to drug resistance and therefore virological failure; however, we did not examine this effect. Furthermore, in the current study most children received an NVP-based regimen. Since it was a cross-sectional study, it was not possible to establish the trend of

October 2014, Vol. 103, No. 10

RESEARCH

viral suppression and viral rebound occurring over a period of time.

In addition, since viral load assessment is not a routine investigation in resource-limited settings such as ours, baseline viral load samples were not available for testing in this study.

In conclusion, we showed that the proportion of virological failure was the highest (57.1%), followed by immunological (25.0%) and clinical failure (11.5%). Children who were on NVP-based regimens had a higher risk of developing virological failure than those on other regimens. The study demonstrated poor performance of currently recommended clinical and immunological criteria to monitor HIVinfected children on ART. Expanding access to viral load testing may improve outcomes for children on ART in Tanzania and help doctors make informed decisions on treating HIV-infected children.

Acknowledgements. We thank the parents/guardians of the HIVinfected children on ART for consenting to participate in the study.

Sincere thanks to Fauster Mgaya, Betty Mchaki and Theofrida Tembo for sample processing and testing in the lab. Special thanks to the Muhimbili University of Health and Allied Sciences, Dr Guerino Chalamila and Prof. Sylvia Kaaya of Management and Development for Health, and Prof. Ferdinand Mugusi (International Clinical, Operational and Health Sciences Research Training Award) for their technical and financial support of this valuable work.

References 1. UNAIDS. Aids Epidemic Update. November 2010. http://www.unaids.org/documents/20101123_ GlobalReport_em.pdf (accessed 1 September 2014).

2. World Health Organization. Antiretroviral Therapy of HIV Infection in Infants and Children: Towards Universal Access: Recommendations for a Public Health Approach â&#x20AC;&#x201C; 2010 Revision. Geneva: World Health Organization, 2010. http://www.who.int/hiv/pub/guidelines/art/en/ (accessed 1 September 2014).

699

3. World Health Organization/UNICEF/UNAIDS. Global Update on HIV Treatment 2013: Results, Impact and Opportunities, Geneva: WHO, 2013. http://www.unaids.org/en/media/unaids/ contentassets/documents/unaidspublication/2013/20130630_treatment_report_en.pdf (accessed 1 September 2014).

4. Kawo G, Kalokola F, Fataki M, et al. Prevalence of HIV type 1 infection, associated clinical features and mortality among hospitalized children in Dar es Salaam, Tanzania. Scand J Infect Dis 2000;32(4):357363. [http://dx.doi.org/10.1080/003655400750044917] 5. UNAIDS. Epidemiological fact sheet on HIV and AIDS: United Republic of Tanzania. 2009. http:// data.unaids.org/pub/report/2009/jc1700_epi_update_2009_en.pdf (accessed 1 September 2014).

6. World Health Organization. Antiretroviral Therapy for HIV Infection in Infants and Children: Towards Universal Access. 2009. www.who.int/hiv/pub/paediatric/paed-prelim-summary.pdf (accessed 1 September 2014).

7. Meya D, Spacek LA, Tibenderana H, et al. Development and evaluation of a clinical algorithm to monitor patients on antiretrovirals in resource-limited settings using adherence, clinical and CD4 cell count criteria. J Int AIDS Soc 2009;12:3. [http://dx.doi.org/10.1186/1758-2652-12-3] 8. Jittamala PPT, Chaiinseeard S, Sirisanthana V, et al. Predictors of virologic failure and genotypic resistance mutation patterns in Thai children receiving non-nucleoside reverse transcriptase inhibitorbased antiretroviral therapy. Pediatr Infect Dis J 2009;28(9):826-830. [http://dx.doi.org/10.1097/ INF.0b013e3181a458f9] 9. Kamya MR, Mayanja-Kizza H, Kambugu A, et al. Predictors of long-term viral failure among Ugandan children and adults treated with antiretroviral therapy. J Acquir Immune Defic Syndr 2007;46(2):187193. [http://dx.doi.org/10.1097/QAI.0b013e31814278c0] 10. Emmett SD, Cunningham CK, Mmbaga BT, et al. Predicting virologic failure among HIV-1-infected children receiving antiretroviral therapy in Tanzania: A cross-sectional study. J Acquir Immune Defic Syndr 2010;54(4):368-375. [http://dx.doi.org/10.1097/QAI.0b013e3181cf4882] 11. Fassinou PEN, Rouet F, Laguide R, et al. Highly active antiretroviral therapies among HIV-1-infected children in Abidjan, Cote dâ&#x20AC;&#x2122;Ivoire. AIDS 2004;18(14):1905-1913. [http://dx.doi.org/10.1097/00002030200409240-00006] 12. Scott ZA, Beaumier CM, Sharkey M, et al. HIV-1 replication increases HIV-specific CD4+ T cell frequencies but limits proliferative capacity in chronically infected children. J Immunol 2003;170(11S):5786-5792. [http://dx.doi.org/10.4049/jimmunol.170.11.5786] 13. Aldous JL, Haubrich RH. Defining treatment failure in resource-rich settings. Curr Opin HIV AIDS 2009;4(6):459-466. [http://dx.doi.org/10.1097/COH.0b013e328331dea5] 14. Davies MA, Boulle A, Eley B, et al. Accuracy of immunological criteria for identifying virological failure in children on antiretroviral therapy. Trop Med Int Health 2011;16(11):1367-1371. [http:// dx.doi.org/10.1111/j.1365-3156.2011.02854.x] 15. Lynen L, van Griensven J, Elliott J. Monitoring for treatment failure in patients on first-line antiretroviral treatment in resource-constrained settings. Curr Opin HIV AIDS 2010;5(1):1-5. [http:// dx.doi.org/10.1097/COH.0b013e3283333762] 16. Bunupuradah T, Puthanakit T, Kosalaraksa P, et al. Immunologic and virologic failure after first-line NNRTI-based antiretroviral therapy in Thai HIV-infected children. AIDS Res Ther 2011;8:40. [http:// dx.doi.org/10.1186/1742-6405-8-40] 17. Cunningham CK, Dorenbaum A, Mofenson L, Culnane M, Sullivan JL, and the PACTG 316 Team. Genotypic resistance analysis in women participating in PACTG 316 with HIV-1 RNA >400 copies/ml. Presented at the 8th Conference on Retroviruses and Opportunistic Infections, 4-8 February 2001, Chicago, USA.

Accepted 26 June 2014.

October 2014, Vol. 103, No. 10

RESEARCH

Quality assurance in diabetic retinal screening in South Africa S Cook,1 MB BCh, FCS (Ophth) (SA); R T Staff,2,3 PhD; K A Goatman,4 PhD; J A Olson,4,5 MD, FRCPE, FRCOphth; and the Scottish Diabetic Retinopathy Screening collaborative e Eye Centre, East London, Eastern Cape, South Africa, and Department of Ophthalmology, Faculty of Health Sciences, Th Walter Sisulu University, Umtata, Eastern Cape, South Africa 2 Aberdeen Biomedical Imaging Centre, University of Aberdeen, Aberdeen, Scotland, UK 3 Aberdeen Royal Infirmary, NHS Grampian, Scotland, UK 4 School of Medicine and Dentistry, University of Aberdeen, Scotland, UK 5 Retinal Screening, Aberdeen Royal Infirmary, NHS Grampian, Scotland, UK 1

Corresponding author: S Cook (dr@eyecentre.co.za) Background. Diabetic retinopathy (DR) is an important biomarker for microvascular disease and blindness. Digital fundus photography is a cost-effective way of screening for DR. Access to DR screening is difficult for many South Africans with diabetes.

Objective. To perform external quality assurance (EQA) on graders registered in the Ophthalmological Society of South Africa DR screening programme.

Methods. Graders registered on the South African (SA) Diabetic Register website were invited to participate in the study. The Scottish EQA software system was used to enable on-line grading of 100 retinal photographs. Expert National Health Service graders provided the consensus expert grading for the image set.

Results. Two hundred and sixty-one participants completed the EQA process, including nine ophthalmologists, 243 optometrists, and nine other graders. A wide range of outcomes were demonstrated, with a mean sensitivity of 0.905 (range 0.286 - 1.000) and mean specificity of 0.507 (0.000 - 0.935). The mean diagnostic odds ratio was calculated to be 12.3 (range 0.147 - 148.2).

Conclusions. This is the first quality assurance study conducted with SA healthcare professionals. The outcomes are of interest to all stakeholders dealing with the diabetes epidemic. The disparity in grader performance indicates room for improvement. The results demonstrate a high referral rate to ophthalmology, suggesting that on average graders are performing safely, but with a high number of inappropriate referrals.

S Afr Med J 2014;104(10):700-704. DOI:10.7196/SAMJ.8678

The incidence of diabetes is increasing globally.

Africa is no exception: the number of adults with diabetes is expected to almost double by 2030 to 23.9 million.[1] Diabetes is clearly becoming a pressing public health problem for Africa, for which effective interventions are required in the near future to avert the anticipated health burden. One such intervention is the introduction of a diabetic retinal screening programme for the early detection of diabetic retinopathy (DR) and the prevention of blindness.

Studies estimating the impact of screening programmes in Europe have concluded that they achieved worthwhile health gains and substantial reductions in the incidence of new blindness due to DR.[2,3] The introduction of a European-style screening programme in the African context is unlikely in the near future. However, raising current screening expertise and fully exploiting the available technology has the potential for significant health gains.

DR screening in South Africa (SA) is done on an ad hoc and opportunistic basis by a spectrum of healthcare providers. These provi足 ders have invested in fundus camera technology capable of producing high-resolution retinal images. This technology is key to established screening programmes, and is core technology for national screening approaches elsewhere. The ability to acquire and record high-quality retinal images is, however, only the first step: effective interpretation is essential to any screening process. How that screening expertise is disseminated and maintained is a challenge for national and professional bodies that wish to address the increasing health burden.

700

The Ophthalmological Society of South Africa (OSSA) has deve足 loped a framework for a national Diabetic Retinopathy Screening Programme that can accommodate the many sectors in the healthcare environment. This includes traditional teaching methods such as lecturing and publication. A key part of this framework is a quality assurance process that will encourage ongoing learning and the monitoring of performance.

The Scottish External Quality Assurance (EQA) process is an internet-based assessment tool for the Scottish Diabetic Retinopathy Screening collaborative. The programme has been in place since 2007. It includes a compulsory twice-yearly procedure that involves all screeners working for the National Health Service in Scotland.

