SAJDVD
The electronic version of the journal is available at www.diabetesjournal.co.za
The South African Journal of Diabetes & Vascular Disease
November 2013
Volume 10 Number 4
Featured in this issue: Diabetes and the audiologist Ideal drug for diabetic macular oedema Digital diabetes and the future Non-nutritive sweeteners CDE Watch 2013 Diabetes Update Symposium
Reviews
Ethics Focus
Achieving Best Practice
Diabetes Educator’s Focus
News
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ISSN 1811-6515
THE SOUTH AFRICAN JOURNAL OF HYPE
RINSULINAEMIA
Diabetes & vascular disease VOLUME 10 NUMBER 4 • NOVEMBER 2013 www.diabetesjournal.co.za
Corresponding Editor DR F MAHOMED Grey’s Hospital, Pietermaritzburg Consulting Editor PROF J-C MBANYA Dr L Lombard National Editorial Board DR A AMOD Centre for Diabetes, Endocrinology and Metabolic Diseases, Life Healthcare, Chatsmed Gardens Hospital, Durban SR K BECKERT Diabetes Nurse, Paarl PROF F BONNICI Emeritus Professor, Faculty of Health Sciences, University of Cape Town and President of Diabetes South Africa PROF R DELPORT Department of Family Medicine, University of Pretoria DR L DISTILLER Director of the Centre of Diabetes and Endocrinology, Houghton, Johannesburg DR F MAHOMED Department of Internal Medicine, Grey’s Hospital, Pietermaritzburg PROF WF MOLLENTZE Head of Department of Internal Medicine, University of the Free State, Bloemfontein PROF CD POTGIETER Specialist Nephrologist, University of Pretoria and Jakaranda Hospital, Pretoria PROF K SLIWA Associate Professor of Medicine and Cardiology, Baragwanath Hospital, University of the Witwatersrand, Johannesburg PROF YK SEEDAT Emeritus Professor of Medicine and Honorary Research Associate, University of Natal, Durban International Editorial Board PROF IW CAMPBELL Physician, Victoria Hospital, Kircaldy, Scotland, UK PROF PJ GRANT Professor of Medicine and head of Academic Unit of Molecular Vascular Medicine, Faculty of Medicine and Health, University of Leeds; honorary consultant physician, United Leeds Teaching Hospitals NHS Trust, UK PROF J-C MBANYA Professor of Endocrinology, Faculty of Medicine and Biomedical Sciences, University of Yaounde I, Cameroon and President, International Diabetes Federation PROF N POULTER Professor of Preventive Cardiovascular Medicine, Imperial College, School of Medicine, London, UK DR H PURCELL Senior Research Fellow in Cardiology, Royal Brompton National Heart and Lung Hospital, London, UK
CONTENTS
Editorial
119
From policy implementation issues to diabetes in the digital age FA Mahomed
Reviews
120
What is the ideal drug for the treatment of diabetic macular oedema? Carl-Heinz Kruse
122
Digital diabetes – looking to the future DJ Wake, SG Cunningham
Research Article
127
Diabetes and the audiologist: is there need for concern regarding hearing function in diabetic adults? K Khoza-Shangase, D Pillay, A Moolla
Diabetes Educator’s Focus
134
Excellence in diabetes: missed opportunities for optimal care N Naidoo
Patient Leaflet
139
Non-nutritive sweeteners: good or bad? R Amod
Diabetes Personality
143
Love and passion make all the difference when managing patients with diabetes P Wagenaar
Page 144
Diabetes News
145
Novo Nordisk Changing Diabetes® cycle relay
Reports
146
Novo Nordisk – Accu-Chek® Diabetes Update Symposium G Hardy
149
CDE Watch, 2013 update from the Centres for Diabetes and Endocrinology P Wagenaar
Page 145
Managing Editor: GLENDA HARDY TEL: 021 976 8129 CELL: 071 819 6425 FAX: 086 610 3395 e-mail: glenda@clinicscardive.com Production Editor SHAUNA GERMISHUIZEN TEL: 021 785 7178 FAX: 086 628 1197 e-mail: shauna@clinicscardive.com Financial & Production Co-ordinator ELSABÉ BURMEISTER TEL: 021 976 8129 CELL: 082 775 6808 FAX: 086 664 4202 e-mail: elsabe@clinicscardive.com Content Manager MICHAEL MEADON (Design Connection) TEL: 021 976 8129 FAX: 086 655 7149 e-mail: michael@clinicscardive.com Gauteng Contributor PETER WAGENAAR CELL: 082 413 9954 e-mail: skylark65@myconnection.co.za Layout RYKIM TEL: 021 715 2449 e-mail: rykim@mweb.co.za
The South African Journal of Diabetes and Vascular Disease is published four times a year for Clinics Cardive Publishing (Pty) Ltd and printed by Durbanville Commercial Printers/Tandym Print. Online Services: Design Connection. Articles in this Journal are sourced as per agreement with the British Journal of Diabetes and Vascular Disease All correspondence to be directed to: THE EDITOR PO BOX 1013 DURBANVILLE 7551 or info@clinicscardive.com TEL: 021 976 8129 FAX: 086 664 4202 INT: +27 (0)21 976-8129 To subscribe to the journal or change address, email elsabe@clinicscardive.com Full text articles available on: www.diabetesjournal.co.za via www.sabinet.co.za The opinions, data and statements that appear in any articles published in this journal are those of the contributors. The publisher, editors and members of the editorial board do not necessarily share the views expressed herein. Although every effort is made to ensure accuracy and avoid mistakes, no liability on the part of the publisher, editors, the editorial board or their agents or employees is accepted for the consequences of any inaccurate or misleading information.
SA JOURNAL OF DIABETES & VASCULAR DISEASE
EDITORIAL
From policy implementation issues to diabetes in the digital age FA MAHOMED
T
his issue of the Journal has several important themes, including excellence in diabetes – missed opportunities for optimal care, the digital age and diabetes, diabetes and audiology, a review of diabetic macular oedema, a discussion on non-nutritive sweeteners, the CDE Watch, notes on the Novo Nordisk Update Symposium, and more. Dr N Naidoo’s article on excellence in diabetes revolves around poor implementation of diabetes policies, and ways of tackling this. Also discussed are the central role of education and the diabetes nurse educator, the involvement of the patient in making key decisions about his/her diabetes care, actively screening for and preventing complications, the Stott model of consultation, and a diabetes record and checklist. This is a pivotal article and if we are to make any progress in diabetes care, we have to heed this guidance. Wake and Cunningham point out the impact of the growing use of mobile apps and sharing of information on the digital highway.
Correspondence to: Dr FA Mahomed Department of Internal Medicine, Grey’s Hospital, Pietermaritzburg Tel: +27 (0) 33 897-3289 Fax: 086 6281 374 e-mail: Fazleh.Mahomed@kznhealth.gov.za S Afr J Diabetes Vasc Dis 2013; 10: 119
Thank you
This will benefit patients and their healthcare professionals and improve their communication and care. They discuss potential problems, such as loss of confidentiality, and different levels of care for those with access to devices as opposed to those who don’t/ can’t access mobile devices. Prof Khoza-Shangase and her colleagues discuss the effect of microvascular damage in type 1 diabetes on cochlea–vestibular function, and its potential to reduce quality of life for diabetics. Although it is a small study and needs to be studied in a larger sample, it nevertheless alerts clinicians to the problem and the need to screen for this condition. Dr Kruse reviews therapy for macular oedema. He covers the role and limitations of photocoagulation, and anti-inflammatory, anti-angiogenesis and other agents, and ends with a guide to the management of macular oedema. Ruwaida Amod explains what non-nutritive sweeteners are and discusses good and bad aspects of these sweeteners. However, this interesting discussion will only be furthered by additional studies. The CDE Watch covers a range of interesting topics from Dr Amod’s ‘Insulin: friend or foe’, and the looming nephropathy disaster, to a lively discussion on bariatric surgery. The Novo Nordisk Update Symposium report includes notes on incretins and hypoglycaemia I thank the local contributors, Prof K Khoza-Shangase, Dr N Naidoo, Dr C-H Kruse and Ms R Amod. We encourage local and continental reviews, case studies and trials in diabetes. I also thank the journal staff for their hard work.
The Director of Clinics Cardive Publishing, Prof Paul Brink and the editorial team thank our authors, reviewers and all others who contributed to our journal during 2013. A special word of thanks to our corresponding editors, Dr Landi Lombard and Dr Faz Mahomed for their hard work and dedication to the journal.
May peace, joy, hope and happiness be yours during this holiday season and throughout the new year. VOLUME 10 NUMBER 4 • NOVEMBER 2013
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What is the ideal drug for the treatment of diabetic macular oedema? CARL-HEINZ KRUSE Introduction Diabetes causes multiple end-organ damage, primarily due to microvascular disease. In the eye, retinal damage (diabetic retinopathy) can broadly be divided into (1) proliferative diabetic retinopathy (PDR) with characteristic vascular proliferation, gliosis and eventual retinal detachment, and (2) diabetic macular oedema (DMO), which leads to eventual destruction of photoreceptors in the central vision. DMO is the leading cause of permanent blindness in diabetics. The pathogenesis of DMO is multifactorial but the major hallmark is hyper-permeability of the retinal microvasculature, leading to retinal oedema and accumulation of proteins and lipids. If left untreated this inexorably leads to loss of vision, typically to the level of legal blindness. Various management options are available for treatment of DMO, including anti-inflammatory drugs, angiogenesis inhibitors, photocoagulation therapy, systemic disease control, vitreolytic agents and other novel drugs. The main goal of this review is to identify the best long-term, vision-preserving treatment option.
Photocoagulation DMO treatment employs laser energy by one of two methods: focal laser to coagulate leaking microaneurisms; and milder, diffuse grid laser to the entire oedematous area to stimulate resorption of the macular fluid by the retinal pigment epithelium. Laser treatment of the macula remains the traditional gold standard of treatment to this day, primarily due to the long track record, effectiveness in limiting vision loss, cost effectiveness and the durability of the treatment.1,2 Despite being the gold standard, photocoagulation is limited by not being equally effective in all patients. The therapy is also primarily aimed at preventing future loss of vision, and very few patients actually gain significant vision (three lines or more) following grid/focal laser.3 In fact, 5% of patients may experience debilitating loss of visual acuity due to the laser treatment itself.4
Anti-inflammatory agents Various inflammatory mediators are responsible for the increased permeability and leakage in DMO, including tumour necrosis factor (TNF-α), interleukins and vascular endothelial growth factors Correspondence to: Dr Carl-Heinz Kruse Department of Opthalmology, University of KwaZulu-Natal, Durban e-mail: ruraleye@gmail.com S Afr J Diabetes Vasc Dis 2013; 10: 120–121
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(VEGF). Corticosteroids are effective in modulating these mediators and are therefore often effective in treating DMO. The limitations of steroid treatment for DMO include the inability to cross the blood–ocular barrier. Steroids therefore have to be injected or surgically placed into the vitreous cavity to be effective. This brings with it all the potential complications of intra-ocular surgery, including endophthalmitis and iatrogenic damage to the lens and retina. The most studied and widely used steroid for intravitreal use is triamcinolone acetonide (Kenalog™). The steroid crystal suspension is injected through the pars plana into the vitreous humour and is effective in reducing macular swelling for four weeks. Newer and longer-lasting preparations include steroids imbedded in a slowly disintegrating matrix, such as Ozurdex™, an injectable, flexible rod impregnated with dexamethasone, which dissolves in four to six months.5 Iluvien™, an injectable non-erodible insert, approved in many European countries, slowly releases fluocinolone acetonide over two to three years.6 Steroids often have a dramatic effect in resolving DMO, often being effective even when laser and anti-angiogenic drugs have failed.5 The effect is, however, transient and repeated injections/ operations are often required. Furthermore, all steroids can cause cataract as well as raised intra-ocular pressure (IOP) which can lead to glaucomatous optic nerve damage.7 Of the patients who received Retisert™, a slow-release steroid, 91% had to have cataract surgery within four years, almost two-thirds had raised IOP and more than a third had surgery for glaucoma resistant to medical treatment.8 Newer, lower-dose devices such as Iluvien™ show some promise in lowering the number of complications.6 Non-steroidal anti-inflammatory drugs have a milder treatment effect and fewer side effects but none have been approved for intra-ocular use in DMO.