Once completed and assessed, feature-based feedback is given to individual screeners and the lead person responsible at each screening site. The process involves each screener grading 100 retinal images.

These grades are compared with a reference standard generated from the consensus of the expert graders, who are experienced ophthalmologists with a high level of proficiency in assessing retinal images. Longitudinal analysis of screener performance has shown that it significantly improves performance for all grades of screener.[4] It has enabled the service to assess individual screeners and sites, to identify strengths and weaknesses, and to improve quality.

Using this software, the current study assessed the performance of volunteer screeners in SA, by comparison with a group of expert graders from the Scottish service. We aimed to assess the feasibility of the EQA process in SA; to compare the performance of

October 2014, Vol. 104, No. 10

RESEARCH

screening groups; and to identify potential improvements in the screening practice of individuals with a view to future personal and group feedback and training.

Methods

Screener recruitment

The Diabetic Retinopathy Screening Programme was advertised and promoted by a variety of means: conference presentations, personal contact, posters, and publications in the SAMJ and the Diabetic Register website (www.diabeticregister. co.za). The Diabetic Register is a closed user group site for healthcare professionals.

Individuals who expressed an interest were invited to participate in the EQA process.

The minimum requirements to take part in the study were access to the internet, an e-mail account, and an occupation with the requirement or opportunity for retinal screening. Those who indicated interest were sent a link to a web-based survey to establish their professional characteristics, e.g. post type, experience and workload (www.surveymonkey.com/s/B6B3BNC).

Once the survey had been completed, a further link was sent explaining how to access the EQA site and carry out the EQA process. The site was open for data collection between November 2013 and January 2014. Technical support in grading was provided by a dedicated employee of the Eye Centre in East London, Eastern Cape, SA. Queries that could not be resolved locally were dealt with by the EQA experts in Scotland.

Running in parallel to this process, expert graders from the Scottish diabetic retinal screening service were asked to participate so as to provide an external consensus reference standard. These graders have all been part of the screening service for more than 5 years, have been tested regularly via the EQA process, have significant screening workloads, and have been shown to be high and consistent performers.

Image selection

The retinal images used in this study were selec­ ted by one of the authors (SC). Anonymised images were selected from the Eye Centre fundus photo database. There was no preselection for quality or level of retinopathy.

The EQA process

The EQA web-based software closely matches the feature-based grading system used in Scotland. The interface (Fig. 1) is compatible with all popular web browsers and consists of an image display on the left, together with controls for contrast, brightness, zoom and red-free colour display, a ruler for measuring the size of features, and a feature grading panel on the right-hand side. The number of times these controls were used was recorded for each screener, along with the time taken for grading all the images. Each grader was presented with the images in a different random order. Screeners were also allowed to use a ‘sandbox’ feature that enabled them

Fig. 1. The External Quality Assurance software interface.

Table 1. A summary of the Scottish Diabetic Retinopathy Grading Scheme Grading

Description

Outcome

R0 (no visible retinopathy)

No visible diabetic retinopathy anywhere

Re-screen in 12 months

R1 (mild)

At least one dot, blot or flame haemorrhage, microaneurysm, exudate or cotton-wool spot anywhere

Re-screen in 12 months

R2 (observable background)

Four or more blot haemorrhages (>AH standard photograph 2a) in one hemi-field only (where the inferior and superior hemi-fields are delineated by a line passing through the centres of the fovea and optic disc)

Re-screen in 6 months

R3 (referable background)

Any of the following features: (i) four or more blot haemorrhages (>AH standard photograph 2a) in the inferior and superior hemi-fields; (ii) venous beading (>AH standard photograph 6a); (iii) intraretinal microvascular anomalies (>AH standard photograph 8a)

Refer to ophthalmology

R4 (proliferative)

Any of the following features: (i) active new vessels; (ii) vitreous haemorrhage

Refer to ophthalmology

R6 (inadequate)

Insufficient clarity or field of view

Slit-lamp examination

M1 (observable maculopathy)

Exudate within a radius of >1 but <2 disc diameters of the centre of the fovea

Re-screen in 6 months

M2 (referable maculopathy)

Any blot haemorrhage or exudate within a radius of 1 disc diameter of the centre of the fovea

Refer to ophthalmology

AH = Airlie House standard photography scheme.[9]

701

October 2014, Vol. 104, No. 10

RESEARCH

to become familiar with the system by grading example images prior to grading the test images.

The software implements the Scottish grading scheme (http://www.ndrs-wp. scot.nhs.uk), summarised in Table 1. The retinopathy grades are derived automatically from the features the grader selects. There are eight possible grading outcomes: four

of these outcomes require referral (M2, R3, R4 and R6), and two indicate more frequent review with a 6-month interval (M1 and R2).

The remaining two categories (R0 and R1) result in re-screening in 12 months.

Results

The promotion process generated interest from 398 individuals. These individuals

Table 2. Participant sample and performance by characteristic n

AUC (SE)

DOR (95% CI)

9

0.922 (0.025)

25.81 (14.41 - 46.24)*

Post Other Ophthalmologist

9

0.842 (0.009)

22.48 (13.53 - 37.36)*

Optometrist

243

0.842 (0.009)

11.57 (10.14 - 13.21)

110

0.825 (0.012)

11.12 (9.35 - 13.21)

Experience (year/s) <1 2-5

60

0.833 (0.026)

11.64 (8.25 - 16.42)

>6

91

0.842 (0.009)

13.68 (11.25 - 16.63)

Competence Novice

115

0.815 (0.011)

10.02 (8.52 - 11.61)*

Competent

122

0.815 (0.011)

12.55 (10.14 - 15.53)*

Experienced

24

0.897 (0.021)

24.11 (16.78 - 34.64)

Workload (examinations/month) ≤10

146

0.838 (0.011)

12.47 (10.69 - 14.53)

11 - 50

60

0.843 (0.019)

11.72 (8.62 - 15.93)

≥51

55

0.843 (0.019)

11.77 (8.73 - 15.87)

AUC = area under the receiver operating characteristic curve; SE = standard error; DOR = diagnostic odds ratio; CI = confidence interval. *Mean statistically significantly different (p<0.05) from the group at the bottom of each section.

1

1– sensitivity

0.8

0.6 Fitted ROC curve Expert graders

0.4

Participant graders

0.2

0 0

0.2

0.4

0.6

0.8

1

1– specificity

Fig. 2. A scatter plot and ROC curve of grader performance in terms of sensitivity and specificity. Each mark represents a single grader. Dark blue squares represent the external expert graders. Lighter blue circles represent the study participants. The ROC line was calculated from the study participants only.

(ROC = receiver operating characteristic.)

702

October 2014, Vol. 104, No. 10

accessed the survey site, filled in the questionnaire and gave permission for their data to be used. Two hundred and sixtyone participants gave all the information requested, and went on to register on the EQA site and complete the process. The characteristics of this group are shown in Table 2.

The nine expert graders achieved a consensus on the grading of 90 out of the 100 images. The responses to these images by each participant were used to assess the participant’s performance. According to the expert external screeners, the 90 images were classified as follows: R0 – 22, R1 – 38, M1 – 2, R2 – 0, R6 – 2, M2 – 13, R3 – 4, R4 – 9.

Fig. 2 shows the sensitivity and specificity of each participant in a receiver operating characteristic (ROC) diagram. Each circle represents a single participant. The squares represent the performance of the external expert graders. All graders were assessed using the consensus grades as the reference standard. The top left-hand corner indicates the best screener performance. The expert graders are shown as dark blue squares. The SA graders are represented as lighter blue circles. Note that the expert graders would be expected to perform better, as they each contributed to the standard.

There is a significant variation in the per­ formance across all graders. For example, at one extreme, a grader detects just over 20% of cases, which would normally be referred to an eye clinic for ophthalmology assessment; while at the other, two graders have 0% specificity – i.e. they are sending everyone to the eye clinic. Table 3 shows the agreement (or lack thereof) between the participants and the external expert screeners. This table shows how images of each grade were graded: the grades along the top show the most serious retinopathy or maculopathy grade according to the standard. The leading diagonal (in bold italics) indicates exact agreement between the standard and the graders. Note that none of the images had a consensus grading of R2 (observable retinopathy) or R6 (technical failure, unassessable image). The bottom left-hand corner (in bold) indicates ‘overgrading’ according to the standard, and the top right-hand corner (in italics) indicates ‘under-grading’ of referable images. The numbers at the end of the rows and columns show the total number of grades in that row or column.

In general, these findings indicate a lack of specificity in those screeners who took part.

The participating group was heterogeneous, with a range of experience, occupations and workloads. The following estimates

RESEARCH

Table 3. Cross-agreement (%) between the external graders (Standard) and the participants* Standard Participants

R0

R1

M1

R2

R6

M2

R3

R4

Total

R0

41.1

15.2

1.5

9.4

1.7

0.0

1.1

4 011

R1

30.1

36.5

18.6

19.5

8.6

1.1

5.4

5 979

M1

1.7

1.6

33.3

3.4

4.0

1.0

1.3

625

R2

0.3

1.1

1.7

0.6

1.1

1.1

0.4

194

R6

1.6

0.5

0.4

35.4

0.3

0.1

0.6

356

M2

10.6

21.4

5.7

9.4

43.1

8.2

8.3

4 554

R3

7.4

15.7

25.1

11.9

31.7

56.8

21.8

4 361 3 410

R4

7.3

7.9

13.6

10.3

9.3

31.8

61.0

Total

5 742

9 918

522

0

522

3 393

1 044

2 349

* The values are the percentage of images that were graded by the participants for each standard grading category. The values at the bottom of each column and at the end of each row represent the total number of images graded into each category by the external graders and participants, respectively.

The leading diagonal (bold italics) indicates exact agreement between the standard and the graders, the bottom left-hand corner (bold) indicates ‘over-grading’ according to the standard, and the top right-hand corner (italics) indicates ‘under-grading’ of referable images.

The grading outcomes are defined in Table 1.

of the performance for each group were calculated: the area under the ROC curve (AUC) and diagnostic odds ratio (DOR) (Table 2). A comparison of the performance using the Metadisc software[5] found that the optometrist performance was inferior to the other two groups. Those who considered themselves experienced screeners performed better than the competent and the novice screeners. No difference was found to be associated with either the number of years of screening or workload.

In order to examine differences in screener behaviour, we ranked the participants in terms of performance (DOR) and divided them into three groups: low performers (DOR≤10.12, n=87), medium performers (10.12<DOR≤22.24, n=87) and high per­ formers (22.24>DOR, n=87). Table 4 shows the time taken and the mean use of the red filter, the zoom and the ruler by each of these performance groups. The use of these tools by the external expert reference group is also included for comparison. Differences between the groups were tested using a oneway analysis of variance and a post hoc Tukey approach. It is clear from this table that the expert reference group took less time and used the tools more. In addition, within the tested groups, the more the tools were used the better the performance.