Angiogenesis inhibitors A number of anti-angiogenic drugs have been approved for treatment of DMO, of which the most studied is ranibizumab (Lucentis™). This humanised monoclonal antibody fragment binds and inactivates VEGF in the vitreous humour, reducing the hyperpermeability of the macular vessels. Avastin™ (bevacizumab) is also increasingly being used to treat DMO as an inexpensive offlabel indication and does not seem to be inferior to ranibizumab.9,10 Pegaptanib (Macugen™) seems to be slightly less effective.10 The advantage of anti-VEGF agents is that they do not cause cataracts and do not usually raise intra-ocular pressure, unlike steroids.11 The treatment effect is often dramatic but also transient, and no sustained-release options are currently available. Most antiVEGF drugs are injected monthly as required, and the average number of ranibizumab injections needed to control the DMO in the first year is nine, and four injections in the second.12 At one year, the anti-VEGF drugs more than doubled the threeline gain in vision, and decreased the loss of three lines of vision in
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DMO by at least two-thirds, compared to grid photocoagulation.10,13,14 This effect was less pronounced at two years compared to laser therapy.12,15 The long-term systemic sequelae of inhibiting VEGF in a vasculopath have not been clearly elucidated. Recent large trials have not shown an increase in thrombo-embolic events or mortality rate at one year in anti-VEGF agents over laser or sham treatments.10,16 Ranibizumab has shown no new safety signals at three years of treatment.17 Aflibercept (VEGF Trap-eye™) was approved by the FDA in 2011 for treating choroidal neovascularisation. This anti-VEGF was shown to be non-inferior to ranibizumab, but the injections need only be injected every eight months instead of four.18 Aflibercept has also been shown to be effective in treating DMO and reduces the treatment and follow-up burden.10
Other treatment modalities Hypoglycaemic, anti-hypertensive and even hypolipidaemic systemic drugs have shown significant results in controlling the progression of diabetic retinopathy and DMO.19,20 Although invasive, total pars plana vitrectomy surgery has been shown to be beneficial in reducing DMO, even in cases that are unresponsive to laser therapy.21,22 The mechanisms involved are probably reduced traction on the macula, temporary dramatic reduction of VEGF as well as increased oxygen saturation to the retina. This therapy seems to be effective even in eyes with no vitreo-retinal traction.23 Medical vitrectomy is an office procedure where enzymatic vitreolytic agents such as microplasmin are injected into the vitreous humour without the need for formal surgery. These agents have shown promise in improving refractory DMO but they have not been widely accepted due to safety concerns.24 Emerging drug technologies include, among others, small interfering RNA, protein kinase C inhibitors and hydroxy-3-methylglutaryl coenzyme A reductase inhibitors.25 None have been approved yet for treatment of DMO.
Combination treatment An approach to capitalise on the positive aspects of the different treatment options would be to give combination therapy. Combining an anti-VEGF with laser therapy should give us a dramatic improvement as well as a sustained effect, respectively. Laser combined with ranibizumab, however, has shown no improvement in final vision but it does reduce the amount of injections needed in the first two years.26 A combination of triamcinolone and ranibizumab has been studied in order to minimise the exposure of the eye to steroids.27 The studies show that after six months, both drugs, used separately, have equal clinical outcomes but an increase in glaucoma in the steroid groups. A combination of the two drugs is no better than single-drug therapy.27
Conclusion Despite being the current gold standard, laser treatment alone seems not to have as good outcomes as intravitreal steroids or anti-VEGF agents. On the other hand, the major problem of the injectable drugs is their short duration of action and recurrence of the oedema. Add to this the propensity of steroids to cause cataract and glaucoma, and the ideal treatment of DMO seems out of our grasp.
REVIEW
The best treatment of DMO currently seems to be a multitherapeutic approach. The management should also be tailored to each patient due to the great variation in individual response. At minimum, this approach should include: (1) strict control of serum glucose levels, blood pressure and lipids, (2) regular screening and early referral for treatment of diabetic retinopathy, (3) focal laser of leaking micro-aneurisms as soon as possible – preferably before a loss in vision, (4) grid laser if the DMO is diffuse, (5) resistant cases should get anti-VEGF or steroids to temporarily flatten the retina to be more receptive to subsequent grid laser, (6) prolonged intravitreal therapy combined with adequate laser for chronic, resistant cases. The choice of intravitreal injection depends on each individual. Steroids should be reserved for post-cataract surgery eyes at a low risk for glaucoma. Patients where regular follow up is difficult may benefit from sustained-release preparations. Anti-VEGF agents are relatively safe in most patients but regular follow up and sustained treatment become crucial. Pars plana vitrectomy or vitreolysis remains a last resort, unless there is evidence of vitreomacular traction, in which case it becomes the primary treatment option for DMO.
References 1.
Photocoagulation for diabetic macular edema. Early Treatment Diabetic Retinopathy Study report number 1. Early Treatment Diabetic Retinopathy Study research group. Arch Ophthalmol 1985; 103: 1796–1806. 2. Mrugacz M, Krajewska M, Bryl A, Szuszkiewicz M. [Evaluate the effectiveness of laser therapy in the treatment of diabetic maculopathy]. Pol Merkur Lek Organ Pol Towar Lek 2013; 34: 351–354. 3. Lima-Gómez V, Milagros Razo-Blanco Hernández D. [Characteristics associated with visual improvement after focal photocoagulation in diabetic macular edema]. Cir Cir 2012; 80: 311–319. 4. Schatz H, Madeira D, McDonald H, Johnson RN. Progressive enlargement of laser scars following grid laser photocoagulation for diffuse diabetic macular edema. Arch Ophthalmol 1991; 109: 1549–1551. 5. Lazic R, Lukic M, Boras I, et al. Treatment of anti-vascular endothelial growth factorresistant diabetic macular edema with dexamethasone intravitreal implant. Retina Phila Pa 2013; Aug 22. (Epub ahead of print). doi:10.1097/IAE.0b013e3182a48958. 6. Sanford M. Fluocinolone acetonide intravitreal implant (Iluvien®). Drugs 2013; 73: 187–193. 7. Bressler SB, Qin H, Melia M, et al. Exploratory analysis of the effect of intravitreal ranibizumab or triamcinolone on worsening of diabetic retinopathy in a randomized clinical trial. J Am Med Assoc Ophthalmol 2013; 131: 1033–1040. 8. Pearson PA, Comstock TL, Ip M, et al, . Fluocinolone acetonide intravitreal implant for diabetic macular edema: A 3-Year multicenter, randomized, controlled clinical trial. Ophthalmology 2011; 118: 1580–1587. 9. Ford JA, Elders A, Shyangdan D, Royle P, Waugh N. The relative clinical effectiveness of ranibizumab and bevacizumab in diabetic macular oedema: an indirect comparison in a systematic review. Br Med J 2012; 345: e5182. 10. Virgili G, Parravano M, Menchini F, Brunetti M. Antiangiogenic therapy with antivascular endothelial growth factor modalities for diabetic macular oedema. Cochrane Database Syst Rev 2012; 12: CD007419. 11. Comyn O, Lightman SL, Hykin PG. Corticosteroid intravitreal implants vs. ranibizumab for the treatment of vitreoretinal disease. Curr Opin Ophthalmol 2013; 24: 248–254. 12. Rajendram R, Fraser-Bell S, Kaines A, et al. A 2-year prospective randomized controlled trial of intravitreal bevacizumab or laser therapy (BOLT) in the management of diabetic macular edema: 24-month data: report 3. Arch Ophthalmol 2012; 130: 972–979. 13. Bandello F, Berchicci L, La Spina C, Battaglia Parodi M, Iacono P. Evidence for antiVEGF treatment of diabetic macular edema. Ophthalmic Res 2012: 48(Suppl 1): 16–20. 14. Thomas BJ, Shienbaum G, Boyer DS, Flynn HW, Jr. Evolving strategies in the management of diabetic macular edema: clinical trials and current management. Can J Ophthalmol J Can Ophtalmol 2013: 48: 22–30. 15. Stewart MW. Anti-vascular endothelial growth factor drug treatment of diabetic macular edema: the evolution continues. Curr Diabetes Rev 2012; 8: 237–246. Continued on page 133
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‘Digital diabetes’– looking to the future Deborah J Wake, Scott G Cunningham Abstract In the UK, 85% of adults use the internet, yet digital technology and web-based applications have been slow to realise their potential within healthcare. Diabetes, a chronic disease requiring extensive self-management, could particularly benefit from an e-health approach. While there are a number of independent on-line diabetes communities, mobile apps, websites and networking opportunities, these operate in silos rather than integrating with mainstream healthcare. This review will explore the political drivers and barriers to e-health, and review current digital opportunities for patients and healthcare professionals within diabetes care.
Keywords: diabetes, digital, technology, social networks, internet, care records, information governance
Introduction In the UK today, many people spend more time communicating through computers than through face-to-face contact; 67% of adults use a computer every day. This trend is not exclusive to the younger generation; 85% of all adults (and at least 80% of households) in the UK have internet access, with further growing trends in access through mobile devices.1,2 Whilst low socioeconomic status may associate with marginally lower technology access, still 92% of lowest earners (<£200/wk) use the internet. The internet can be accessed almost anywhere in the world through a variety of handheld devices, and computers. It has influenced the way people learn, consume, buy, socialise and support one another. One of the biggest rises in the last 5 years has been through social networking sites such as Facebook, which has recently announced reaching 1 billion users worldwide (equivalent to the third largest country in the world!).3 Twitter, a free networking and blogging tool, has seen massive growth across the personal and corporate world. Social networks are not just transforming our social lives, but have been shown to support knowledge transformation, communication and understanding, and can lever change, promote the uptake of beneficial behaviours, and encourage ownership.4–10 Despite its potential benefits,5 the healthcare sector has been slow to embrace the digital revolution, in comparison to industry,
Correspondence to: Dr Deborah Jane Wake Medical Education Institute/Medical Research Institute, Level 5, University of Dundee, Ninewells Hospital, Dundee, DD1 9SY, UK. Email: d.j.wake@dundee.ac.uk Scott G Cunningham Clinical Technology Centre, University of Dundee, Ninewells Hospital, Dundee, UK Originally in: Br J Diabetes Vasc Dis 2013; 13(1): 13–20 S Afr J Diabetes Vasc Dis 2013; 10: 122–126
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particularly banking and retail. Chronic diseases like diabetes could potentially benefit from technology driven approaches to care.
Background The recorded prevalence of diabetes in the UK is around 2.9 million and rising,11 andis expected to double over the next 15 years.11-14 This will place considerable strain on the National Health Service (NHS).15 There is an urgent need to develop and test innovative methods to address the gap between demand for and availability of services. A recent report in Diabetic Medicine15 predicts NHS annual spending on diabetes will increase from £9.8 to £16.9 billion over the next 25 years (17% of the entire NHS budget). Taking into account indirect wider society costs this rises to £23.7 billion currently (£39.8 billion by 2035). A large percentage goes into treating complications. A focus on early management and complication prevention could therefore have a huge economic impact.
Political drivers In 2008, the Technology in the NHS report outlined a vision to transform care and interaction in the NHS through technology, including web-based communication.6 A subsequent review made promotion of innovation a legal duty for health authorities. Engaging Patients in their Health concluded that the use of technology is “underdeveloped and poorly deployed” in the NHS.16 The internet and electronic patient held records have the potential to change the balance of power from healthcare providers to healthcare users and reduce the burden of care by engaging patients in managing their own health and illness.16,17 NHS England has pledged through ‘The Power of Information’ strategy to allow all patients access to their GP records by 2015.18 NHS Scotland’s “Delivering for Health”, promotes a focus on care delivery which is quicker, more personal and closer to home, in addition, to promoting wellness, and decreasing costly acute care necessitated by illness events.19 The Scottish Diabetes Action Plan20 and the Healthcare Quality Strategy (2010) emphasise the importance of “putting people at the heart of the NHS”, with high quality, evidence based and patient-focused care.21 In reality, healthcare provision is organised around healthcare staff availability with little support between infrequent clinic appointments. Significant and innovative changes to healthcare delivery are required to improve diabetes care in the current climate.16 Selfmanagement, education and empowerment are key to good glycaemic control and “Interactive behaviour change technology” and on-line tools could be a cost effective option for the management of people with diabetes.4,5,22
Diabetes digital healthcare systems (health informatics) Clinical Management Systems including unified electronic patient records and clinical portals are becoming increasingly mainstream in
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Figure 1. SCI-DC (National Diabetes Registry for NHS Scotland); a screen shot from an electronic clinical care record with fictitious patient data.
modern healthcare, although in most centres they still compliment rather that replace traditional paper based records. Electronic diabetes registries in the context of good managed clinical networks have the potential to dramatically improve care23,24 but are rarely used to capacity. Clinical Management Systems are particularly useful for chronic disease management where multiple care providers are involved. A good exemplar is SCI-Diabetes, a shared electronic record for diabetes care developed by NHS Scotland and the University of Dundee24,25 (see Fig. 1). SCI-Diabetes (previously SCI-DC) facilitates the collection of data from multiple sources within primary, secondary and tertiary care into one fully consolidated, patient-focused view. The system covers the entire national population of diabetes patients, meaning that data can be viewed by all authorised users at the point of care, therefore avoiding any duplication of effort. Secondary data use Electronic systems may also capture vast volumes of data, suitable for record linkage and exploitation to improve service, enhance the clinical evidence base and to provide benchmarks.12,25,26 Clinical research networks throughout the world26,27 now support the use of clinical data in epidemiological research and clinical trials.28,29 Secure linkage and anonymisation of data from relevant datasets is required prior to analysis in order to maintain information governance standards. This process does not detract from the quality of the data being analysed, but ensures that the identities of those whose records contribute are protected.