Discussion

DR has been identified as a valuable biomarker for systemic risk of microvascular complications of diabetes mellitus. With the publication of the Atherosclerosis Risk Study findings by Wong et al.[6] and the subsequent publication of the findings of the Japanese Diabetes Complications Study,[7] there has been a new appreciation

Table 4. Screener use of the image manipulation tools and time taken Group

Time taken (hours) mean (SD)

Red filter (%) mean (SD)

Zoom (%) mean (SD)

Ruler (%) mean (SD)

Low

3.91 (0.24)

57.62 (4.11)*

10.71 (1.98)*

9.39 (1.82)

Medium

4.17 (0.22)*

63.61 (3.58)*

25.30 (3.46)*

11.44 (1.53)

High

4.70 (0.27)*

69.38 (3.16)*

36.21 (3.67)

14.46 (1.74)

Expert

2.02 (0.23)

98.12 (1.18)

57.23 (13.20)

22.44 (5.12)

*Groups in which there is a significant difference between the participant group and the expert group (p<0.05).

of the importance of detecting any retinopathy. These studies demonstrated a significantly (approximately two times) increased risk of coronary heart disease and stroke in the study groups. This has changed the emphasis of screening for DR from a blindness prevention initiative (detection of advanced retinopathy) to a primary healthcare initiative (detection of any retinopathy). The importance of a biomarker for systemic complications at primary healthcare level cannot be overstated, particularly in a resource-poor setting. DR provides such characteristics.

There has been a general decline in the provision of screening by GPs in SA. This is because GPs only have ready access to direct ophthalmoscopy, a technology that has low sensitivity,[8] even in the best hands, and is unpopular with patients because it requires the pupils to be dilated. In the ophthalmic world, fundus photography has transformed the ability to detect disease as well as creating a permanent digital record.

Fundus photography rather than direct ophthalmoscopy will therefore probably become the standard of care for DR. Patientfriendly, good-quality fundus photography relies on image acquisition utilising non-

703

October 2014, Vol. 104, No. 10

mydriatic cameras. These are capitalintensive items that have not been available on a widespread basis in SA. The OSSA DR programme has strived to lower the barriers to access to screening opportunities for people living with diabetes. OSSA has endorsed the use of nonophthalmologist graders to try to cope with the burden of disease. There is a widespread appreciation of the value of non-medical personnel as graders. These graders need the backing of a robust, scientific-quality assurance system. This initiative, coupled with optometrist interest, has seen the introduction of many new cameras into the SA healthcare market. A key public health issue has been to establish a responsible way of implementing quality assurance, encouraging participation and ongoing learning. Fundus photo screening is a new discipline in SA. This means that there is a wide range of levels of competence. A system of accreditation was required. This needed to be on an ongoing basis rather than a once-off pass/fail scenario. The system should encourage improvement over time.

The Scottish EQA system has demonstrated these characteristics in the Scottish Diabetic Retinopathy Screening collaborative.

RESEARCH

The Scottish Retinopathy Grading System was chosen for imple­ mentation in SA because of its simple, hierarchical grading of retinopathy characteristics. Simplicity and clear cut-offs for referrals are vital for management of DR. The inclusion of R2 with more frequent review at screening (primary) level is important for the public sector eye clinics, which are already swamped with blindness prevention work. The Scottish system and algorithm for referral has been moderated for the SA scenario to increase safety. The modifications are that any maculopathy (M1 or M2) is to be referred to ophthalmology, and the concept of systemic risk has been incorporated into the algorithm. This is particularly important in SA, where levels of control of diabetes and hypertension are generally very poor. The risk calculator developed by Prof. Einar Steffanson (www.risk.is) has been introduced for use in Africa (www.riskafrica. co.za). This enables non-medical graders to calculate risk and modify the review period for poor control.

The outcomes were significantly better for the ophthalmologist group than for the optometrist group. More experienced graders had higher scores than those with less time since qualifying and a lower level of perceived experience. No significant difference was noted in outcome between the different daily workload groups. The wide range of performance across the groups was larger than that observed in the first Scottish EQA in 2008.[4] It is expected that this will be reduced and overall performance be improved over repeated EQAs, as happened in Scotland.

Safety of non-ophthalmologist graders was a concern. The results show that this group tended to over-refer rather than underrefer. This was reassuring from a safety point of view, but it does mean that more cases than necessary would have been referred.

Specificity will be the key aspect of training initiatives in order to address this. Furthermore, 12.6% of cases that should have been referred were not (compared with 4.6% calculated from the Scottish 2010 EQA round).

The time taken to complete the task was similar between the different performance groups. Use of the tools increased with performance, with the high-performance group making the most use of the red-free filter, zoom and ruler controls. After the EQA process was completed, individual feedback and results were given anonymously to each participant. The individual was able to see his or her outcome relative to the peer group. Our plan is to repeat this process on an annual basis, encouraging new participants and monitoring performance. This system is thought to be ideal for the SA environment, where many graders possess their own cameras and would respond better to a peer group-driven incentive to improve rather than an absolute pass/fail outcome.

704

Study limitations

This study has a number of weaknesses that should be addressed in future work. Not all grading groups were present in our test set.

When selected, the imaging mix was thought to contain examples of all possible outcomes. However, consensus was not reached by the expert graders, so grade R2 was not represented in the study set. It is difficult to assess experience and training as a predictor of performance. One would expect the more experienced and better trained to have superior performance, as we have crudely shown in Table 2. However, a better, more refined assessment of these factors will inform where educational efforts could best be focused. In general, our sample is a self-selected group who have expressed an interest; how these findings can be applied to the broader population performing such screening processes is unclear, although we have no reason to expect that our sample is not representative.

Conclusion

The process was well supported by participants and was able to demonstrate safety and areas of weakness that require training. The next SA EQA is scheduled to run in November 2014.

Acknowledgements. The authors thank all the participants for their time and interest and the members of the Scottish Diabetic Retinopathy Screening Collaborative who acted as the external standard: Alison Bow, Anne Fairley, Anne Sinclair, Brian Power, Mohan Varikkara, Saileela Hanumanthu, Sonia Zachariah, Usha Zamvar and William Wykes.

References 1. Shaw JE, Sicree RA, Zimmet PZ. Global estimates of the prevalence of diabetes for 2010 and 2030.

Diabetes Res Clin Pract 2010;87(1):4-14. [http://dx.doi.org/10.1016/j.diabres.2009.10.007] 2. Backlund L, Algvere P, Rosenqvist U. New blindness in diabetes reduced by more than one-third in Stockholm County. Diabet Med 1997;14(9):732-740. [http://dx.doi.org/10.1002/(SICI)10969136(199709)14:9<732::AID-DIA474>3.0.CO;2-J] 3. Ryder R. Screening for diabetic retinopathy in the 21st century. Diabet Med 1998;15(9):721-722. [http://dx.doi.org/10.1002/(SICI)1096-9136(199809)15:9<721::AID-DIA694>3.0.CO;2-B] 4. Goatman KA, Philip S, Fleming AD, et al. External quality assurance for image grading in the Scottish Diabetic Retinopathy Screening Programme. Diabet Med 2012;29(6):776-783. [http://dx.doi. org/10.1111/j.1464-5491.2011.03504.x] 5. Zamora J, Abraira V, Muriel A, et al. A software for meta-analysis of test accuracy data. BMC Med Res Methodol 2006;6:31. [http://dx.doi.org/10.1186/1471-2288-6-31] 6. Wong T, Klein R, Sharrett A, et al. Diabetic retinopathy and risk of ischemic stroke: The atherosclerosis risk in communities study. Invest Ophthalmol Vis Sci 2004;45(Suppl 2):U617-U617.

7. Kawasaki R, Tanaka S, Tanakas AS, et al.; Japan Diabetes Complications Study Group. Ophthalmology 2013;120(3):574-582. [http://dx.doi.org/10.1016/j.ophtha.2012.08.029.

8. Harding SP, Broadbent DM, Neoh C, White MC, Vora J. Sensitivity and specificity of photography and direct ophthalmoscopy in screening for sight threatening eye disease: The Liverpool Diabetic Eye Study. BMJ 1995;311(7013):1131-1135. [http://dx.doi.org/10.1136/bmj.311.7013.1131] 9. Early Treatment Diabetic Retinopathy Study Research Group. Grading diabetic retinopathy from stereoscopic color fundus photographs â&#x20AC;&#x201C; an extension of the modified Airlie House classification: ETDRS Report Number 10. Ophthalmology 1991;98(5):786-806. [http://dx.doi.org/10.1016/S01616420(13)38012-9]

Accepted 20 August 2014.

October 2014, Vol. 104, No. 10

Amloc 5 mg. Each tablet contains amlodopine maleate equivalent to 5 mg amlodopine. Reg. No.: RSA S3 38/7.1/0183 NAM NS2 06/7.1/0011 BOT S2 BOT0801198. Amloc 10 mg. Each tablet contains amlodopine maleate equivalent to 10 mg amlodopine. Reg. No.: RSA S3 38/7.1/0183 NAM NS2 06/7.1/0011 BOT S2 BOT0801198. For full prescribing information, refer to the package insert approved by the Medicines Control Council, 12 August 2006. 1) IMS, MAT unit sales, 1 July 2013 - 30 June 2014. 2) Dahlof B, Sever PS, Poulter NR, et al. for the Ascot investigators. Prevention of cardiovascular events with an antihypertensive regimen of amlodopine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial - Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial.

Lancet 2005;366:895-906. 3) Nissen SE, et al. Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and nromal blood pressure. The CAMELOT study: A randomised controlled trial. JAMA 2004;292:2217-2226. 4) Department of health website: http//www.doh.gov.za - Accessed 27/08/2014. ACC118/10/2014.

GUEST EDITORIAL

Atopic dermatitis The articles in this issue of CME reflect the views of a number of individuals who developed the guideline for the management of atopic dermatitis (AD) to improve the outcome of its treatment in South Africa (SA). AD has a major impact on the quality of life of sufferers and it is hoped that the articles and the guidelines they embody, if implemented, play a role in achieving these outcomes.

Not only is AD the most common skin disease in children, but it causes tremendous morbidity. Engaging with many of these suffering children and their parents daily, is emotionally draining and energy sapping. No other skin condition places such demands on resources, time and the human spirit.

It is therefore essential that the management of AD should be optimal, with a thorough understanding of the pathogenesis, approaching it in a multi-professional manner. Understanding the disease will also contribute towards eliminating unnecessary investigations, unnecessary and inappropriate interventions and unsubstantiated treatment modalities. The simplistic way of approaching AD as â&#x20AC;&#x2DC;an allergyâ&#x20AC;&#x2122; is long outdated, as the complexity of the condition becomes increasingly apparent with the publication of new information. All healthcare workers involved in the management of AD should take note of these guiding principles and try to implement them in clinical practice whenever possible.

The basis of each topic was developed through general consensus by a panel of four dermatologists and five paediatricians (including three allergists) from SA, based on evidence from an extensive literature review.

Draft documents were made available for comment via the internet. All input, where appropriate, was then incorporated into the guideline.

This issue of CME consists of six full-length articles, covering the following topics: aetiopathogenesis,[1] epidemiology,[2] diagnosis,[3] patient education and specialist referral,[4] non-pharmacological treatment[5] and pharmacological treatment.[6] Summaries of the general approach to and guideline for the management of AD are also provided (available online only).[7] A disclaimer has to be added: these guidelines do not represent all possible methods of management applicable to all patients, do not exclude any other reasonable methods, and will not ensure successful treatment in every situation. The responsible physician should

DynavalCo2014CME island.pdf

2

2014/09/08

take the unique circumstances of each patient into consideration regarding decisions about a specific therapy.

The pharmaceutical companies Astellas Pharma and Galderma generously co-sponsored the meeting of the work group and all costs generated by the meeting.

We trust that all who read this issue will find it stimulating, informative and helpful in daily practice to improve the condition of these suffering children and adults.

Werner Sinclair Department of Dermatology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa sinclairw@ufs.ac.za

Robin J Green Department of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa robin.green@up.ac.za

1. Jordaan HF, Todd G, Sinclair W, Green RJ. Aetiopathogenesis of atopic dermatitis. S Afr Med J 2014;104(10):706-709. [http://dx.doi.org/10.7196/SAMJ.8840] 2. Todd G. Epidemiology of atopic dermatitis. S Afr Med J 2014;104(10):710. [http://dx.doi.org/10.7196/SAMJ.8843] 3. Sinclair W, Aboobaker J, Green RJ, Levin ME. Diagnosis of atopic dermatitis: From bedside to laboratory. S Afr Med J 2014;104(10):711. [http://dx.doi.org/10.7196/SAMJ.8850] 4. Green RJ, Pentz A, Jordaan HF. Education and specialist referral of patients with atopic dermatitis. S Afr Med J 2014;104(10):712. [http://dx.doi.org/10.7196/SAMJ.8857] 5. Todd G, Manjra A, Sinclair W, Levin M, Green RJ. Non-pharmacological treatment modalities for atopic dermatitis. S Afr Med J 2014;104(10):713. [http://dx.doi.org/10.7196/SAMJ.8860] 6. Puterman A, Lewis H, Sinclair W, Green RJ. Topical and systemic pharmacological treatment of atopic dermatitis. S Afr Med J 2014;104(10):714. [http://dx.doi.org/10.7196/SAMJ.8870] 7. Green RJ, Sinclair W. General approach to and summary of the guideline for the management of atopic dermatitis. S Afr Med J 2014;104(10). [http://dx.doi.org/10.7196/SAMJ.8876]

S Afr Med J 2014;104(10):705. DOI:10.7196/SAMJ.8865

9:30 AM

C

M

Y

CM

MY

CY

CMY

K

705

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

REVIEW

Aetiopathogenesis of atopic dermatitis H F Jordaan,1 MB ChB, MMed (Derm); G Todd,2 MB ChB, FCDerm (SA), PhD; W Sinclair,3 MB ChB, MMed (Derm); R J Green,4 MB BCh, DCH, FCP(SA), DTM&H, MMed, FCCP, PhD, Dip Allergology (SA), DSc 1 Division of Dermatology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa 2 Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa 3 Department of Dermatology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa 4 Department of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa Corresponding author: W Sinclair (sinclairw@ufs.ac.za)

The aetiopathogenesis of atopic dermatitis (AD) is complex and during recent years much has been learnt regarding the genetic predisposition to the development of this condition and how its interaction with the environment influences clinical manifestations. AD is not a simple allergic condition. An inherited stratum corneum barrier defect, transepidermal water loss, early antigen exposure through the skin and over-hygienic care of the young child seem to be the major drivers in the manifestation of the disease. Many other, more specific, environmental factors may influence the clinical picture in individual patients; some of these have an allergic basis, while others do not.

In this article, the terminology used in this issue of CME is explained, the evidence for the different aetiopathological factors is presented and the factors that worsen or improve AD are listed.

S Afr Med J 2014;104(10):706-709. DOI:10.7196/SAMJ.8840

Definitions and terminology

The word eczema derives from the Greek word for ‘boiling over’. Eczema periodically flares up (or boils over).

The term dermatitis refers to inflammation of the skin, analogous to appendicitis (inflammation of the appendix), hepatitis (inflammation of the liver), etc. Currently, the terms dermatitis and eczema are generally regarded as synonyms.

Internationally, however, there is no agreement on the use of these terms. The word eczema tends to be a layman’s term, while dermatitis is more often used in a scientific context.

Eczema/dermatitis is not a diagnosis. The most common forms of eczema/dermatitis are atopic, seborrhoeic, primary irritant, allergic contact, photoallergic, phototoxic, nummular, asteatotic, stasis and dyshydrotic.

Atopy may be defined as a clinical hypersensitivity state subject to hereditary influences, including hay fever, asthma and eczema, developing against a complex genetic background – the so-called atopic diathesis. In the 1980s, Hanifin and Rajka proposed a list of criteria, leading to agreement regarding the clinical concept of atopic dermatitis (AD). In 1994, a UK Working Party refined these criteria in a concise and validated set of survey-based diagnostic criteria useful for the purposes of epidemiological studies, as set out below.

Atopic in the term atopic eczema is simply an indicator of the frequent association of this condition with atopy and the need9:30 to DynavalCo2014CME island.pdf 2 2014/09/08

separate this clinical phenotype from other forms of eczema. The terms atopic eczema and AD are synonymous.

According to the position paper of the Nomenclature Review Committee of the World Allergy Association,[1] the term atopic eczema/dermatitis syndrome (AEDS) should be used as the umbrella term covering the different subtypes of AD. The new nomenclature (AEDS) underlines that AD is not one single disease entity, but rather an aggregation of several diseases that have certain clinical characteristics in common.

Intrinsic AD (non-allergic AEDS (NAAEDS) or atopiform dermatitis) fulfils the most commonly used diagnostic criteria for AD. Patients with intrinsic AD have no associated respiratory diseases, such as bronchial asthma or allergic rhinitis, present with normal total serum IgE levels, have no specific IgE, and manifest negative skin-prick tests to aeroallergens or foods.

In one study, intrinsic AD was more common in females and disease onset was later. This group comprised at least 20% (up to 60%) of cases.[2] Extrinsic AD (allergic AEDS (AAEDS)) is commonly associated with respiratory allergies such as rhinitis and asthma, high levels of serum IgE, specific IgE, and positive skin-prick tests to aeroallergens or foods. Immunological differences between NAAEDS and AAEDS AMcan be found in the cell and cytokine patterns in peripheral blood and

C

M

Y

CM

MY

CY

CMY

K

706

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

affected skin, and also by phenotyping characterisation of epidermal dendritic cells. This group comprises 40 - 80% of patients.[2] The classification into AAEDS and NAAEDS at each stage of life, i.e. infancy, childhood, adolescence and adulthood, is essential for the allergological management of patients regarding allergen avoidance, secondary allergy prevention, and immunotherapy. The risk of an ‘atopy march’ is significantly lower in children with NAAEDS than in those with AAEDS.[3] This subdivision is controversial. Cases may transform from one type to another and this division may not be applicable to adults. Until the exact genetic and causative agents are known, one should consider the clinical disease as one condition.

Acute eczema/dermatitis is characterised by oedema, erythema, vesiculation, exudation and crusting. Chronic eczema/dermatitis is characterised by lichenification, which refers to thickening of the skin with exaggeration of normal markings. Flat-topped, shiny, quadrilateral coalescing papules are enclosed. Subacute eczema/ dermatitis shows features that overlap with those of acute and chronic eczema/dermatitis, i.e. commonly slightly elevated, and red, brownish or purplish in colour, with variable scaling. Generally, the subacute presentation of eczema/dermatitis is more common.

The morphology, distribution and evolution of eczema/dermatitis in atopic eczema/dermatitis are highly characteristic and age dependent: • Infant phase (birth - 2 years): red scaly lesions typically develop on the cheeks, usually sparing the peri-oral and perinasal areas.

The chin is typically involved and cheilitis is common. A small but significant number of infants develop a generalised eruption, and involvement of the scalp is not uncommon. The nappy area is often spared, but sometimes the cubital/popliteal fossae or other parts of the limbs are involved.

• Childhood phase (2 - 12 years): eczema/dermatitis involves the flexural areas (i.e. the cubital and popliteal fossae) and the neck, wrist and ankles.

• Adolescent and adult phases (12 years - adulthood): involvement is similar to the childhood phase. Additionally, hand, peri-ocular and anogenital eczema/dermatitis are common. Sometimes lesions occur on extensor surfaces, and follicular accentuation may be prominent.

Morphologically, lesions may be classified as acute, subacute or chronic. Atopic eczema is a difficult disease to define, as the clinical features are highly variable with regard to morphology, body site and time. Diagnosis is therefore essentially clinical.[4]

Aetiopathogenesis

The aetiopathogenesis of AD is probably multifactorial. Current thinking favours a skin barrier defect as the most significant predisposing factor, where mutations in the filaggrin gene feature strongly.[5,6] MostDynavalCo2014CME studies on the causes of AD have been performed island.pdf 2 2014/09/08 9:30

in children. There is little to suggest that adult AD should have a different aetiopathogenesis, except for some clinical features that differ, such as the predominant involvement of the hands and the head and neck.[7]

Genetics

Population-based family studies in Europe suggest that in atopic families up to 50% of offspring will have AD.[8] Twin studies showing a concordance rate of 0.75 for monozygotic twins and 0.20 for dizygotic twins support a genetic basis for AD.[8-10] Candidate genes are further evidence for a genetic predisposition.[8,10]

Allergic sensitisation

The predisposition for IgE hyper-responsiveness to allergens defines the term atopy.[1] A systematic review of the published evidence for allergic sensitisation and dermatitis in 12 population studies worldwide has shown that IgE hyper-responsiveness does not necessarily equate to AD, even though it may be associated with the disease phenotype, especially in severe disease.[2,11] Geographical location was associated with the risk of being atopic among those with AD compared with normal healthy controls.