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necessary technology is “highly context dependent and research … is essential to inform strategic decision making”.17 Patient access to personal health records has the potential to improve self care and influence clinical decision making. Patients may better understand their clinical conditions and be motivated to ask appropriate questions during consultations. Online pre-clinic assessments can be used to allow the consultation to proceed more efficiently. In the UK, there are a limited number of online systems that allow patient access to clinical records, with various levels of success. EMIS Access33 and Renal PatientView34,35 allow access to a subset of clinical data from primary and secondary care respectively. They have both reported a reduction in administration overheads, and an improvement in appointment attendance as a result of records access. EMIS Access offers appointment booking and repeat medication ordering capabilities, to extend the user experience and the convenience available. Renal Patient View’s evaluation of its uptake also reported benefits including improved understanding of kidney health, enhanced ability to self care and improved patient– professional communication. My Diabetes My Way36 (Fig. 2) is an example of a diabetesfocused shared personal record, functioning in NHS Scotland. Patients have online access to the most relevant data fields within the main database, which is linked to an extensive education resource website. Whilst still in its infancy, user feedback has been positive. Patient quote: “it is an essential component to aid selfmanagement”. Mobile apps Patient self care can be supported further by the use of mobile phone software applications or ‘apps’. There are a huge number of smart phone apps available (many free) to diabetes patients (see Fig. 3) across all service provider markets. They have various features including; blood glucose recorders (with trend analysis), medications recorders with reminder alerts, activity and exercise monitors, calorie counters, recipe finders, and carbohydrate/insulin calculators. Some have links to wider diabetes communities for peer support. There are a number of apps specifically supporting nutritional aspects of diabetes including Carbs and Cals (for carbohydrate
Diabetes self care: a digital approach Patient record access A 2007 Nuffield Trust report30 on Electronic Personal Health Records (ePHR’s) stated that: “ePHRs have the potential to improve communication between providers and patients by sharing information, to enhance the quality of records by highlighting inaccuracies, and to reduce the burden of care by engaging patients in managing their own health and illness” In the US, Kaiser Permanente’s My Health Manager31 is one of largest and most advanced patient access systems. It has reported significant decreases in primary care office visits and telephone contacts.32 Whilst useful, it has been highlighted that the implementation of the
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Figure 2. My Diabetes My Way: A personal health record for diabetes care (anonymised data shown).
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Nutrition: Fooducate Carbs and Cals Carb Master Free Carb counting with Lenny (kids) Calorie Counter Calorie Tracker Daily Burn Lose it! Sparkpeople Food and fitness Tracker GoMeals Weight Watchers Mobile Exercise: Fitness/ Exercise My Fitness Pal Workout Trainer Run Tracker Diabetes News: Diabetes Headline News
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Glucose: • Bant • Blood Glucose Tracker • On Trak • Diabetes App • Diabetes Companion (dLife) • Diabets Buddy Lite • Diabetes Log • GluCoMo • Glucose Buddy • WaveSense Diabetes Manager • Glucool • Glooko • Handylogs sugar • Islet- diabetes assistant • Diabetes Reference • Dbees.com • dLife • Glucose Meter • Diabetes Log Book • GlucaTrend Diabetes • Diabetes Tracker Life • SiDiary • vRee for Diabetes • On Track
Figure 3. Examples of mobile phone applications available currently (Dec 2012) to help people with diabetes self managed their condition.
counting) and Fooducate, which allows users to scan products in shops and learn more about their nutritional value. In addition, new plug in smart phone ‘widgets’ such the iBG star, can allow a iPhone to essentially function as a home glucose monitor. Devices and software Diabetes has benefited hugely from the development of electronic devices ranging form simple home blood glucose monitors through to insulin pumps and continuous glucose monitoring systems (CGMS), the later two providing a major breakthrough in the management of type 1 diabetes. The success of a fully effective ‘artificial pancreas’ will depend on the development of sophisticated algorithms to predict blood glucose readings, and allow alteration of insulin administration appropriately. Even for those patients not using pumps, predictive glucose software is now available to allow more accurate insulin dose calculation. ManageBGL37 for example claims to be able to able to offer “a simulated or virtual insulin pump” for type 1 diabetes through use of an online software programme. Current and previous blood glucose results, carb intake, exercise, insulin doses and longer term glucose trends are used to predict future glucose readings and aid auto-calculation of bolus doses of insulin. These systems do require intensive user input to achieve their goals and have not been validated in widespread trials. Communication systems Increased contact between healthcare professionals and patients has been shown to improve glucose control and reduce complications. The average person with diabetes patients will spend on average around 3 hours with healthcare professions in the year, and self manages their condition 8 757 hours of the year.38 Provision of additional face-to-face care is costly, but a more efficient solution could be provided by digital technology through the use of virtual
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clinics and messaging systems to provide on-going ‘needs driven’ support throughout the year. Whilst free communication software is widely available (such as Skype, WebEx, message boards and social networks), integration into existing healthcare systems with the required security, governance and confidentially is more difficult. Patients Know Best39 is an example of a social enterprise that has developed electronic communication strategies and patient driven clinical record ownership. This has been successfully integrated with some healthcare systems, suggesting these barriers are not insurmountable. The evidence base for the use of on-line communication/ telemedicine in diabetes care is limited, however a small US study suggests potential benefits.40 It demonstrating a dramatic improvement in HbA1C (9.5 versus 8.2%) and a 4% mean weight reduction compared with conventional care using a telemedicine (virtual clinic) approach. Simple one way SMS (text) messaging has also been shown to be beneficial in diabetes care in small studies,41–45 increasing adherence and health related behaviours. Tang et al.46 trialled a multi-approach online diabetes management system in over 400 patients, reporting significant improvements in HbA1C at 6 months, although it was unclear whether these benefits were sustained. The true impact of wide spread adoption of online communication tools across diabetes services is still to be proven. Online learning With the continued growth of the world-wide web, online knowledge support for disease management is vast. This mainly comes from websites provided by government and non-governmental organisations, pharmaceutical companies, or increasingly from independent sources. Online blogs, diabetes specific encyclopaedias (Diapetadia)47 and search engines (Diaboogle)48 contribute to the information mix. In addition, interactive eLearning courses for patients are emerging in key areas such as carbohydrate counting, which is traditionally taught through intensive group education over several days.49 Online support tools such as mood-gym can additionally provide patient with self help modules to deal with psychological problems.50 Mainstream education providers including the Open-University, also provide free online courses about diabetes and its complications which may be useful for both patients and health care workers.51 Social networks/blogging Social networking platforms such as Facebook, Bebo and LinkedIn52–54 have seen an explosion in use in recent years, for both social and business use. The healthcare sector has only begun to realise the potential of these tools. Rather than providing didactic knowledge transfer, social networks can encourage learning and development through community sharing and peer support. They can also provide a sense of community and have the potential to problem-solve on a large scale (using techniques such as crowd sourcing). Many healthcare trusts, and patient support charities (e.g. Diabetes UK) have Facebook pages. PatientsLikeMe8 is an example of a chronic disease social network with over 170 000 users that allows users to ‘meet’ other patients with similar problems, enter into group discussions and share data online. The data generated from users has resulted in a number of significant publications.7 DLife,55 Diabetes.co.uk,56 Diabetic Connect57and Sugar Stats,58 are other examples of diabetes focused online communities.
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Patient Opinion is a relatively new website for any patients, that allow users to share healthcare experiences in an open and free environment.59 Twitter is a popular free social networking/blogging tool. It focuses on following a specific activity/person for information rather than supporting equal contributions and community development, but can be of use in knowledge sharing. Although best recognised for its use by celebrities and their followers, many businesses and field experts now also use twitter for marketing, networking and information dissemination. Simple SMS text messaging has been shown to be successful in behaviour change/motivation in diabetes and other areas of healthcare,41,60 but the benefits of using blogging and networking tools like Twitter and Facebook in diabetes care is yet unknown.
Barriers to eHealth Whilst technology has the potential to transform, it also has the potential to divide and care should be taken in the design of systems so they do not disadvantage certain users such as those with physical or visual impairment, literacy problems, nonnative language speakers or patients from low socio-economic backgrounds.61,62 In addition, any data sharing through technology needs to be grounded in good information governance to protect patients and minimise security risks. The Caldicott principles go some way to defining basic information standards for all, but organisations need to carefully consider the implications of any new data sharing project.63
Conclusions Internet-based technology has huge potential to transform diabetes care. Most diabetes patients have access to the internet and most are computer literate. Technology can improve care, particularly for those currently disadvantaged by current service delivery (see Fig. 4, case study) including hard-to-reach populations such as the geographically remote, young adolescents, busy professionals, patients with physical disabilities, patients with social phobias and those with a record of poor engagement with traditional clinics. Patients, social enterprises and commercial companies, rather than the healthcare professionals are the current drivers of the digital revolution, realising opportunities through development of apps, programs, gadgets and software to aid care management. One of the biggest challenges is focusing and linking this plethora
We recently reviewed a man in his late 20s, with type 1 diabetes for 15 years on the high dependence unit. He was requiring regular intensive care input, having being admitted with severe diabetic ketoacidosis, profound acidosis and reduced conscious state (GCS 3 on admission). Thankfully he made a full recovery over the coming days, but had he presented any later, his chance of survival would have been slim. The emergency services had broken down his door, following a phone call from a social networking friend from the USA (who he had never met in person). The caller had become worried when the patient hadn’t been messaging online for a few days. The patient who admitted a degree of social phobia, hadn’t attended diabetes clinics for 3 years and spent several hours a day socialising online. Figure 4. Case study: This is an anonymised real case highlighting a population group who do not engage with mainstream care, but who may benefit from a technology based approach to care.
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of technology and online activity with mainstream healthcare so that patient really benefits. Many technology tools and systems currently operate in silos; for example patients use glucose monitors and diabetes apps to manage their diabetes at home but this information is never fully shared with their healthcare providers thus missing an opportunity for inaction and intervention. Technology that allows individuals to contribute information to their care record between appointments, leading to a much more complete picture of their current health, may go some way to achieving this. Technology development in healthcare has been hampered by concerns around security, and lack of expertise. Digital health will however play an increasingly important role in diabetes care over the coming decades, and mainstream health providers need to find innovative ways to overcome these barriers and work with commercial and non-governmental partners to achieve the best care for their patients.
Conflict of interest The authors have no conflicts of interest to declare
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. David Matthews O for NS. Internet Access Quarterly Update, Q3 2012 [Internet]. Office for National Statistics. 2012 [cited 2012 Nov 30]. Available from: http:// www.ons.gov.uk/ons/rel/rdit2/internet-access-quarterly-update/2012-q3/stbiaqu.html#tab-User-engagement 2. Office for National Statistics. Internet Access- Households and individuals [Internet]. 2011. Available from: http://www.ons.gov.uk/ons/publicationsrereference-tables.html?edition=tcm%3A77-226727 3. Associated Press. Number of active users at Facebook over the years [Internet]. [cited 2012 Aug 12]. Available from: http://finance.yahoo.com/news/numberactive-users-facebook-over-years-214600186--finance.html 4. Brown L. A review of web-assisted interventions for diabetes management: maximizing the potential for improving health outcomes. J Diabetes Sci Technol 2007; 1: 892–902. 5. Ramadas A, Quek KF, Chan CK, Oldenburg B. Web-based interventions for the management of type 2 diabetes mellitus: a systematic review of recent evidence. Int J Med Inform 2011; 80: 389–405. 6. Liddell A. Technology in the NHS : transforming the patient’s experience of care. London: King’s Fund; 2007. 7. Wicks P, Vaughan TE, Massagli MP, Heywood J. Accelerated clinical discovery using self-reported patient data collected online | a patient-matching algorithm. Nat Biotechnol 2011; 29: 411–4. 8. Patients LIke Me [Internet]. 2012 [cited 2012 Jan 12]. Available from: www. patientslikeme.com 9. Diabetes.co.uk [Internet]. Facebook. [cited 2012 Dec 1]. Available from: http:// www.facebook.com/Diabetes.co.uk 10. Diabetes UK [Internet]. Facebook. [cited 2012 Dec 1]. Available from: http:// www.facebook.com/diabetesuk 11. Diabetes UK. Diabetes in the UK 2012: Key statistics on diabetes [Internet]. Diabetes UK; Available from: http://www.diabetes.org.uk/Professionals/ Publications-reports-and-resources/Reports-statistics-and-case-studies/Reports/ Diabetes-in-the-UK-2012/ 12. International Diabetes federation. Diabetes Atlas [Internet]. 2011. Available from: www.diabetesatlas.org 13. Scottish Executive. Scottish Health Survey: Topic Report; Obesity [Internet]. 2011 [cited 2012 Jun 26]. Available from: http://www.scotland.gov.uk/ Publications/2011/10/1138/0 14. Scottish Executive. The Scottish Health Survey: Topic Report: Older People’s Health [Internet]. 2011 [cited 2012 Jun 26]. Available from: http://www.scotland.gov.uk/ Publications/2011/11/24083430/0 15. Hex N, Bartlett C, Wright D et al. Estimating the current and future costs of Type 1 and Type 2 diabetes in the UK, including direct health costs and indirect societal and productivity costs. Diabet Med 2012; 29: 855–62.