In five studies that included adolescents and adults, the findings were essentially similar. In a cross-sectional household survey from Ethiopia, which included adults and children, 15% of those with AD and 8% of those without AD were atopic on skin-prick testing.[12] This lack of association between AD and allergen sensitisation in that setting was confirmed in a cross-sectional survey and nested casecontrolled study in children.

Environment

An increasing prevalence of AD over the past 50 years is not consistent with genetic drift alone, but supports a strong environmental influence as evidenced by population migration studies.[13] These environmental influences, which affect initial disease expression or aggravation of established disease, are summarised below. However, population studies from Africa seldom confirm a role for the environmental factors.[12] Interestingly, many are surrogate markers of urbanisation[14] and increased socioeconomic status,[14] which appear to be the only fairly consistent associations across all population groups.

The aetiopathogenesis of AD is best explained by the concept of a damaged barrier function, whether intrinsically normal or dysfunctional, that induces a state of epidermal repair, coupled with aberrant responses to epidermal insults of the affected skin.[8,10,14,15] In Africa, this hypothesis has not yet been validated. A novel filaggrin gene defect has been documented in a single Ethiopian case of AD.[16] What evolutionary advantage the skin barrier defect conveyed to the populations now exposed to environmental influences precipitating AMatopic disease, is unknown.

C

M

Y

CM

MY

CY

CMY

K

707

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

Environmental influences

The following factors have been shown to increase the risk for/ prevalence of AD: • rural compared with urban living (hygiene hypothesis)[13,14,17,18] • maternal AD history (parent-of-origin effect)[10,18,19] • higher socioeconomic status[12,14,20] • higher educational level of parents[21] • smaller family size (hygiene hypothesis)[17,22] • improved basic hygiene (hygiene hypothesis)[17] • antibiotic use early in life (hygiene hypothesis)[17,21] • caesarean section delivery[23] • increased maternal age[19] • environmental tobacco smoke (major risk)[13] • contact dermatitis[24,25] • cooler climates[13] • clothing with rough fibres[26] • environmental pollution[13,17] • psychosocial stress.[21,23]

something in their diet; however, it is rarely diet alone that triggers AD. Tests for food allergy should not routinely be done in all cases of AD. Concomitant or causative food allergy should be considered in patients with a convincing history of food allergy and those with moderate to severe eczema that does not respond to appropriate and adequate topical treatment.

Sensitisation to foods (raised ImmunoCAP values or positive skin-prick tests) is common in AD, but not synonymous with clinically relevant food allergy. About 60% of patients with AD are sensitised to food allergens[29] – a much higher percentage than the overall prevalence of food sensitisation in the general population.

In 2011, infants attending a tertiary dermatology clinic for AD were shown to have high sensitisation rates (66% to at least one food), most commonly to egg (52%), peanuts (39%) and cow’s milk (25%).[30] Approximately 30 - 40% of children with AD have a co-existing food allergy,[29] but this is much less common in adults.

References

The following factors have been shown to decrease the risk for/ prevalence of AD: • day-care attendance[17] • animal exposure early in life (hygiene hypothesis)[17,21,23] • endotoxin exposure in early infancy (hygiene hypothesis)[17] • infections early in life (hygiene hypothesis)[17] • breastfeeding[19,27,28] • fully hydrolysed formula feeds[21,27,28] • vaccination (hygiene hypothesis).[17,19] The following factors have not been inconclusively shown to affect the risk for/prevalence of AD: • parasite infestation[15,17] • maternal diet[18,19,23,26,28] • maternal probiotic use[19,23,26] • diet restriction[21,27] • elemental diet[21,27] • organic food[21] • solid food introduction[21,27] • diet supplementation with antioxidants, essential fatty acids, probiotics[18,19,21,26-28] • staphylococcal control[18,21,26] • hard water – no effect if calcium carbonate is removed[20] • reduced house dust mite exposure[18,21,26] • clothes softeners.[26]

Food allergy

The inter-relationship between AD and food allergy is complex.

Many patients and/or their carers believe that it is caused by DynavalCo2014CME island.pdf

2

2014/09/08

1. Johansson SGO, Bieber T, Dahl R, et al. Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. J Allergy Clin Immunol 2004;113:832-836. [http://dx.doi.org/10.1016/j.jaci.2003.12.591] 2. Flohr C, Johansson SGO, Wahlgren C-F, Williams H. How atopic is atopic dermatitis? J Allergy Clin Immunol 2004;114:150-158. [http://dx.doi.org/10.1016/j.jaci.2004.04.027] 3. Tokura Y. Extrinsic and intrinsic types of atopic dermatitis. J Dermatol Sci 2010;58:1-7. [http://dx.doi. org/10.1016/j.jdermsci.2010.02.008] 4. Simpson EL, Hanifin JM. Atopic dermatitis. Med Clin N Am 2006;90:149-167. [http://dx.doi. org/10.1016/j.mcna.2005.09.002] 5. Wolf R, Wolf D. Abnormal epidermal barrier in the pathogenesis of atopic dermatitis. Clin Dermatol 2012;30:329-334. [http://dx.doi.org/10.1016/j.clindermatol.2011.08.023] 6. Irvine AD, Irwin McLean WH, Leung DYM. Filaggrin mutations associated with skin and allergic disease. N Engl J Med 2011;365:1315-1327. [http://dx.doi.org/10.1056/NEJMra1011040] 7. Sandström Falk MH, Faergemann J. Atopic dermatitis in adults: Does it disappear with age? Acta Derm Venereol 2006;86:135-139.

8. Schultz Larsen F. Genetic epidemiology of atopic dermatitis. In: Williams HC. Atopic Dermatitis. The Epidemiology, Causes and Prevention of Atopic Dermatitis. Cambridge: Cambridge University Press, 2000:113-124. [http://dx.doi.org/10.1017/CBO9780511545771.010] 9. Schultz Larsen F. Atopic dermatitis: A genetic-epidemiologic study in a population-based twin sample. J Am Acad Dermatol 1993;28:719-723. http://dx.doi.org/10.1016/01909622(93)70099-F] 10. Morar N, Willis-Owen SAG, Moffatt MF, Cookson WOCM. The genetics of atopic dermatitis. J Allergy Clin Immunol 2006;118:24-34. [http://dx.doi.org/10.1016/j.jaci.2006.03.037] 11. Williams H, Flohr C. How epidemiology has challenged 3 prevailing concepts about atopic dermatitis. J Allergy Clin Immunol 2006;118:209-213. [http://dx.doi.org/10.1016/j. jaci.2006.04.043] 12. Yemaneberhan H, Flohr C, Bekele Z, et al. Prevalence and associated risk factors of atopic dermatitis symptoms in rural and urban Ethiopia. Clin Exp Allergy 2004;34:779-785. [http://dx.doi.org/10.1111/ j.1365-2222.2004.1946.x] 13. Burrell-Morris C, Williams HC. Atopic dermatitis in migrant population. In: Williams HC. Atopic Dermatitis. The Epidemiology, Causes and Prevention of Atopic Dermatitis.

Cambridge: Cambridge University Press, 2000:169-182. [http://dx.doi.org/10.1017/ CBO9780511545771.015] 14. Obeng BB, Hartgers F, Boakye D, Yazdanbakhsh M. Out of Africa: What can be learned from the studies of allergic disorders in Africa and Africans? Curr Opin Allergy Clin Immunol 2008;8:391-397. [http://dx.doi.org/10.1097/ACI.0b013e32830ebb70] 15. Roduit C, Wohlgensinger J, Frei R, et al. Prenatal animal contact and gene expression of innate immunity receptors at birth are associated with atopic dermatitis. J Allergy Clin Immunol 2011;127:179-185. [http:// dx.doi.org/10.1016/j.jaci.2010.10.010] 16. Winge MCG, Bilcha KD, Lieden A, et al. Novel filaggrin mutation but no loss-of-function variants found in Ethiopian patients with atopic dermatitis. Br J Dermatol 2011;165:1074-1080. [http://dx.doi. org/10.1111/j.1365-2133.2011.10475.x] 17. Flohr C, Pascoe D, Williams HC. Atopic dermatitis and the ‘hygiene hypothesis’: Too clean to be true? Br J Dermatol 2005;152:202-216. [http://dx.doi.org/10.1111/j.13652133.2004.06436.x]

9:30 AM

C

M

Y

CM

MY

CY

CMY

K

708

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

18. Shams K, Grindlay DJC, Williams HC. What’s new in atopic dermatitis? An analysis of systematic reviews published in 2009-2010. Clin Exp Dermatol 2011;36:573-578. [http://dx.doi. org/10.1111/j.1365-2230.2011.04078.x] 19. Godfrey K. Fetal and perinatal origins of atopic dermatitis. In: Williams HC. Atopic Dermatitis.

The Epidemiology, Causes and Prevention of Atopic Dermatitis. Cambridge: Cambridge University Press, 2000:125-138. [http://dx.doi.org/10.1017/CBO9780511545771.011] 20. McNally N, Phillips D. Geographical studies of atopic dermatitis. In: Williams HC. Atopic Dermatitis.

The Epidemiology, Causes and Prevention of Atopic Dermatitis. Cambridge: Cambridge University Press, 2000:71-84. [http://dx.doi.org/10.1017/CBO9780511545771.012] 21. National Institute for Health and Clinical Excellence. Atopic dermatitis in children. Management of atopic dermatitis in children from birth up to the age of 12 years. NICE Clinical Guideline 57. London: NICE, 2007.

22. McNally N, Phillips D. Social factors and atopic dermatitis. In: Williams HC. Atopic Dermatitis.

The Epidemiology, Causes and Prevention of Atopic Dermatitis. Cambridge: Cambridge University Press, 2000:139-154. [http://dx.doi.org/10.1017/CBO9780511545771.012] 23. Williams HC, Grindlay DJC. What’s new in atopic dermatitis? An analysis of systematic reviews published in 2007 and 2008. Part 1. Definitions, causes and consequences of dermatitis. Clin Exp Dermatol 2009;35:12-15. [http://dx.doi.org/10.1111/j.1365-2230.2009.03733.x]

24. Bonitas NG, Tatsioni A, Bassioukas K, Ioannidis PA. Allergens responsible for allergic contact dermatitis amongst children: A systematic review and meta-analysis. Contact Dermatitis 2011;64:245257. [http://dx.doi.org/10.1111/j.1600-0536.2010.01860.x] 25. Czarnobilska E, Obtulowicz K, Dyga W, Spiewak R. A half of schoolchildren with ‘ISAAC dermatitis’ are ill with allergic contact dermatitis. J Eur Acad Dermatol Venereol 2011;25:1104-1107. [http:// dx.doi.org/10.1111/j.1468-3083.2010.03885.x] 26. Hoare C, Li Wan Po A, Williams H. Systematic review of treatments for atopic dermatitis. Health Technology Assessment 2000;4(37):1-191.

27. Batchelor JM, Grindlay DJC, Williams HC. What’s new in atopic dermatitis? An analysis of systematic reviews published in 2008 and 2009. Clin Exp Dermatol 2010;35:823-828. [http://dx.doi.org/10.1111/j.13652230.2010.03901.x] 28. Muche-Borowski C, Koop M, Reese I, et al. Allergy prevention. Dtsch Arztebl Int 2009;106:625-631. [http://dx.doi.org/10.3238/arztebl.2009.0625] 29. Suh K-Y. Food allergy and atopic dermatitis: Separating fact from fiction. Semin Cutan Med Surg 2010;29:72-78. [http://dx.doi.org/10.1016/j.sder.2010.03.007] 30. Gray C. A prospective descriptive study to determine the prevalence of IgE-mediated food allergy in South African children with atopic dermatitis attending a tertiary medical centre: Review of the first 80 patients.

Abstract. South African Journal of Child Health 2011;5(3):99.

ABSTRACT

Is BCG vaccination effective against Mycobacterium tuberculosis in children?

We know from numerous efficacy trials over several decades that bacillus Calmette-Guérin (BCG) has 60 - 80% protective efficacy against severe forms of tuberculosis (TB) in children, particularly meningitis, but that its efficacy against pulmonary disease varies geographically. The latter is probably because BCG does not seem to protect against disease when given to those already infected or sensitised to environmental mycobacteria. The purpose of this recent study was to determine whether BCG vaccination protects against Mycobacterium tuberculosis infection, as assessed by interferon γ release assays (IGRA) in children.

Roy et al. conducted a systematic review and meta-analysis using searches of electronic databases from 1950 to November

2013. Inclusion criteria were vaccinated and unvaccinated children under 16 years of age with known recent exposure to patients with pulmonary TB. Children were screened for M. tuberculosis infection with IGRA. Primary analysis included 14 studies and 3 855 participants. The estimated overall risk ratio was 0.81, indicating a protective efficacy of 19% against infection among vaccinated children after exposure compared with unvaccinated children. Among those infected, protection against progression to disease was 58%. This study suggests that BCG protects against M. tuberculosis infection and progression from infection to disease.

Roy A, Eisenhut M, Harris RJ, et al. Br Med J 2014;349:g4643. [http://dx.doi.org/10.1136/bmj.4643]

The full version of the abstract is available online. Use the QR code above to access.

DynavalCo2014CME island.pdf

2

2014/09/08

9:30 AM

C

M

Y

CM

MY

CY

CMY

K

709

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

ARTICLE

Epidemiology of atopic dermatitis G Todd, MB ChB, FCDerm (SA), PhD Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa Corresponding author: G Todd (gail.todd@uct.ac.za)

Epidemiological studies on atopic dermatitis, primarily performed in children, have shown that the one-year prevalence rate of symptoms is population and area dependent. The few studies that have been done in South Africa among children of different age groups showed one-year prevalence rates of 1 - 13.3%. In adults, the burden of disease is significant. The prevalence rates and age-related percentages of those affected vary between the countries where studies were undertaken. While about 60% of cases show spontaneous clearing by puberty, the condition may recur in adults.

S Afr Med J 2014;104(10):710. DOI:10.7196/SAMJ.8843

How common is atopic dermatitis and who gets it?

Much of the work on the epidemiology of atopic dermatitis (AD) has been done in children,[1-3] employing a variety of prevalence measures, including lifetime prevalence, point prevalence and one-year prevalence rates.

The International Study of Asthma and Allergies in Childhood (ISAAC) Phases One and Three[4,5] has documented that the oneyear prevalence rate for AD symptoms varies worldwide, dependent on the population and geographical area studied (globally, nationally or locally). A comparison of the two studies shows a general decline or plateau one-year prevalence rate in the developed world, but an increasing prevalence in the developing world.[6] Few studies address the prevalence of AD in South African (SA) populations. The Phase One ISAAC study[4] of 13 - 14-year-old schoolchildren in Cape Town showed an 8.3% one-year prevalence rate of AD symptoms, with 2.3% having severe disease (sleep disturbance for >1 night per week). The Phase Three follow-up study[5] documented an increased one-year prevalence of 13.3% among children of the same age. No children 6 - 7 years of age were included for SA in either study.

In normal 3 - 11-year-olds, the one-year prevalence rate was 1 - 2.5% in amaXhosa children, depending on the methodology used to define AD and whether they came from urban or rural environments.[7] While it is accepted that AD is a particular problem in children, the burden of disease is significant in adults. A study in adults in Scotland showed a 0.2% one-year period prevalence for AD in persons >40 years of age. Adults accounted for 38% of the AD population.[8] Studies from Nigeria and Ethiopia show that 40 - 60% of patients with Pearinda2014CME AD were >19 years of age.[9,10] 1 2014/09/08 9:29 island.pdf

Few incidence studies on the condition have been done; these were in cohorts of children in Europe.[3]

Natural history and severity

Studies on the natural history of AD record up to 60% spontaneous clearing by puberty.[3,8,11] However, AD may recur in adults and the risk is associated with a family history, early onset, severity and persistence of childhood AD and presence of mucosal atopy.[8] In adults the clinical picture may be altered: patients presenting with hand dermatitis were possibly exposed to additional insults such as irritants (wet work, detergents, chemicals and solvents) or head and neck involvement.[12] The concept of the â&#x20AC;&#x2DC;atopic marchâ&#x20AC;&#x2122;, where children with AD develop mucosal forms of atopic disease,[13] has been challenged by some cohort studies.[14] An early wheeze and a specific sensitisation pattern (wheat, cat, mite, soy and birch) were predictors of wheezing at school age in a German-birth cohort study, irrespective of the presence of AD. The development of rhinoconjunctivitis is more strongly associated with AD than asthma.[15] It is probable that there are many subsets of the AD phenotype.

Studies in Europe assessing the severity of AD in children revealed that 84% had mild, 14% moderate and 2% severe disease.[16] In adult cohorts, those who had severe disease accounted for 12%, using the scoring AD (SCORAD) system.[12] In a Japanese population survey, 70 - 90% of cases were mild, dependent on age group. Moderate to severe AD occurred predominantly in early adolescence and adulthood.[17] AM References available online at http://dx.doi.org/10.7196/SAMJ.8843

C

M

Y

CM

MY

CY

CMY

K

710

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

ARTICLE SUMMARY

Diagnosis of atopic dermatitis: From bedside to laboratory W Sinclair,1 MB ChB, MMed (Derm); J Aboobaker,2 MB ChB, FFDerm (SA), FRCP (Lond), PhD; R J Green,3 MB BCh, DCH, FCP (SA), DTM&H, MMed, FCCP, PhD, Dip Allergology (SA), DSc; M E Levin,4 MB ChB, FCPaed (SA), Dip Allergology (SA), MMed (Paed), PhD, EEACI (UEMS), FAAAAI, FACAAI Department of Dermatology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa epartment of Dermatology, University of KwaZulu-Natal, Durban, South Africa D 3 Department of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa 4 Division of Asthma and Allergy, Department of Paediatrics, Faculty of Health Sciences, University of Cape Town and Red Cross War Memorial Children’s Hospital, Cape Town, South Africa 1 2

Corresponding author: W Sinclair (sinclairw@ufs.ac.za)

Atopic dermatitis (AD) is essentially diagnosed clinically.

In babies and young children, the diagnosis is usually straightforward. Dry, very pruritic dermatitis starts on the cheeks, often involving the neck and trunk, but the nappy area is spared. Limb involvement follows later – first extensoral, later classically flexural. The foregoing clinical picture is what most people recognise as AD. In adults, the presentation may vary widely. Classic flexural dermatitis may persist, but erythroderma (wholebody involvement), head and neck dermatitis, isolated hand dermatitis and nummular dermatitis may be more difficult to identify as AD. In the past, the so-called Hanifin criteria were used to diagnose AD, but these were complicated and not always reproducible.

Currently, the diagnostic criteria of the UK Working Party on AD are used. According to these, the patient must have pruritus and ≥3 of the following: • history of flexural dermatitis (front of elbows, back of knees, front of ankles, neck, around the eyes) or involvement of cheeks and/or extensor surfaces in children aged ≤18 months • visible flexural dermatitis involving the skin creases (or the cheeks and/or extensor surfaces in children ≤18 months of age) • history of a dry skin during the past year • history of asthma or hay fever (or atopic disease in a first-degree relative in children <4 years of age) • onset <2 years of age (only for children aged ≥4 years at time of diagnosis).

Treatment decisions are based on the estimation of the severity of the dermatitis. Complicated scoring systems are used only in a research

Pearinda2014CME island.pdf

1

2014/09/08

environment, not in daily clinical practice. We propose a more practical system to classify the dermatitis as mild, moderate or severe: • Measure the area involved in percentage of body surface, where 1% body surface approximates the size of one of the patient’s hands (including the fingers).

• Establish acute, subacute or chronic changes, where acute changes imply more severe dermatitis.

• Determine the impact on the patient’s quality of life, e.g. sleep disturbances, absenteeism, visible scratch marks, social withdrawal.

Laboratory investigations (e.g. IgE levels, skin biopsy) are not required for the diagnosis, but may be useful to exclude conditions in the differential diagnosis and to identify environmental trigger factors.

Total IgE levels are normal in about half of the cases. ImmunoCAP assays for specific IgE and skin-prick tests may be done to confirm the atopic nature of the patient’s condition. Skin-prick tests are often used to try to identify specific allergens that may trigger AD; interpretation of the results is complicated and always has to be correlated with the clinical condition of the patient. ImmunoCAP assays provide the same information.

Other investigations that may be useful in individual cases are patch tests (where superimposed allergic contact dermatitis is suspected), scratch, patch and skin application tests (for foods), atopy patch tests, and tests to exclude immunodeficiency and herpes infection (Tzanck smear, rapid polymerase chain reaction and electronmicroscopy).