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39. Patients Know Best Ltd. Patients Know Best; Manage Your Health [Internet]. 2012 [cited 2012 Jan 12]. Available from: http://www.patientsknowbest.com/ 40. Whitlock WL, Brown A, Moore K, et al. Telemedicine improved diabetic management. Mil Med 2000; 165: 579–84. 41. Franklin VL, Waller A, Pagliari C, Greene SA. A randomized controlled trial of Sweet Talk, a text-messaging system to support young people with diabetes. Diabet Med 2006; 23: 1332–8. 42. Franklin VL, Greene A, Waller A et al. Patients’ engagement with “Sweet Talk” – a text messaging support system for young people with diabetes. J Med Internet Res 2008; 10: e20. 43. Franklin V, Waller A, Pagliari C, Greene S. “Sweet Talk”: text messaging support for intensive insulin therapy for young people with diabetes. Diabetes Technol Ther 2003; 5: 991–6. 44. Arora S, Peters AL, Agy C, Menchine M. A mobile health intervention for inner city patients with poorly controlled diabetes: proof-of-concept of the TExT-MED program. Diabetes Technol Ther 2012 14: 492–6. 45. Louch G, Dalkin S, Bodansky J, Conner M. An exploratory randomised controlled trial using short messaging service to facilitate insulin administration in young adults with type 1 diabetes. Psychol Health Med 2012 May 30. 46. Tang PC, Overhage JM, Chan AS et al. Online disease management of diabetes: Engaging and Motivating Patients Online With Enhanced Resources-Diabetes (EMPOWER-D), a randomized controlled trial. J Am Med Inform Assoc 2012 Nov 20. 47. European Association for the Study of Diabetes. Diapedia. The Living Textbook of Diabetes [Internet]. [cited 2012 Jan 12]. Available from: http://www.diapedia. org 48. Farrell B. Diaboogle. Your Diabetes-Minded Search Engine [Internet]. 2008 [cited 2012 Jan 12]. Available from: diaboogle.com 49. Bournemouth Diabetes and Endocrine Centre. BDEC Diabetes Learning Programme [Internet]. 2012 [cited 2012 Jan 12]. Available from: http://www. bdec-e-learning.com/ 50. Australian National University. The Mood Gym [Internet]. [cited 2012 Jan 12]. Available from: https://moodgym.anu.edu.au/welcome 51. The Open University. Living with Diabetes [Internet]. 2012 [cited 2012 Jan 12]. Available from: http://openlearn.open.ac.uk/course/view.php?id=3947 52. Facebook [Internet]. [cited 2012 Jan 12]. Available from: www.facebook.com 53. bebo [Internet]. Available from: http://www.bebo.com/ 54. LinkedIn [Internet]. 2012 [cited 2012 Jan 12]. Available from: http://uk.linkedin. com/ 55. dLife [Internet]. [cited 2012 Jan 12]. Available from: http://www.dlife.com/ 56. Diabetes.co.uk. Diabetes.co.uk: the global diabetes community [Internet]. 2012 [cited 2012 Jan 12]. Available from: http://www.diabetes.co.uk/ 57. Diabetic Connect [Internet]. 2012 [cited 2012 Jan 12]. Available from: http:// www.diabeticconnect.com/ 58. SugarStats [Internet]. 2012 [cited 2012 Jan 12]. Available from: https://sugarstats. com/ 59. Patient Opinion [Internet]. [cited 2012 Dec 8]. Available from: https://www. patientopinion.org.uk/ 60. Free C. Smoking cessation support delivered via mobile phone text messaging (txt2stop): a single-blind, randomised trial. The Lancet. 2011; 378: 49-55. 61. Sarkar U, Karter AJ, Liu JY et al. The literacy divide: health literacy and the use of an internet-based patient portal in an integrated health system-results from the diabetes study of northern California (DISTANCE). J Health Commun 2010; 15 (Suppl 2): 183–96. 62. Sarkar U, Karter AJ, Liu JY et al. Social disparities in internet patient portal use in diabetes: evidence that the digital divide extends beyond access. J Am Med Inform Assoc 2011; 18: 318–21. 63. Department of Health. The Caldicott Committee: Report on the Review of Patient-Identifiable Information. 1997.
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Diabetes and the audiologist: is there need for concern regarding hearing function in diabetic adults? K KHOZA-SHANGASE, D PILLAY, A MOOLLA Abstract Background: The main aim of the current pilot study was to describe the auditory function of individuals diagnosed with type 1 diabetes mellitus (T1DM) in Johannesburg, Gauteng. Methods: A quasi-experimental, non-equivalent control-group design was used. A non-probability purposive sample of nine adults with T1DM and nine healthy adults with normal hearing were recruited and assessed at the University’s Speech and Hearing Clinic (USHC). Data collection involved detailed case history taking, otoscopic examination, tympanometry, puretone audiometry, speech audiometry and diagnostic distortion product otoacoustic emissions (DPOAE) testing. Findings were analysed descriptively and through inferential statistics (Fisher’s exact test and the independent samples t-test). Results: Individuals with T1DM presented with normal middle ear function and no middle ear pathology, as suggested by the otoscopic examination and impedance audiometry. Hearing levels were within normal limits even though thresholds were elevated at 6 000 Hz. Speech audiometry results were found to be elevated in this group, with reduced DPOAE amplitudes in the high frequencies. Conclusion: Current findings imply that microvascular complications of T1DM may cause damage to the outer hair cells, resulting in reduced DPOAE amplitudes and elevated thresholds in the high frequencies as well as in speech reception and discrimination levels. These findings highlight the need for future studies on a larger sample size for generalisability, with inclusion of older participants with T1DM.
Keywords: type 1 diabetes mellitus, distortion product otoacoustic emissions, cochleovestibular, pure tones, microvascular
Background The causes of hearing loss vary widely, and dysfunctions in the metabolism of carbohydrates, thyroid disturbances and other metabolic disorders have been listed as some of the frequent causes of vestibular and auditory abnormality. Among the glucose metabolism disorders, type 1 diabetes mellitus (T1DM) is most commonly related to auditory disorders.1 Regardless of Correspondence to: Prof Katijah Khoza-Shangase Speech and Hearing Clinic, Witwatersrand University, Johannesburg Tel: +27 0(11) 717-4565 Fax: 086 553 6055 e-mail: Katijah.Khoza@wits.ac.za D Pillay, A Moolla Speech and Hearing Clinic, Witwatersrand University, Johannesburg S Afr J Diabetes Vasc Dis 2013; 10: 127–133
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the cause of hearing loss, documented consequences of hearing loss include a profound negative impact on speech and language development, educational achievement, vocational performance, social interactions and psychological well-being. Although there is a lack of good data on T1DM prevalence in developing countries, and in particular in sub-Saharan Africa, epidemiologically, developing countries have a lower incidence of T1DM compared to developed countries. The incidence of T1DM in developing countries is reported to be limited but accounts for approximately 0.9 to 5% of all diabetics in these countries.2 The low prevalence of the condition may reflect inaccessible and/or unaffordable healthcare that may result in the misdiagnosis or lack of diagnosis of T1DM, poor prognosis as well as low incidence. The low prevalence could also be explained by factors such as quality of diabetes care and survival rates. Despite a low recounted T1DM incidence, prevalence of diabetes has been documented to be increasing in Africa, specifically South Africa, estimated to be home to 841 000 affected people.3 This raises concerns for the assessment and management of individuals with this condition, as changes in diets as well as management may change the presentation of the disease, including audiological presentation. Diabetic microangiopathy is one morphological aspect that is common in diabetes mellitus. It is defined as diffuse thickness of the basal membrane, which may also occur with the vascular endothelium.1,4 It may lead to microvascular complications, which result in retinopathy, nephropathy and neuropathy.5 Diabetic neuropathy is known to affect the sensory and motor nerves in a distal to proximal pattern, producing diabetic polyneuropathy, which is a common complication of T1DM.6 Examinations of temporal bones in patients with T1DM have revealed cochlear damage, characterised by microangiopathy of the inner ear vessels, stria vascularis atrophy and spiral ligament and hair cell loss. Researchers believe this may result in hearing loss.7 A number of international research studies have confirmed a relationship between diabetes mellitus and sensorineural hearing loss but with conflicting findings.8-13 More specifically, research by Lisowska et al.4 concluded that individuals with T1DM may have alterations in both the cochlear and retrocochlear auditory pathway and that the hearing impairment is mild and subclinical, which can only be detected by accurate and objective audiometric methods. The motivation for inclusion of a combination of the basic audiometric and physiological testing (using a combination of audiometric testing procedures such as pure-tone audiometry, tympanometry, otoacoustic emissions and auditory brainstem responses) assisted us to determine if the auditory alteration in individuals with T1DM indicate impairment at the cochlear level or in the acoustic neural pathways.10 Despite the aforementioned studies, which used a combination of audiometric testing with large sample sizes and inclusion and exclusion criteria that varied widely, generalisation of findings to the whole diabetic population becomes a challenge. The majority of these studies were conducted internationally with very little evidence
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from developing countries where the diagnosis, presentation and management of the disease may be different from that in developed countries, hence the importance of the current study. In addition to individuals with T1DM having a mild highfrequency sensorineural hearing loss, the literature also suggests that they may also present with cochleovestibular symptoms such as tinnitus, which precedes the hearing loss, as well as vertigo.8,14 Lasisi, Nwaorgu and Bella’s study15 on diabetic subjects further confirmed this. A prevalence of cochleovestibular dysfunction (benign paroxysmal positional vertigo, tinnitus and sensorineural hearing loss) was evident. However, the prevalence of these symptoms specifically for T1DM was not specified. Diabetic neuropathy caused by diabetic microangiopathy may cause damage to the inner ear, resulting in a hearing impairment. It is therefore important that audiologists recognise and manage the microvascular complications of diabetes in order to provide optimal care and treatment for this growing population. Moreover, audiologists should have a clear understanding of the disease process, which will allow them to be able to conduct appropriate assessment and management of individuals who present with T1DM. Currently, there is a dearth of research in South Africa regarding auditory function in individuals diagnosed with T1DM. Therefore, the current study aimed at describing the auditory function of individuals diagnosed with T1DM in Gauteng, South Africa. This pilot study proposed to answer the following research questions: • What is the prevalence of cochleovestibular symptoms such as tinnitus and vertigo in T1DM? • How can the results of the basic audiological assessment for the individuals diagnosed with T1DM and the control group be described? • What are the DPOAE characteristics of both groups? • Are DPOAE measures more sensitive in detecting the early signs of cochlear dysfunction in individuals with T1DM, when compared to the pure tone test battery? • Is there a relationship between the auditory function in individuals with T1DM and duration of T1DM?
Methods A quasi-experimental, non-equivalent control-group research design was used, with the aim of determining the relationship between T1DM and auditory function. The study setting was an out-patient clinic at the University’s Speech and Hearing Clinic (USHC) in Johannesburg, Gauteng. Participants were recruited through a nonprobability purposive sampling technique. Participants were invited to participate if they had medical confirmation of the diagnosis of T1DM, were between the ages of 19 and 40 years of age, and were able to provide informed consent. Participants who had a congenital/family history of hearing impairment, head and/or neck trauma, including ear operations, and participants who had been or were at the time of the study on ototoxic medication were excluded from participating in the study. Participants with an occupational/personal history of noise exposure were also excluded. The participants responded to poster advertisements that were placed at various diabetes centres as well as to word of mouth in Gauteng. Prior to recruitment, consent and information letters were sent to all relevant authorities to obtain permission to conduct the study.
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Measurements A structured test battery was used that included a questionnaire and audiology tests. The following section briefly describes the measurements used in this study. The testing procedure commenced with a detailed case history taking for each participant using a questionnaire. The questionnaire consisted of a biographical information section, medical history and hearing history section. The questionnaire provided background information and cochleovestibular symptoms which could relate to a hearing loss such as tinnitus and vertigo; information that when used together with the audiometric results could contribute to the interpretation of the results and guide treatment planning.15 The audiological test battery consisted of the following. Otoscopic examination: this was conducted using a Welch Allyn Pocket otoscope to allow the audiologist to detect middle and outer ear pathology.16 In addition, malformations of the auricle or the external auditory canal, signs of trauma or infection and cerumen obstruction or collapse of the external auditory canal were observed.16 Impedance audiometry: tympanometry and acoustic reflexes (both ipsilateral and contralateral) were conducted using a Grason Stadler Inc, 38 Version 4 tympanometer on all participants. The single-frequency 226-Hz probe tone was used. The tympanogram results were analysed according to the types of tympanograms: A, B, C, As and Ad. Type A tympanograms were recorded as normal and all other types were considered abnormal.17 Acoustic reflexes were recorded as normal if elicited between 70 and 110 dB at 500, 1 000, 2 000 and 4 000 Hz.18 Pure-tone audiometry: air- and bone-conduction testing was conducted on each participant using an AC 40 audiometer. Air conduction was done at 250, 500, 1 000, 2 000, 3 000, 4 000, 6 000 and 8 000 Hz bilaterally. A pure-tone average (PTA) was obtained for the right and left ear, respectively. Pure-tone averages below 26 dB were regarded as indicative of hearing function within normal limits.19 Bone conduction was done at 250, 500, 1 000, 2 000 and 4 000 Hz bilaterally. This was only conducted in participants who had air-conduction thresholds greater than 25 dB at any of the frequencies. As air- and bone-conduction testing was done together, it was possible to differentiate between the types of hearing loss: conductive, sensorineural or mixed.20 Speech audiometry: speech reception threshold (SRT), and speech discrimination (SD) testing was performed using an AC 40 audiometer. SRT was used to verify the pure-tone audiometry results.21 The Central Institute for the Deaf version 1 (CID W-1) word list was used for SRT testing, while speech discrimination was carried out bilaterally at 5 and 25 dB SL and at TD-10, using the NAL AB word list with monitored live voice if hearing thresholds were not within normal limits.21 If the hearing thresholds were within normal limits, it was carried out at 25 dB SL.21 For interpretation, a good correlation between SRT and PTA was considered to exist if they were within 6 dB of each other, a fair correlation existed if the scores were between ± 7 and ± 12 dB of each other, and a poor correlation existed if the scores differed by ± 13 dB or more.21 It is acknowledged that the use of monitored live voice and a word list that is not South African normed were limitations in the current study.
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Distortion product otoacoustic emissions (DPOAEs): DPOAEs for the current study were evaluated on the Capella Madsen diagnostic machine, as it can measure the response of the cochlear amplifier in discrete frequency ranges. The stimulus parameters that were used for DPOAEs are as follows: intensity (L1 = 65 dB SPL, L2 = 55 dB SPL), ratio (f2/f1 = 1.22) and frequency range (500–8 000 Hz). To be considered a valid DPOAE, the DP amplitude had to exceed the noise floor value by at least 6 dB and fall within the normative region.22 Statistical analysis For data management and analysis, qualitative and quantitative statistical analysis of the results was performed. Descriptive statistics were used to describe socio-demographic characteristics of the sample and to evaluate whether DPOAE tests are more sensitive in detecting the early signs of cochlear dysfunction than the basic pure-tone test battery.23 Fisher’s exact test was used to determine the prevalence of cochleovestibular symptoms in order to test the significance of any association of difference between two independent samples.24 The independent-samples t-test helped assess the results of the basic audiological assessment and the DPOAE, assessing the significant difference between the means of two groups on the dependent variable.25 Pearson’s correlation coefficient was used to determine the relationship between the auditory function in individuals with T1DM and age of onset, as it measures the degree of relationship between two variables and allows making predictions from one variable to another.26
Results As indicated in Table 1, the experimental group consisted of nine individuals (two males and seven females) who were medically diagnosed with T1DM. The control group consisted of nine individuals (two males and seven females) without T1DM and with no known hearing loss. The age of the participants ranged between 19 and 40 years. The mean age for the experimental group was 26.5 years (standard deviation = 6.54) and the mean age for the control group was 26.2 years (standard deviation = 4.65). Prevalence of cochleovestibular symptoms such as tinnitus and vertigo in T1DM The statistical results from the Fisher’s exact test conducted indicated no relationship between the cochleovestibular symptoms and T1DM. The corresponding p-value, if below 0.5, indicated a relationship between T1DM and the cochleovestibular symptoms. However descriptively (as depicted in Table 2), vertigo was most prevalent in the experimental group (56%), with tinnitus at 11%. Results of basic audiological assessment for T1DM individuals and controls The otoscopic examination for the experimental and control group was clear. This means that no obstruction was present and normal tympanic membranes were clearly visible in all participants. No differences were noted between the groups. Impedance audiometry Tympanometry: the p-value for the middle ear static compliance, ear canal volume and middle ear pressure are indicated in Table 3. There were no significant differences in the scores for the experimental and control group.
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Table 1. Demographic profile of the participants. Group 1 (19–25 years)
Group 2 (26–31 years)
Group 3 (32–40 years)
Factor
Exp
Control
Exp
Control
Exp
Control
Number of participants
4
4
3
3
2
2
Age (mean)
21
21
27.3
28.3
36.5
33.5
Males/females
1/3
0/4
0/3
1/2
1/1
1/1
Table 2. Prevalence of cochleovestibular symptoms for the experimental and control groups. Factor
Tinnitus
Vertigo
Yes
No
Yes
No
Experimental
1
8
5
4
Control
1
8
0
9
p-value
9
undefined
Acoustic reflexes: an independent samples t-test was conducted to compare the acoustic reflexes at each frequency, bilaterally in both groups. The p-values for the acoustic reflexes at each frequency are presented in Table 3. There were no statistically significant differences in the scores for the experimental and control groups. These results suggest that T1DM does not have a statistically significant effect on acoustic reflexes. Pure-tone audiometry: an independent samples t-test was conducted to compare the intensity values at each frequency in the experimental and control groups. The p-value for the intensity values at each frequency is shown in Table 3. Again, there were no statistically significant differences in the scores for the experimental and control groups. These results suggest that T1DM did not have an effect on pure-tone audiometry in the current sample. Fig. 1 illustrates the mean values of right and left ear pure tones, and mean pure-tone average values for both groups, respectively. Visual descriptive analysis of the data illustrates that although the mean values for the right and left ear pure tones were within normal limits for the experimental group, they were higher than those of the control group. The greatest difference was noted at 6 000 Hz. Speech audiometry There was no statistically significant difference for SRT values (p = 0) and SD values (p = 0.7) in the experimental and control groups when the independent samples t-test was conducted. These results suggest that T1DM did not have a statistically significant effect on SRT or SD. However, descriptively, mean SRT and SD values were higher in the experimental group compared to the control group. For the experimental group: SRT (RE) = 12.22 dB HL, SRT (LE) = 10 dB HL; SD (RE) = 98 dB HL, SD (LE) = 97 dB HL. For the control group: SRT (RE) = 5 dB HL, SRT (LE) = 5 dB HL; SD (RE) = 95 dB HL, SD (LE) = 96 dB HL.
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Table 3.p-values of impedance audiometry, pure-tones audiometry and DPOAEs for left and right ears. Tympanometry
Right ear
Left ear
Static compliance
0.72
0.59
Ear canal volume
0.461
0.79
Ear pressure
0.4
0.96
Acoustic reflex frequency (kHz)
0.5
1
2
4
0.5
1
2
4
Ipsilateral
0.8
0.9
0.3
0.6
0.8
0.5
0.7
0.6
Contralateral
0.15
0.43
0.8
0.71
0.43
0.52
0.91
0.87
Pure-tone frequency (kHZ)
0.25
0.5
1
2
3
4
6
8
0.25
0.5
1
2
3
4
6
8
1
0.4
0
0
0
0.4
0
0
0.5
0.1
0
0
0
0
0
0.2
DPOAEs frequency (kHZ)
0.5 0.18
0.75 0.88
1 0.14
0.5 0.39
0.75 0.32
1 0.04
1.5 0.61
2 0.93
3 0.08
4 0.56
6 0.25
8 0.56
1.5 0.95
2 0.83
3 0.08
4 0.26
6 0.16
8 0.55
DPOAE characteristics of both groups An independent samples t-test indicated a statistically significant difference in the scores for the left ear in the experimental and control groups at 1 000 Hz (p = 0.04). No statistically significant difference was found in the scores for both ears in the experimental and control groups for the other frequencies (Table 3). The mean values of the right and left ear DPOAE characteristics indicate that the DPOAE results were within normal limits for both groups at all frequencies except 500 Hz in the experimental group (Fig. 2). The reliability of the mean DPOAE amplitude at 500 Hz is questionable as DPOAE amplitudes may fall below the lower end of the normal range for all frequencies except 500 Hz.27 The mean DPOAE values in the experimental group were lower in the right and left ears than in the control group, except at 1Â 500 Hz. This suggests that the mean DPOAE values in the experimental group were closer to 6 dB, although within normal limits, which may suggest an early sign of outer hair cell (OHC) dysfunction. This is particularly important to note in the
current sample which comprised a relatively young age of T1DM subjects.
Fig. 1. Mean auditory threshold of left and right ears.
Fig. 2. Mean DPOAE values of left and right ears.
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DPOAE measures for detecting the early signs of cochlear dysfunction in individuals with T1DM compared to puretone test battery The mean values of the right ear DPOAEs and pure tones (Fig. 3) were within normal limits for all frequencies except at 500 Hz. The auditory threshold value at 6 000 Hz, although within normal limits, was the lowest compared to all other frequencies. The mean values of the DPOAEs were found to be lower at 6 000 and 8 000 Hz compared to pure tones. This indicates that the DPOAE measure may be more sensitive in detecting early signs of cochlear dysfunction as the values are close to 6 dB. The mean values of the left ear DPOAEs and pure tones (Fig. 3) were within normal limits. The mean values of the DPOAEs at 6 000 and 8 000Hz indicate that the DPOAE measure may be more sensitive in detecting the early signs of cochlear dysfunction
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Fig. 3. Mean values of left and right ear DPOAEs and pure tones.
as the values are close to 6 dB, the minimum limit for normal DPOAE measurements. Relationship between auditory function in individuals with T1DM and duration of T1DM Fig. 4 indicates that the PTA was highest for an individual with a 20-year duration of T1DM. However, the PTA decreased for individuals who had had TIDM for 21 years and longer. The Pearson correlation coefficient was 0.047. This statistical value had no significance but this may have been due to the small sample size of the current study.
Discussion According to the research literature, auditory function has been reported in individuals with T1DM, using a combination of audiometric testing procedures such as pure-tone audiometry, tympanometry, OAEs and ABRs.11,13,14,28-31 The results from the auditory characteristics in individuals diagnosed with T1DM in Gauteng, South Africa, are discussed in accordance with the subaims of the study. On examination of prevalence of cochleovestibular symptoms such as tinnitus and vertigo in T1DM, the current results indicated that vertigo was most prevalent (56%), with tinnitus presenting in 11% of the sample. This is consistent with the literature, which suggests that individuals with T1DM may have cochleovestibular symptoms such as tinnitus and vertigo,8, 32,33 and tinnitus has been found to precede hearing loss.14 The current findings have implications for audiologists who should be cognisant of these cochleovestibular symptoms when assessing and managing individuals diagnosed with T1DM. Vertigo can have detrimental effects in an individual if not treated in terms of propensity to falls; and both vertigo and tinnitus can have a serious and negative impact on quality of life. Probing for these symptoms during routine medical follow up of individuals with T1DM can ensure early identification and intervention. With regard to the description of the results of the basic audiological assessment of individuals diagnosed with T1DM and the controls, otoscopic examination in both groups indicated normal middle ear function bilaterally. The findings from impedance
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audiometry indicated no differences between the control and experimental groups, suggesting that T1DM does not have a negative effect on impedance audiometry. These findings are consistent with published data,30 which concluded that individuals with T1DM have normal impedance audiometry. Pathophysiologically, it can be argued that middle ear function would not be expected to be impacted on by T1DM. The results of the pure-tone audiometry indicated no statistically significant difference between the experimental and control group data. Furthermore, none of the individuals with T1DM had a clinical hearing loss based on the PTA (i.e. all PTAs were below 26 dB). However the mean auditory threshold of each frequency in the right and left ear and the PTA value in both ears were higher at all frequencies in the experimental group, compared to those in the control group. This was more clearly noted at 6 000 Hz for both ears and was noteworthy at 8 000 Hz as well. These findings indicate that individuals with T1DM have auditory thresholds that are higher than those without T1DM. This finding is supported by Ferrer et al.29 and Pessin et al.14 In addition, the elevated thresholds at 6 000 and 8 000 Hz may be an indication of progression of a possible high-frequency hearing loss. This is characteristic of T1DM, which affects predominantly the higher frequencies.31 It is crucial that audiologists in South Africa are mindful that individuals with T1DM have elevated thresholds in the high frequencies, specifically 6 000 and 8 000 Hz. The mild degree of clinical audiological changes in the current sample could have been a feature of T1DM or it may have been influenced by the younger age range of the participants as well as the small sample size. Nonetheless, the findings indicate a need for more in-depth research in this group with a wider range of participants who have had T1DM for a longer period of time. Speech audiometry results also indicated no statistically significant difference between the experimental and control group data. This finding is the same as that by Parving et al.32 who also found no significant difference between individuals with T1DM and healthy individuals and their corresponding mean values for SRT and SD. However, the mean SRT and SD speech level values were again found to be elevated in the experimental group. This is consistent with the elevated pure-tone audiometry results in the T1DM group. Impaired speech audiometry findings have a significant impact on quality of life of the impaired individual as
Fig. 4. Duration of T1DM in years versus PTA.