S Afr Med J 2014;104(10):711. DOI:10.7196/SAMJ.8850

9:29 AM

C

M

Y

CM

MY

CY

CMY

K

711

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

ARTICLE SUMMARY

Education and specialist referral of patients with atopic dermatitis R J Green,1 MB BCh, DCH, FCP (SA), DTM&H, MMed, FCCP, PhD, Dip Allergology (SA), DSc; A Pentz,1 MB ChB, DCH, FCPaed (SA), MMed (Paed), Dip Allergology (SA), Cert Pulmonology (SA) Paed, FCCP; H F Jordaan,2 MB ChB, MMed (Derm) 1 2

epartment of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa D Division of Dermatology, Department of Medicine, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa

Corresponding author: R J Green (robin.green@up.ac.za)

Educating patients with atopic dermatitis (AD) is an essential and unavoidable component of therapy.

If the disease involves young children, education of parents is mandatory. Without adequate attention to education all therapies are futile and the patient is doomed to an impaired quality of life. Practitioners treating patients with AD must be aware that the disease is one of the most important medical conditions that affects quality of life, which usually involves the entire family.

While many of the educational principles centre on an adequate explanation of the therapies and their appropriate application and timing, there are a number of matters that must be addressed independently, including: • an explanation of the aetiology and pathology of the disease process • avoidance of generic (cigarette smoke, irritants) and individual specific (allergens) trigger factors • attention to skin hygiene and care • attention to itch prevention (adequate moisturisation, nail clipping – keeping nails short, and avoiding hot bedrooms, woollen clothing, over-dressing and soaps) • an explanation of the chronic and relapsing nature of the disease • an explanation that all therapies can only treat, not cure, the condition • an honest discussion about medication side-effects

Pearinda2014CME island.pdf

1

2014/09/08

• a discussion about the scientific basis of alternative therapies (homoeopathy, reflexology, naturopathy, acupuncture and herbal therapy). Such discussion should suggest that, even though these therapies are not grounded by the same evidence required for allopathic medicine, many individuals feel compelled to try them owing to desperation. Such desperation can usually be overcome by careful attention to skin care and medicine use.

Educational messages need to be frequently repeated. Patients and parents must be given adequate opportunity to raise concerns and ask questions.

AD consultations, even follow-up visits, usually require lengthy periods of time. Education is greatly aided by providing information leaflets, reputable website addresses and contact details of support groups.

The majority of patients with AD respond to dedicated conservative treatment. Indications for referral to a specialist include the following: suspected eczema herpeticum (Kaposi’s varicelliform eruption) (immediate (same-day) referral); severe AD that has not responded to optimal topical therapy after one week or failed treatment of bacterially infected AD (urgent referral (seen within two weeks)); a diagnosis that is or has become uncertain; AD on the face that has not responded to appropriate treatment; AD associated with severe and recurrent infections; suspected contact allergic dermatitis; or AD giving rise to serious social or psychological problems for the child, parent or carer (routine (non-urgent) referral).

S Afr Med J 2014;104(10):712. DOI:10.7196/SAMJ.8857

9:29 AM

C

M

Y

CM

MY

CY

CMY

K

712

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

ARTICLE SUMMARY

Non-pharmacological treatment modalities for atopic dermatitis G Todd,1 MB ChB, FCDerm (SA), PhD; A Manjra,2 MB ChB, FCPaed (SA), Dip Allergology (SA), FAAAAI (USA), M Clin Pharm; W Sinclair,3 MB ChB, MMed (Derm); M Levin,4 MB ChB, FCPaed (SA), Dip Allergology (SA), MMed (Paed), PhD, EAACI (UEMS), FAAAAI, FACAAI; R J Green,5 MB BCh, DCH, FCP (SA), DTM&H, MMed, FCCP, PhD, Dip Allergology (SA), DSc Department of Medicine, Faculty of Health Sciences, University of Cape Town, South Africa Private practice, Westville Hospital, Durban, South Africa 3 Department of Dermatology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa 4 Division of Asthma and Allergy, Department of Paediatrics, Faculty of Health Sciences, University of Cape Town and Red Cross War Memorial Childrenâ&#x20AC;&#x2122;s Hospital, Cape Town, South Africa 5 Department of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa 1

2

Corresponding author: G Todd (gail.todd@uct.ac.za)

Non-pharmacological measures to improve the management of atopic dermatitis (AD) are considered as important as pharmacotherapy if true healing of the skin is to be achieved. Skin dryness (which contributes to inflammation, loss of suppleness leading to fissuring, impaired barrier function, and increased adherence of Staphylococcus aureus organisms) can be overcome by the use of emollients. Ointments and creams provide better barrier function than lotions. In general, oily preparations are better emollients, but these may be too messy for routine use. Different preparations may be needed for the face and the body. Best results are obtained if emollients and medications are applied within three minutes of bathing to retain hydration. Sufficient quantities must be prescribed, e.g. 250 g/wk for children and 500 g/wk for adults for whole-body coverage.

When emollients (excluding bath emollients) and other topical products are used at the same time of day to treat AD in children, the different products should ideally be applied one at a time with several minutes between applications, when practical. Inform children with AD and their parents or carers that emollients should be used in larger amounts and more often than other treatments, on the whole body after AD has cleared up, and while using other treatments.

Aqueous cream is not a suitable emollient, as the alkaline detergent (sodium lauryl sulphate) used as the emulsifier can aggravate the dermatitis. The alkaline pH created on the skin has been found to increase transepidermal water loss and disruption of the skin barrier function. Any product containing unbuffered sodium lauryl sulphate emulsifier should therefore not be used as a leave-on emollient.

Pearinda2014CME island.pdf

1

2014/09/08

Bathing is an important part of the management of AD. Regular, once-daily bathing in warm (not hot) water to hydrate the skin and debride crusts is important. After bathing, pat the skin dry and apply emollients immediately. Scented soaps should be avoided and replaced by a moisturising cleanser.

Routine use of topical or systemic antibacterial or antifungal agents is not recommended for AD, but during flares such agents may be invaluable. There is limited evidence that laundry practices have an effect on AD control, but logic would support adopting methods that are simple and reduce undue exposure to potential allergens and irritants in patients with impaired skin barrier function. Wool intolerance is a minor criterion for diagnosis in AD. Fabric roughness, not the type of textile, determines skin irritation.

Avoidance of any textile reported by the patient as irritating is advised.

There is no specific diet for the treatment of AD. Elimination diets are not routine treatment and are potentially harmful. Food elimination should be reserved for those children who have been proven to be allergic to the specific food.

A recent review on the use of occlusive dressings (wet or dry) found little beneficial evidence for their use. They are more efficacious when used in combination with topical steroids and reduce the absolute amount of topical steroid required. Wet wraps are safe as a second-line short-term (14-day) intervention, although increase in infections with use is a documented side-effect.

S Afr Med J 2014;104(10):713. DOI:10.7196/SAMJ.8860

9:29 AM

C

M

Y

CM

MY

CY

CMY

K

713

October 2014, Vol. 104, No. 10

CONTINUING MEDICAL EDUCATION

ARTICLE SUMMARY

Topical and systemic pharmacological treatment of atopic dermatitis A Puterman,1 MB ChB, FCPaed (SA); H Lewis,2 MB ChB, FCPaed (SA); W Sinclair,3 MB ChB, MMed (Derm); R J Green,4 MB BCh, DCH, FCP (SA), DTM&H, MMed, FCCP, PhD, Dip Allergology (SA), DSc Private practice, Claremont, Cape Town, South Africa Private practice, Centurion, Pretoria, South Africa 3 Department of Dermatology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa 4 Department of Paediatrics and Child Health, Faculty of Health Sciences, University of Pretoria, South Africa 1 2

Corresponding author: A Puterman (putall@global.co.za)

Topical corticosteroids (TCSs) continue to be the mainstay of atopic dermatitis (AD) treatment.

For more than four decades TCSs have provided effective flare control by means of their antiinflammatory, antiproliferative, immunosuppressive and vasoconstrictive actions. They suppress the release of inflammatory cytokines and act on a variety of immune cells, including T lymphocytes, monocytes, macrophages, dendritic cells and their precursors. Various strengths and formulations of TCSs are available.

The extent to which they induce cutaneous vasoconstriction and inhibit inflammation corresponds to their potency.

The extensive use of TCSs in clinical practice is supported by an ever-expanding body of clinical trial data, which assists in providing physicians with sensible recommendations for the quantity, frequency and duration of TCS therapy. Preparations of very weak or moderate strength are used on the face and genital area, whereas those of moderate or potent strength are used on other areas of the body.

Patients should be educated about the different steroid potencies to minimise untoward side-effects.

The vehicle through which the active steroid is delivered plays an important role in absorption and can enhance its efficacy. Generally, ointments are more effective than creams, as the emollient action and occlusive effect result in better skin penetration. Ointments also require fewer preservatives; therefore, the potential for irritant and allergic reactions is lower. Wet wraps and application under occlusion enhance absorption of topical steroids.

Topical steroids may be used for 10 - 14 days when the dermatitis is active, followed by ‘holidays’ with emollients only. TCSs may also be used in bursts of 3 - 7 days to treat exacerbations. This rationale can be extended to using potent TCSs for a few days to initiate control, followed by a milder-potency TCS and/or emollient. For Pearinda2014CME island.pdf

1

2014/09/08

chronic lichenified eczema, frequent applications of potent steroids are required for much longer periods. A possible regimen for TCSs as maintenance treatment for stable disease is ‘weekend use’, where the product and emollients are applied on weekend days only, while continuing with emollients only during the rest of the week.

The quantity of TCS that should be used is a common practical problem for patients. The fingertip unit is useful: the index finger from distal crease to fingertip approximates 0.5 g. This aids the monitoring of compliance and use. There is no clear evidence to suggest that a twice-daily application of TCS is better than a oncedaily application. It may be justified to use once-daily corticosteroids as a first step in all patients with AD, thus decreasing the cost, improving compliance and reducing side-effects.

Topical calcineurin inhibitors (TCIs) (pimecrolimus and tacrolimus) are complex macrocyclic compounds that result in selective inhibition of cytokine transcription in activated T cells.

They are registered for short-term and non-continuous chronic treatment of moderate to severe AD in immunocompetent patients ≥2 years old. Clinically, pimecrolimus lowers the incidence of flares and significantly reduces pruritus. Both pimecrolimus and tacrolimus are safe and effective in reducing the severity of AD symptoms in children and adults.