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this epitomises human contact. Provision of aural rehabilitation in the form of amplification and/or communication strategies would ensure enhanced communication functioning for the individual with T1DM. The mean DPOAE amplitude values were notably reduced in the experimental group compared to the control group. These changes in the experimental group were significantly reduced in the high frequencies: 6 000 and 8 000 Hz. These finding indicate that there was outer hair cell dysfunction in the inner ear, as DPOAEs provide information on the OHCs located in the cochlear,34,35 and can detect when the function of the cochlear amplifier is impaired.36 DPOAEs are also known to be more sensitive to subclinical hearing changes long before they can be detected on the audiogram. Microangiopathy of the inner ear vessels, stria vascularis atrophy, and spiral ligament and hair cell loss are likely to result in hearing loss.7,36 Moreover the ear-specific microvascular complications of the inner ear have been reported to be the source of the hearing loss related to T1DM.7 All of these factors could alter the OHCs function and consequently the DPOAE, as evidenced in the current sample. The reduced DPOAE amplitudes in this study are consistent with previous literature that indicated reduced amplitudes for the mid to high frequencies on this phenomenon.11-13 DPOAEs are known to be an excellent physiological measure to identify hearing loss, and the identification of hearing loss is better at mid to high frequencies than at lower frequencies.36 A comparison of the DPOAE amplitudes and auditory thresholds at each frequency indicated that DPOAEs are more sensitive in detecting the early signs of cochlear dysfunction in individuals with T1DM compared to pure-tone audiometry. DPOAEs are more sensitive as the DPOAE amplitudes at the high frequencies, 6 000 and 8 000 Hz, were significantly reduced, indicating damage to the OHCs. However, the auditory thresholds on pure-tone assessment only showed an increase in threshold at 6 000 Hz. An increase in threshold was also noted at 8 000 Hz but this was not as notable when compared to the increased threshold at 6 000 Hz. This finding is consistent with previous literature. For example, Ottaviani et al.13 also found that the use of DPAOEs demonstrated alterations of the cochlear function despite the participants having normal pure auditory thresholds. The current findings on the reduced DPOAE amplitudes in individuals with T1DM as well as DPOAEs being more sensitive in detecting the early signs of cochlear dysfunction have implications for audiologists who are assessing individuals with T1DM. They indicate that the audiologist should ensure that DPOAEs form part of the protocol when assessing the hearing status of individuals with T1DM. Results of the auditory function and its relationship with T1DM and age of onset indicated that the PTAs were highest for an individual who had had T1DM for 20 years. However, the PTA decreased for individuals who had had T1DM for 21 years and longer. These results are inconclusive, possibly due to the small sample size. Ferrer et al.29 concluded that the duration of T1DM is significantly correlated with the auditory thresholds at 1 000, 2 000 and 8 000 Hz. In summary, results from the current study revealed that tinnitus and vertigo were prevalent cochleovestibular symptoms in T1DM. The otoscopic and immittance findings were within normal limits for the experimental and control groups. Additionally, the puretone audiometry results indicated the absence of hearing loss.
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However, auditory thresholds were elevated at 6 000 Hz in the experimental group. Speech audiometry results were found to be not statistically significantly different between the two groups but the SRT and SD results were elevated in the experimental group. DPOAEs amplitudes were reduced in the experimental group at all frequencies but were most statistically significantly reduced at 6 000 and 8 000 Hz. DPOAEs were found to be more sensitive than the pure-tone assessment battery in detecting the early signs of cochlear dysfunction in individuals with T1DM. Limitations of the study Due to the small sample size, the current study is presented as a pilot study. Therefore its results need to be considered in relation to the identified limitations. Firstly, the small sample size. The results could have been more conclusive and generalisable had there been a larger sample size, with a wider age range cohort, which is an indication for future studies. Secondly, ultra-high frequency audiometry testing did not form part of the test protocol due to a lack of equipment. The use of high-frequency audiometry testing at 10 000 and 12 000 Hz could have identified the high-frequency hearing loss that is characteristic of T1DM, which may have been missed in the current sample. Finally, a larger sample size would have allowed for more powerful statistical analysis to be conducted to support the current findings. The findings of this study have important implications for the assessment and management of individuals with T1DM by audiologists. Despite the fact that the low prevalence and high cost mean that T1DM is likely to be low on the list of priorities for the ministry of health in South Africa, all efforts should be made to improve the quality of life of individuals diagnosed with this condition, and that might include audiological management. The key findings of this study suggest the importance of incorporating audiological assessment for individuals with T1DM. When assessing individuals with T1DM, the assessment should include the basic audiometric test battery as well DPOAEs. Importantly, hearing loss may be present with DPOAE assessment but absent with pure-tone audiometry. The use of DPOAEs as a test procedure in any basic audiometric test battery is paramount as it is able to detect early signs of cochlear dysfunction. The elevated thresholds at 6 000 Hz in individuals with T1DM can reasonably be ascribed to T1DM itself due to the strict inclusion and exclusion criteria that were adhered to. Finally, further replicated research with the same protocol and a larger sample is required to obtain more conclusive and generalisable results.
Conclusion This study provides preliminary understanding of the concerns regarding hearing function in people living with T1DM in South Africa. The main conclusion drawn from the study was that microvascular complications of T1DM may cause damage to the OHCs, resulting in reduced DPOAE amplitudes in the high frequencies. This may also result in elevated auditory thresholds at 6 000 Hz. Furthermore, individuals with T1DM appear to have normal middle ear function and no middle ear pathology, as suggested by the otoscopic examination and impedance audiometry. Such individuals identify speech sounds at an elevated threshold. These study findings provide valuable information about the assessments necessary for long-term management of persons with T1DM. Because of the small sample size in the current study as well as
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the young age range of the participants, the findings cannot be generalised to the entire population with T1DM. Nonetheless, the current findings highlight the need for future studies on larger sample sizes. This is particularly important, as the incidence of T1DM in developing countries is observed to be gradually increasing annually.
Acknowledgements The authors acknowledge Ms Ifeanyi Oranye for acting in the role of research assistant during the write up of this article.
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Continued from page 121 16. Campbell RJ, Bell CM, Paterson JM, et al. Stroke rates after introduction of vascular endothelial growth factor inhibitors for macular degeneration: a time series analysis. Ophthalmology 2012; 119: 1604–1608. 17. Silva, R, Axer-Siegel R, Eldem, et al. The SECURE study: long-term safety of ranibizumab 0.5 mg in neovascular age-related macular degeneration. Ophthalmology 2013; 120: 130–139. 18. Semeraro F, Morescalchi F, Parmeggiani F, et al. Aflibercept in wet AMD: specific role and optimal use. Drug Des Devel Ther 2013; 7: 711–722. 19. Kumar B, Gupta SK, Saxena R, Srivastava S. Current trends in the pharmacotherapy of diabetic retinopathy. J Postgrad Med 2012; 58: 132–139. 20. Toth PP, Simko RJ, Palli SR, et al. The impact of serum lipids on risk for microangiopathy in patients with type 2 diabetes mellitus. Cardiovasc Diabetol 2012; 11: 109. 21. Yanyali A, Nohutcu AF, Horozoglu F, Celik E. Modified grid laser photocoagulation versus pars plana vitrectomy with internal limiting membrane removal in diabetic macular edema. Am J Ophthalmol 2005; 139: 795–801. 22. Recchia FM, Ruby AJ, Carvalho Recchia CA. Pars plana vitrectomy with removal
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Diabetes Educator’s Focus EXCELLENCE IN DIABETES: MISSED OPPORTUNITIES FOR OPTIMAL CARE Dr N Naidoo Specialist family physician and district medical officer, New Hanover, KwaZulu-Natal. e-mail: docnn@iafrica.com
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T
he exponential increase in incidence of diabetes and other non-communicable diseases, such as cardiovascular diseases, hypertension, stroke, hyperlipidaemias and certain cancers are associated to a large extent with a growing epidemic of obesity, and lifestyle issues, mainly as a result of lack of exercise, dietary indiscretion, smoking and excessive alcohol consumption.1 Most people with these diseases and other chronic non-communicable diseases in South Africa are treated in public-sector clinics, where both acute and chronic conditions are managed together. This situation rarely provides adequate care for those with chronic conditions or attempts to address their risk factors, nor is it organised to detect early complications and generally lacks patient-centred initiatives to enable patients to become active partners in their own care. Planning to improve the organisation of how primary healthcare services deal with chronic non-communicable diseases is lacking. This is in vast contrast to how some communicable diseases, such as tuberculosis (TB) and human immunodeficiency virus (HIV), are currently organised and managed. The reality in South Africa is that non-communicable diseases are far more common and have a greater impact than communicable diseases with regard to morbidity and mortality rates if not adequately assessed, managed and funded at the primary level of care. As a result of this, there are deficiencies in the levels and standards of care, with a high prevalence of unrecorded diabetic, hypertensive and cardiovascular complications and sub-optimal glycaemic and blood pressure control, as well as an almost total absence of essential laboratory tests to manage
progress of the disease or detect early complications at the primary level. The result often is polypharmacy and a repetition of the same medications without an attempt to treat to target or change treatments if contraindicated, either as result of side effects or renal or hepatic impairments. A major problem that is often encountered is failure to refer to a higher level of care when indicated.2 Despite improvements in measurement of blood pressure and blood glucose levels, current guidelines are often not followed, with the result that over 60% of diabetics and 50% of hypertensive patients and those with cardiovascular disease are sub-optimally managed.3,4 It is surprising that despite these findings, the trend recently has been to close wellfunctioning chronic non-communicable disease clinics or not to establish these where the need exists, even though the National Department of Health has made policy progress and established chronic disease care on the health agenda, such as the South African Declaration for Prevention and Control of Non-Communicable Diseases 2020 targets. Diabetes and other chronic non-communicable diseases require not only continuing medical care but also planning and organisation with regard to continuing patient self-management skills, patient education, health professional education, nutritional education and on-going evaluation of lifestyle modification, to ensure optimal care. A comprehensive approach that extends beyond glycaemic control (Steno 2 study) showed that intensive multifactorial interventions, which included cardiovascular riskfactor assessments, hypertension and dyslipidaemia management and attention to lifestyle matters was more cost-effective than conventional treatment.5
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The gold standard of diabetes care currently in South Africa is outlined in the 2012 SEMDSA guidelines.6 To achieve excellence in diabetes care, these guidelines should be implemented by all healthcare professionals, especially family physicians who are community based. However, the road to excellence in diabetes care is littered with a number of obstacles or barriers that have to be overcome and addressed effectively. These include various cultural, economic, social, environmental, political, educational and health-management issues.7 This article highlights some of the obstacles or barriers encountered in everyday practice that impact on achieving excellence in diabetes care. These include, among others, the management of pre-diabetes, implementing behavioural change, risk-factor assessment, prevention and early detection of complications, patient and health professional education, managing patients to achieve targets, patient-centred care, and comprehensive, integrative approaches to care, smoking cessation, medical nutritional therapy, organisation of chronic care, achieving optimal glycaemic control, screening of high-risk individuals and keeping of diabetes records that easily profile progress and detect trends or abnormalities that require action or referral. PRE-DIABETES This is a term used to describe the state of impaired fasting glucose (6.1–6.9 mmol/l) or impaired glucose tolerance (fasting < 7 mmol/l and two-hour 7.8–11 mmol/l). Pre-diabetes has a high risk of progression to develop diabetes mellitus (25–50% lifetime risk). Its importance lies in the fact that pre-diabetes increases the risk of cardiovascular complications by 1.5-fold, and diabetes increases the risk by two- to four-fold, making the importance of prevention through lifestyle changes imperative.8 Research studies have highlighted the value of lifestyle changes in the prevention of type 2 diabetes. There are several national and international studies and initiatives that have addressed preventive measures successfully. This fact emphasises the need for education and lifestyle modifications, and in some cases, the addition of medication for the prevention of diabetes. This role is best filled by a diabetes educator who will teach the skills needed to live a healthy life. These skills will enable patients to change their health through responsible self-care, knowledge and diabetes skills training. Changes in attitude, motivation, adherence and strict care with regard to diet and exercise are more effective in delaying diabetes onset than medication. High-risk individuals should be screened for diabetes. This includes individuals with a family history of type 2 diabetes, hypertension, hyperlipidaemia, high-risk ethnic groups, the obese (body mass index > 35 kg/m2), increased waist circumference (> 94 cm in men and > 80 cm in women), a history of gestational diabetes, patients with the metabolic syndrome, underlying cardiovascular disease, the presence of polycystic ovarian syndrome, those with impaired glucose tolerance and impaired fasting
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glucose levels, sedentary lifestyle, alcohol abuse and those on certain medications such as long-term steroids, beta-blockers, thiazide diuretics, etc. People who are not controlled with lifestyle modifications and who are at high risk would benefit from the addition of metformin.9 ASSISTING PATIENTS WITH DIABETES TO MAKE CHANGES People with diabetes need knowledge, skills and motivation to assess their risks in order to understand how they will benefit from changing behaviours or lifestyle, and to act on that understanding by engaging in appropriate behaviour. Diabetes is a self-managed condition. It requires those with it not only to understand the nature of their condition and its consequences, but also to take practical action in a number of ways on a daily basis in order to prevent diabetes from impacting negatively on their lives. These actions include monitoring blood glucose levels and blood pressure, and recording these in a diabetes diary, injecting insulin correctly, taking tablets regularly, detecting and dealing with hypoglycaemia, and paying attention to the amount, type, content and timing of food and drink intake, as well as physical activity. Thinking and planning ahead is essential to prevent problems with various activities such as driving, employment or working in risky environments and engaging in social activities. Living successfully with diabetes is more about taking knowledgeable decisions or actions than simply having knowledge. It is a behavioural condition. Knowledge alone will not change behaviour. Collaborative self-management interventions where people responded to clinical information and goal setting were more effective in improving clinical outcomes. Promoting self-management and a partnership in decision making is the key skill of a health professional such as a family physician. There are a number of models that inform how to do this. These include chronic disease self-management, therapeutic patient education, a heart manual, and patient empowerment. As health professionals and especially as family physicians, our role is about promoting active and successful decision making by addressing the patient’s thoughts, ideas, feelings, fears, beliefs, myths, as well as their knowledge. Patients are more likely to adhere to decisions they have made themselves and to goals they have set themselves, i.e. to promote self-efficacy or confidence in their ability to take action for their own benefit. This will promote behavioural change.10 Brief motivational interviewing (BMI) is an approach to motivating behavioural change and has great potential if used in general healthcare settings, especially in managing chronic conditions such as diabetes.11 Our role as healthcare practitioners is to enquire whether the patient is ready to change, does he/she understand the need for change, have appropriate treatment targets been set, are monitoring programmes in place, and is referral necessary, e.g. dietician, exercise physiologist, clinical psychologist.
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Factors that patients with diabetes should be encouraged to take responsibility for include dietary matters, smoking cessation,12 exercise, ownership of their diabetes care, identifying their needs, misconceptions, motivations and wants, and knowledge of their condition. Family physicians and healthcare workers should ensure a good or satisfactory patient relationship through a patient-centred approach by being nonjudgemental, establishing a good rapport with the patient and being open and honest, attentive, and reflecting and praising achievements however small, relinquishing some control to the patient, explaining the significance of various findings, including their test results and risks of developing complications, identifying the patient’s agenda and jointly setting goals, defining timelines and developing action plans. Evidence shows that people with diabetes who do not receive appropriate education and knowledge have a four-fold risk of a major complication. Education should therefore be a planned life-long process in diabetes management as the condition evolves and life circumstances change.10 PREVENTION AND EARLY DETECTION OF COMPLICATIONS It should be remembered that 30 to 50% of people with type 2 diabetes have complications at the time of diagnosis due to prolonged insulin resistance (10 to 15 years) before hyperglycaemia is detected clinically. The acute complications of diabetes include hypoglycaemia, which is characterised by a low blood glucose level (< 2.7 mmol/l), diabetic ketoacidosis (DKA) characterised by high blood glucose levels, ketosis and acidosis and hyperosmolar non-ketotic coma (HONK) characterised by high blood glucose levels. Other complications include blurred vision or acute neuropathic symptoms and insulin oedema. Understanding of the pathogenesis, causes and symptoms of the above, and their early detection and effective management is vital to avoid long-term complications. The importance of early detection of hypoglycaemia and its avoidance is very important as it is accompanied by cardiovascular complications, especially acute myocardial infarction. This is as a result of the stimulation of a number of inflammatory markers including cytokines that are induced as a result of the hypoglycaemia.13 Chronic complications include both micro- and macrovascular complications. Microvascular complications include retinopathy, nephropathy, neuropathy, dermopathy and cardiomyopathy. Risk factors for microvascular disease include the duration of diabetes, poor glycaemic control, genetic predisposition, hypertension, hyperlipidaemia and smoking. Some of these will need timeous intervention from the treating health professional. There is a continuous relationship between HbA1c level and microvascular complication rate. Therefore, it is imperative that this is always managed to the individual’s target as per the guidelines. In the young diabetic, the HbA1c level should be < 6.5%. In the elderly and dependant this should be between 7.5 and 8.5%.
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Screening for these complications and their early detection, management and referral is the hallmark of good diabetes practice. These will include regular annual, or six monthly visits if indicated, to the ophthalmologist, cardiologist, nephrologist if urinary albumin or albuminuria is present, neurologist if indicated for the early detection of various neuropathies, podiatrist for the prevention and early detection of foot problems, and the dietician for medical nutritional management especially in obese patients. Smoking cessation therapy must be instituted in all patients. Aspirin should be used in all patients who have a greater than 10% risk assessment for cardiovascular disease. Sexual dysfunction in the male is common and should alert one as a marker for more widespread vascular disease. This should be evaluated, especially for cardiovascular and other macro- and microvascular targetorgan involvement. It must be remembered that the key to successful management and prevention of the above complications lie in achieving early and on-going glycaemic control, especially early morning and post-prandial glucose control, blood pressure control according to the JNC7 guidelines, lipid control according to the current 2012 guidelines, the total abstinence from smoking, and lifestyle management of visceral abdominal adiposity and obesity. Macrovascular complications include coronary artery disease, atherosclerosis, cerebro-vascular disease and peripheral vascular disease. Early screening, prevention and detection of these complications are essential to avoid serious disability, morbidity and mortality. Diabetes is largely a vasculopathic disease and a coronary artery risk equivalent. Once again, the mainstay of prevention and the avoidance of complications are to maintain long-term glycaemic control, satisfactory control of blood pressure and lipid levels, anti-coagulation therapy according to the current guidelines, and very importantly, smoking cessation.14 THE ABCS OF FOOT CARE IN DIABETES: ASSESSING THE RISK FACTORS Foot examination and management in the diabetic patient is discussed as an example of risk-factor assessment for diabetes-related foot problems. Healthcare workers should be familiar with the ABCss of diabetes care: HBA1c level (glycosylated haemoglogin) (A), blood pressure control (B), cholesterol (C), smoking cessation (s) and salicylates (s). These refer to the risk factors for diabetes-related complications.15 The ABCS of foot care in patients with diabetes refer to the risk factors for diabetes-related foot problems, as people with diabetes are prone to peripheral neuropathy, peripheral vascular disease and often need special care to avoid problems, especially as they are likely to have abnormal foot structure.16 This can be summarised as follows: A: Anaesthesia (i.e. peripheral neuropathy) B: Blood supply (i.e. peripheral vascular disease)
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C: Care (i.e. routine preventive foot care) S: Structure (i.e. abnormal foot structure). Foot problems are second only to cardiovascular problems in terms of healthcare costs and morbidity in patients with diabetes. The foot risk factors, the ABCS, are important for those over 60 years of age who have had diabetes for 20 years or more, or who have significant macro- and/or microvascular complications. Table 1 summarises the ABCS of foot care and the five As of assessment as a framework for foot care in everyday practice. The patient can be classified as being in danger (red light), with impaired circulation and reflexes, no pulses, skin breakdown; or to be cautious (amber light) because of abnormal findings such as reduced stimuli, reflexes and pulses, skin changes or corns and calluses; or having a healthy foot (green light). Depending on the assessment, appropriate action should be implemented. A CONSULTATION APPROACH FOR DIABETES MANAGEMENT Nigel Stott described a model for a comprehensive and integrative interviewing technique in primary care, which he referred to as the ‘surface anatomy of the consultation’.17 This can also be used as an organised management plan for diabetes care to achieve excellence and successful outcomes and patient satisfaction. The four areas referred to as ABCD are discussed below. A: A patient-centred clinical method is employed in all consultations. This includes exploring both the disease and the illness experience with regard to the patient’s ideas, feelings concerns, fears and expectations and knowledge of the disease and family support, understanding the Table 1. Summarising the five As assessment and the ABCS of foot care.16 Advise about foot care and or foot ware
Arrange reviews and or referrals
ABCS of foot care
Ask about symptoms
Assess the signs
Anaesthesia
Any tingling or numbness?
Sensation
Daily footcare routine Inappropriate foot wear
Podiatry assessment and review action plan
Blood supply
Any claudication or cold feet?
Pulses
Daily footcare routine Inappropriate foot wear
Podiatry assessment and review action plan
Care
What foot care routines are followed?
Nails and skin (thickening, drying, cracking)
Foot-care routines Appropriate foot wear
Education on-going review
Structure
Any foot soreness?
Foot arches, angles and abnormalities when standing
Special foot wear
Orthotic, podiatry and or physiotherapy review
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whole person, enhancing the doctor–patient relationship, finding common ground with regard to management decisions, being realistic and taking economic factors into account, and incorporating the family and community resources to the benefit of the patient. The choice of medications, dosage and dosage adjustments, and side effects and lifestyle modifications are discussed and follow-up visits arranged. Basic investigations are done, such as HbA1c level, full blood count (FBC), thyroid stimulating hormone (TSH), renal function test, lipid levels, liver function test, fasting or random blood glucose test, and urine examination for albumin and ketones. An ECG will be arranged. Appointments will be made where indicated to the ophthalmologist, podiatrist, dietician and other specialities. B: Behaviour-modifying intervention. This includes modifying help-seeking behaviour, diabetes education, individualised diet plan and calorie intake, and modifying lifestyle, especially with regard to an exercise schedule and active weight loss if overweight or obese. Advice on over-the-counter preparations and alternate medicines will be discussed. C: Continuity of care and monitoring other on-going chronic conditions and problems related to diabetes or other conditions. This is also the opportunity to review all blood results, reports, ECGs and the early detection of complications and co-morbidities, and to arrange for their treatment and or referral, especially with regard to cardiovascular and other risk factor assessments. Enquire if the patient is on antiretrovirals, as this will need modification since some of these medications cause hyperglycaemia, hyperlipidaemia, insulin resistance, lypodystrophy and neuropathy. It is important to treat to target with regard to HbA1c, blood pressure and lipid levels and to adjust medications accordingly. A full foot assessment should be undertaken or arranged with the podiatrist. The urine, body mass index and waist circumference are done at every visit. The follow-up visits are usually arranged every three or six months, as indicated. D: Opportunistic intervention for preventive and promotive healthcare. This includes lifestyle issues of diet, exercise, weight loss, alcohol consumption and smoking. Enquire about sexual dysfunction and screen for prostate disorders with PSA estimation. Screen for TB, and advise on mammogram and PAP smear tests. THE DIABETES RECORD To achieve excellence in diabetes and to ensure optimal care, an adequate medical record is essential. In addition to the usual demographic data, it should also contain the following elements: data on the duration of diabetes and family history, home glucose monitoring, habits related to smoking, alcohol, drugs, medications, adherence to lifestyle issues, especially diet and exercise, past medical and surgical history, the
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All current medications are listed as a record for the information of other health professionals the patient may consult, for example the private doctor, or the district hospital or clinic nurse. The plan of action, or management decisions, or changes to the treatment is recorded. The next appointment date is recorded. A copy of the record is retained in the patient file and a copy handed to the patient for the use of other professionals he/she may consult. The above is all contained in the diabetes service record, which is currently in use at the Edendale Diabetes Clinic (Fig. 1). This is presented as a guide and example to achieve optimal diabetes care. In addition to the above diabetes record, the diabetes diary, and sometimes an Accu-Chek 360 View Smartpix print out, various risk-assessment tools are available and should be used to guide on-going management, such as the cardiovascular, type 2 diabetes and chronic kidney disease risk-assessment tool to assess combined risk.18,19 Acknowledgements I acknowledge the contributions made by Dr Faz Mahomed and Dr Rekha Mohan from Greys Hospital, Pietermaritzburg. References 1. 2.
3. 4. Fig. 1. Diabetes service record.
presence of HIV and CD4 count and details of HAART, current or past medications and allergies, and the presence of any cardiovascular diseases or complications. The height, weight, body mass index, waist circumference, and blood pressure and pulse both sitting and lying down, and fasting or random blood glucose tests are done on the day of examination. The presence or absence of carotid or abdominal bruits is noted. A urine dipstix examination is done on the day of the visit to detect albuminuria, ketones, nitrites and any other abnormality. Visual acuity and fundal examinations are arranged. Examination of the cardiovascular and respiratory system, feet, peripheral pulses, nerves, skin, injection sites and thyroid is undertaken at every visit. Sexual health should be enquired about as it may be related to wider vascular diseases. Dental hygiene and health should be recorded and attended to. An ECG is done to exclude any ischaemia or other abnormality. All blood tests are recorded at the six-monthly visit. Any abnormality is acted upon, e.g. potassium, creatinine, urea, lipids, vitamin B12, HbA1c, FBC, TSH and liver function. Appointments with the ophthalmologist, dietician, podiatrist and cardiologist are confirmed or arranged.
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5. 6. 7. 8. 9. 10. 11.
12. 13.
14. 15. 16. 17. 18. 19.
Ali AT, Crowther NJ. Factors predisposing to obesity: a review of the literature. J Endocrinol Metab Diabetes 2009; 14(2): 81–84. Steyn K, Levitt NS, Patel M, Fourie J, Lombard C, Everett K. Hypertension and Diabetes: Poor care for patients at community health centres. J Endocrinol Metab Diabetes S Afr 2008; 13(2): 64–70. Klisiewicz AM, Raal FJ. Sub-optimal management of type 2 diabetes mellitus. A local audit. J Endocrinol Metab Diabetes S Afr 2009; 14(1): 13–16. Amod A, Riback W, Schoeman HS. Diabetes guidelines and clinical practice: is there a gap? The South African Cohort of the International Diabetes Management Practices Study. J Endocrinol Metab Diabetes 2012; 17(2): 85–90. Klisiewicz AM,Huddle KRL, Management of type 2 diabetes mellitus for general practitioners. J Endocrinol Metab Diabetes S Afr 2011; 16(2): 75–84. The 2012 SEMDSA Guidelines for the Management of Type 2 Diabetes. J Endocrinol Metab Diabetes S Afr 2012; 17(1): S1–94. Bonnici F. The silent epidemic of the 21st Century. Address on World Diabetes Day to Diabetes SA as National President. Diabetes Focus 2001; 33: 38–39. Van der Merwe L. Prediabetes: a focus on the role of diabetes education in prevention of type 2 diabetes. J Endocrinol Metab Diabetes S Afr 2011; 16(1): 64–65. Prevention/delay of type 2 diabetes mellitus in high risk individuals. 2012 SEMDSA Guidelines. J Endocrinol Metab Diabetes S Afr 2012; 17(1): 90–92. Certificate in Diabetes Care (CIDC). University of Warwick. Warwick Diabetes Care 2006; 69–77. Mash RJ, Allen S. Managing chronic conditions in a South African primary care context: exploring the applicability of brief motivational interviewing. S Afr Fam Pract 2004; 46(9): 21–26. Bolliger C, van Biljon X. Successful smoking cessation. Strategies for the GP. Mod Med S Afr 2004; 29(9): 44–48. Cambell I. Bute School of Medicine. St Andrews University, Scotland. Guide your patients on their journey with diabetes. Talk given on 24 July 2013. Lifescan CME meeting, Durban. The CDE three-day advanced course in diabetes care for health professionals. Durban, 15–17 August 2008. Phillips P. The ABCSs of diabetic care. Mod Med S Afr 2008; 33(3): 38–42. Phillips P, Evans A. The ABCS of foot care in diabetes: assessing the risk factors. Mod Med S Afr 2010; 35(4): 48–51. Stott NCH. Primary Health Care. Bridging the gap between theory and practice. Springer-Verlag, 1983: 13–20. Blom DJ. Cardiovascular risk assessment. S Afr Fam Pract 2011; 53(2): 121–128. Alssema M, et al. One risk assessment tool for cardiovascular disease, type 2 diabetes, and chronic kidney disease. Diabetes Care 2012; 35: 741–748.