Systemic corticosteroids are frequently used for short-term therapy of severe AD, but their use is controversial. Oral antibiotics do not benefit AD when used for skin that is not clinically infected, but infected dermatitis should be treated with penicillinase-resistant penicillins, cephalosporins or clindamycin.

Complementary/alternative therapies have no proven benefit in AD.

S Afr Med J 2014;104(10):714. DOI:10.7196/SAMJ.8870

9:29 AM

C

M

Y

CM

MY

CY

CMY

K

714

October 2014, Vol. 104, No. 10

PROFESSIONAL ADVERTISING Tel: 021 681 7000 | E-mail: bronlyne.granger@hmpg.co.za www.hmpg.co.za | www.professionalads.co.za We accept credit card payments - Visa or MasterCard.

URGENT - Specialists needed in Qatar New medical facility needs specialists in following fields: One year contracts - extensions negotiable.

1. Female Consultant Dermatologist 2.Consultant Histo-pathologist 3.Interventional radiologist 4.Intensivist/Anesthesiologist

5.Neurologist.

6. Pulmonolgist 7.Endodontist 8. Pedodonist 9.Aviation Medical specialist

Packages negotiable - all expenses taken care of. T&C’s apply

Please send detailed CV’s to brenda@i-recruit.co.za or contact me on 082 449 3950

PRIVAATPRAKTYK TE KOOP PRIVAATPRAKTYK TE KOOP IN DIE NOORDE VAN PRETORIA.PRAKTYK BESTAAN REEDS 40 JAAR.GROOT AANTAL PASIENTE,GOEIE INKOMSE, LAE HUUR, ALLE MEUBELS EN VOORRAAD INGESLUIT.EIENAAR WAS SELF 15 JAAR BY DIE PRAKTYK.R150 000 OF NAASTE AANBOD. BETROUBARE PERSONEEL WAT KAN AANBLY. OOK MEER AS 13 JAAR VOLTYDS BETROKKE. CONTACT DR SANET PRETORIUS TEL:012 543 0366/7

PRAKTYK TE KOOP OOSKAAP Finansiele gevestigde solo-praktyk te koop by die see. Goeie lewenskwaliteit en kleindorpse hartelikheid.

Baie werk. Goeie omset. Selde nagwerk.

Eienaar tree af.

Kontak Sanet 0825743446

GP REQUIRED

Opportunity for GP in new upmarket Medical & Dental suites, Centurion.

GP required to join a multi-disciplinary practice serving the local community, University & Schools. Based in Grahamstown which is close to the coast and boasts several good schools.

New up-market Medical & Dental practice has a great opportunity for a GP Doctor to establish themselves in the Highveld, Centurion.

Please contact Dr. Barbara Bull (bull@highstmed.co.za) or Alix Whittington-Jones (Whittington-jones@highstmed.co.za) at 046 636 2063.

The Suites come fully equipped with furniture, PC & networking, Internet, reception services, security, parking, electricity/water, cleaning services.

Call Peter 0836544544

PROFESSIONAL ADVERTISING

MEDICAL PRACTITIONER: HEAD OFFICE Qualifications MB ChB, HPCSA Registered, CPD system compliance Experience 10 years post-graduate clinical experience & epidemiology and statistics Outputs Deliver professional and effective corporate medical services; Assessment of disability- dread disease, functional impairment, sickness benefit claims; Interpretation of exercise ECG’s, lung function tests, pathology results; Research and training of underwriters and claims assessors; Assisting with underwriting queries; Assistance with product design and development; Marketing assistance through presentations to sales force Apply www.sanlam.co.za by 10 November 2014.

Working for PathCare always produces excellent results!!

Pathologist PathCare Laboratories have a position available in Welkom for an Anatomical Pathologist or a Pathologist qualified in any one of the clinical disciplines.

If you believe you would thrive in a multi-disciplinary private laboratory, and have similar goals and values to our own, we encourage you to contact us for this position.

Requirements: ▪ M.Med or FC Pathology (SA) ▪ Current registration with the HPCSA as a Pathologist ▪ Relevant working experience ▪ Excellent communication and interpersonal skills ▪ Ability to maintain confidentiality and impartiality.

To apply, please email lindyg@pathcare.co.za Closing date: 31 October 2014. www.pathcare.co.za

www.strate

o.za gy-rm.c

PROFESSIONAL ADVERTISING

Advertisement: Clinical Pathologist Van Rensburg Pathologists Inc., a fast growing independent and private pathology firm in Bloemfontein, has a position available for a Clinical Pathologist.

Candidates, meeting the following requirements, can mail their CV to Lourika van der Walt, lourika@vrpath.co.za Requirements: MMed or FC Pathology (SA) Current Registration with the HPCSA as a Clinical Pathologist Relevant working experience Good leadership and communication skills

HSE – MIDLAND REGIONAL HOSPITAL, IRELAND Midland Regional Hospital, Mullingar, Ireland is a 215 bedded hospital providing services including General Medicine, General Surgery, Anaesthesia, Emergency Medicine, Obstetrics/Gynaecology and Paediatrics. The hospital offers an excellent opportunity to work in a dynamic service where all medical staff are actively involved in education and training. The hospital is an affiliated teaching site for the medical schools of Royal College of Surgeons in Ireland and University College Dublin. It is also a recognised teaching centre for postgraduate medical education across all specialties.

Opportunities exist for Non-Consultant Hospital Doctors in the following areas:

n Registrar Emergency Medicine n Registrar General Medicine n Special Lecturer/Clinical Tutor in General Medicine n Registrar Obstetrics/Gynaecology n SHO Paediatrics Irish Medical Council registration is mandatory.

Applicants should apply by CV to: Danny Connaughton, Email: danny.connaughton@hse.ie Informal enquiries to: Danny Connaughton on Tel: +353 (0)44 9394146.

Closing date for receipt of CVs: Friday, 26th September 2014.

For further information and application details log on to www.hse.ie/eng/jobs

www.hse.ie/eng/jobs Easy Access • Public Confidence • Staff Pride

SAMAREC/CPD SERVICES AVAILABLE: 타

SAMAREC:

CPD:

Evaluating the ethics of research

Assisting health professionals to

protocols developed for clinical

maintain and acquire new and

South African Medical Association

trials conducted in the private

updated levels of knowledge, skills

Continued Professional

healthcare sector. Ensuring the

and ethical attitudes that will be of

Development Accreditation

protection and respect of rights,

measurable benefit in professional

safety and well-being of

practice and to enhance and

participants involved in clinical

promote professional integrity. The

trials and to provide public

SA Medical Association is one of

health to the nation

assurance of the protection by

the institutions that have been

o

Excellent Service

reviewing, approving and providing

appointed by the Medical and

o

Quick Turnaround

comment on clinical trial protocols,

Dental Professions Board of the

o

Efficiency

the suitability of investigators,

Health Professions Council of SA

facilities, methods and procedures

to review and approve CPD

used to obtain informed consent.

applications.

South Africa Medical Association Research and Ethics Committee SAMAREC

타

타

WHAT WE ARE ABOUT

Our Mission: o

Empowering Doctors to bring

For further information please contact the SAMAREC/CPD Secretariat on 012 481 2000 OR email us on samarec@samedical.org or cpd@samedical.org

CPD

OCTOBER 2014

Effective in 2014, the CPD programme for SAMJ will be administered by Medical Practice Consulting: CPD questionnaires must be completed online at www.mpconsulting.co.za

True (A) or false (B): Non-communicable diseases in South Africa 1. The losses to South Africa’s gross domestic product from diabetes, stroke and coronary heart disease between 2006 and 2015 are estimated at US$1.88 billion.

2. Mandatory salt regulations, beginning in 2016, will save 6 400 lives from stroke and 4 300 from non-fatal stroke, and cut hospitalisation costs by ZAR300 million annually.

3. The proportion of years of life lost due to non-communicable diseases is highest in the rural areas.

Preventing diabetic blindness, and quality assurance in diabetic retinal screening 4. About 55% of people with diabetes are likely to suffer from diabetic retinopathy (DR).

5. DR is an important biomarker for microvascular disease.

6. Direct ophthalmoscopy has low sensitivity, and is unpopular with patients as it requires their pupils to be dilated.

7.

Fundus photography rather than direct ophthalmoscopy is likely to become the standard of care for DR (and smart-phone technology is now being tested for screening for DR using mobile phones).

Look before you strip varicose veins 8. Lower limb varicosities can arise from ‘reverse’ venous flow from inferior vena cava obstruction, and cursory physical examination in such cases may result in underlying pathology being overlooked or misdiagnosed.

The influence of glucocorticoids on lipid and lipoprotein meta­ bolism and atherosclerosis 9.

Patients managed with glucocorticoids should have their cardiovascular risk assessed, especially if long-term treatment is planned, with special attention given to management of dyslipidaemia.

Meeting adolescents’ sexual and reproductive health needs 10.

There are strong associations of high HIV rates with high incidences of sexually transmitted infections and high rates of unplanned teenage pregnancy.

Aetiopathogenesis of atopic dermatitis 11.

Atopic dermatitis is not one single disease, but rather an aggregation of several diseases with certain clinical characteristics in common.

12. The morphology, distribution and evolution of eczema/dermatitis in atopic eczema/dermatitis are highly characteristic and age dependent.

Epidemiology of atopic dermatitis 13. Few adults suffer from atopic dermatitis.

14. Up to 60% of cases of atopic dermatitis clear spontaneously by puberty.

Diagnosis of atopic dermatitis: From bedside to laboratory 15. Total IgE levels are normal in about half of cases of atopic dermatitis.

16. Skin biopsy is essential to the diagnosis of atopic dermatitis.

Education and specialist referral of patients with atopic dermatitis 17. Inadequate itch control is a reason for referral.

Non-pharmacological treatment modalities for atopic dermatitis 18.

Non-pharmacological treatments are at least as important as pharmacological treatments in atopic dermatitis.

Topical and systemic pharmacological treatment of atopic dermatitis 19. Topical corticosteroids continue to be the mainstay of atopic dermatitis treatment.

20. Clinical trial data have proved that pimecrolimus reduces the incidence of flares and has a significant effect on reducing pruritus.

CPD questions include articles from CME. The full versions of each article can be found on the SAMJ website (http://www.samj.org.za)

A maximum of 3 CEUs will be awarded per correctly completed test.

INSTRUCTIONS 1. Read the journal. All the answers will be found there.

2. Go to www.mpconsulting.co.za to answer the questions.

Accreditation number: MDB001/007/01/2014 (Clinical)

October 2014, Vol. 104, No. 10