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Keep and Copy Series NON-NUTRITIVE SWEETENERS: GOOD OR BAD? Ruwaida Amod Dietitian, Pietermaritzburg e-mail: ruwaida.jogiat@gmail.com
S Afr J Diabetes Vasc Dis 2013; 10: 139–141
There is much debate surrounding the use of non-nutritive sweeteners (NNS) among consumers and more so in the diabetic population. Previous uses of artificial sweeteners included to improve glycaemic control, achieve energy balance and assist in weight reduction. Current research is examining whether the benefits of utilising NNS to achieve these goals outweigh the risks, primarily on a long-term basis.
H
umans have a natural preference for foods that taste sweet. The most commonly used substance to sweeten foods is sucrose. In 2010 about 300 million people were estimated to have type 2 diabetes mellitus (T2DM) globally and this number is expected to rise to nearly 450 million by 2030. In 2009 the American Heart Association (AHA) released a scientific statement calling for a reduction in sugar intake as a way of decreasing obesity and heart disease.1 A high-sugar, high-fat diet is one of the factors to be blamed for the rise in T2DM and obesity.2,3 As a result of the negative effects of sugar, an alternative many patients are consuming is nonnutritive sweeteners (NNS).2 However, how useful NNS are in improving dietary choices is controversial.4 According to the Academy of Nutrition and Dietetics, NNS have caused many concerns among healthcare practitioners and the general public.5 The Calorie Control National Consumer Survey which was conducted in the USA found that of nearly 200 million consumers in the USA, 85% of the population use NNS, and 8–11% of consumers do not use NNS due to concerns over their health.6 DEFINITION OF A NNS A NNS offers little or no energy when it is ingested. They are also known as low-calorie sweeteners, artificial sweeteners, non-caloric sweeteners and
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intense sweeteners.5,7 An ideal artificial sweetener should not affect glucose homeostasis and have no hormonal effects pertaining to hunger.4 NNS are many times more intense than sucrose, at approximately 30 to 13 000 times sweeter.2 As an example, sucralose, which is one of the most current sweeteners on the market, is about 600 times sweeter than sucrose.8 The first NNS to be introduced to the commercial market was saccharin in the late 1800s.9 Common artificial sweeteners currently on the market are aspartame, sucralose and acesulfame-K.10 A new NNS that has emerged on the market, Stevia, has extracts from the plant Stevia rebaudiana and shows great promise as a natural NNS.7 NNS can be found in a number of commercially manufactured products such as beverages, ice cream, chewing gum, chocolate, jams and yoghurts.2 USES OF NNS Some of the most common uses of NNS include: • to sweeten foods so that individuals with diabetes can enjoy a variety of foods and beverages without the increases in kilojoules in the diet2,9 • to achieve the aim of good blood glucose control • to achieve energy control in patients who are aiming to lose weight • to increase the palatability of foods.2,5,9
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GOOD Many healthcare practitioners have proposed that NNS provide a beneficial effect in food and beverages.11 According to the American Dietetic Association (ADA) ‘Sugar alcohols and NNS are safe when consumed within the daily intake levels established by the Food and Drug Administration (FDA)’. For patients with diabetes, choosing an NNS rather than sucrose can assist with regard to moderating carbohydrate intake.5 The Academy of Nutrition and Dietetics concluded in a review conducted in 2010 that NNS do not affect glycaemic response in people with diabetes.5 In patients with TD2M who had the NNS sucralose added to their diet, fasting blood glucose and insulin responses were not affected.4 Hubrich stated that individuals who use NNS have an increased intake of fruit and vegetables and a lower intake of fat, thereby indicative of a healthier diet. Furthermore, in studies carried out in individuals with TD2M, those drinking diet cool drinks were found to consume less refined sugar, fats and processed meats.6 Bellisle et al. conducted a meta-analysis of 16 randomised controlled trials in which sugar was replaced with NNS. This resulted in a 10% reduction in energy intake on a daily basis and an average of 0.2 g/week of weight loss. There was also less weight gain after weight loss. A study of individuals who had maintained > 10% weight loss for over five years showed that they consumed less dietary fat and more artificially sweetened beverages. These individuals were also more physically active.6 In a study conducted by Mozaffarian et al. cited by Malik et al., it was found that diet cool drink was associated with weight loss when combined with changes in diet and lifestyle.1,7 This is due to the fact that food and lifestyle changes are intertwined.3,9 This is supported by Grotz et al., who state that NNS can be used to decrease the energy intake of the diet as well as assist in maintaining body weight.8 As the management of obesity is multifactorial, there is no conclusive evidence to suggest that the use of NNS causes weight gain in adults.2 More specifically, the NNS sucralose is safe to use during pregnancy and thus may be a viable option for gestational diabetics attempting to lose weight, as well as in assisting to achieve an improved glycaemic control in this patient population.8 Furthermore, no birth defects were noted in mice that ingested high doses of sucralose.8
One possible explanation for the increase in weight is that the subjects used in these studies might have been at risk for weight gain. Another explanation is that substituting foods and beverages containing NNS with foods containing nutritive sweeteners may cause the subjects to overeat.1,12 A few studies have reported positive associations between the consumption of diet cool drinks, weight gain and an increased risk of the metabolic syndrome. However the authors state that these observations may have been due to reverse causation, as diet cool drink consumption is higher in individuals with T2DM than in those without T2DM.1 According to Bellisle et al., NNS may have a lower satiety than sugar. This could result in the body being tricked into overeating, or in the overstimulation of taste receptors, thereby creating a sweet-taste addiction.6,13 This is particularly relevant to intense sweeteners that are 160–13 000 times sweeter than sucrose.1 Malik et al. also state that diet cool drink may enhance appetite by cephalic phase stimulation. This area however remains controversial. There have been some reports that long-term use of NNS can lead to side effects such as dizziness, nausea, cancer (lung, bladder and brain tumours) chronic respiratory disease, hallucination, hypersensitivity and heart failure.10 Another side effect of some NNS is that they are poorly absorbed and are fermented in the gastrointestinal tract, leading to lower intestinal fermentation byproducts such as gas.8 This leads to abdominal discomfort.
BAD Recent data suggest that NNS may have physiological effects that alter appetite and or glucose metabolism.12 There have been various epidemiological studies conducted using NNS, primarily in the form of diet cool drinks.4,12 Diet cool drinks are flavoured with NNS such as aspartame, sucralose, saccharin, acesulfame potassium and neotame.1 Results of these studies demonstrated increased weight gain, the metabolic syndrome and diabetes in subjects tested.12
CONCLUSION To date there is no conclusive evidence to support or refute the use of NNS, particularly in the diabetic patient population. It is anticipated that further long-term studies will be required in order to determine the toxicity and carcinogenicity of NNS. Human studies would also be useful to confirm the safety of consuming NNS on a long-term basis. More specifically, in the diabetic patient population, studies are required to assess whether NNS have an effect on insulin sensitivity or glucose homeostasis.
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RECOMMENDATIONS According to Shankar et al., consumers do not have adequate information to make informed choices with regards to NNS. Consumers should be advised to be cautious with regard to the use of NNS. It is important that symptoms related to allergies and intolerances be monitored, even if NNS are consumed in small quantities.2 The use of NNS in conjunction with dietary management of diabetes is to optimise glycaemic control. This is widely practiced by healthcare practitioners on a global scale.2 To ensure optimal health, however, it is recommended that minimal quantities of both NNS and sucrose be consumed. More emphasis should be placed on a balanced diet that includes whole grains, vegetables, fruits, legumes, low-fat dairy products and lean meats. The use of processed foods should also be limited.2,3
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4.
Key messages 5.
â&#x20AC;˘ The use of NNS in T2DM is controversial. â&#x20AC;˘ New varieties of NNS are emerging that originate from plant sources. â&#x20AC;˘ More research is required in order to determine the long-term effects of NNS in human subjects. References 1. 2. 3.
Malik VS, Hu FB. Sweeteners and risk of obesity and type 2 diabetes: the role of sugar-sweetened beverages. Curr Diab Rep 2012; 12: 195â&#x20AC;&#x201C;203. Shankar P, Ahuja S, Sriram K. Non-nutritive sweeteners: Review and update. Nutrition 2013; 1â&#x20AC;&#x201C;7. Sievenpiper JL, Souza RJ. Are sugar-sweetened beverages the whole story ?Am J Clin Nutr 2013; 98: 261â&#x20AC;&#x201C;263.
6. 7.
8. 9.
10. 11. 12. 13.
Brown AW, Bohan Brown MM, Onken KL, Beitz DC. Short-term consumption of sucralose, a non-nutritive sweetener, is similar to water with regard to select markers of hunger signaling and short-term glucose homeostasis in women. Nutr Res 2011; 31: 882â&#x20AC;&#x201C;888. Position of the Academy of Nutrition and Dietetics: Use of Nutritive and Nonnutritive Sweeteners. J Acad Nutr Dietetics 2012; 112: 739â&#x20AC;&#x201C;758. Bloomgarden ZT. Nonnutritive sweeteners, fructose and other aspects of diet. Diabetes Care 2011; 34: e46â&#x20AC;&#x201C;e51. Gardener C, Wylie-Rosett J, Gidding SS, Steffen LM, Johnson RK, Reader K, Lichtenstein AH. Nonnutritive sweeteners: current use and health perspectives. Diabetes Care 2012; 35: 1798â&#x20AC;&#x201C;1808. Grotz VL, Munro IC. An overview of the safety of sucralose. Regulatory Toxicol Pharmacol 2009; 55: 1â&#x20AC;&#x201C;5. Wiebe N, Padwal R, Field C, Marks S, Jacobs R, Tonelli M. A systematic review on the effect of sweeteners on glycemic reponse and clinically relevant outcomes. BMC Med 2011; 9: 1â&#x20AC;&#x201C;18. Shrivastav A, Srivastava S. Human sweet taste receptor: complete structure prediction and evaluation. Int J Chem Analyt Scie 2013; 4: 24â&#x20AC;&#x201C;32. Swithers SE. Artificial sweeteners produce counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab 2013: 1â&#x20AC;&#x201C;11. Brown RJ, Rother KI. Non-nutritive sweeteners and their role in the gastrointestinal tract. J Clin Endocrinol Metab 2012; 97(8): 2597â&#x20AC;&#x201C;2605. Rudenga KJ, Small DM. Amygdala response to sucrose consumption is inversely related to artificial sweetener use. Appetite 2012; 58: 504â&#x20AC;&#x201C;507.
Submit case reports to the South African Journal of Diabetes and Vascular Disease: www.diabetesjournal.co.za Specifications: Total word count 1 500; maximum three illustrations/images Title Abstract t JODMVEJOH XIZ UIF DBTF JT OPWFM PS NFSJUT SFWJFX Describe the case according to timeline t NFEJDBM IJTUPSZ t SFMFWBOU EBUB GSPN DMJOJDBM JOWFTUJHBUJPOT t JOUFSWFOUJPOT Discussion on clinical relevance t XIZ UIJT JT OPWFM PS XPSUI SFWJFX t DPNQSFIFOTJWF MJUFSBUVSF SFWJFX t EFSJWF OFX LOPXMFEHF t QSPWJEF SFDPNNFOEBUJPOT References Types of case report 1. Diagnosis related t VOVTVBM PS OFX EJTFBTF t VOVTVBM QSFTFOUBUJPO PG LOPXO EJTFBTF t OFX NFUIPET PG EJBHOPTJT t VOVTVBM PS OFX BFUJPMPHZ t VOFYQFDUFE BTTPDJBUJPO CFUXFFO EJTFBTFT PS TZNQUPNT
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2. Management related t OFX PS JNQSPWFE USFBUNFOU UZQF t OFX PS SBSF TJEF FòFDUT PS DPNQMJDBUJPO PG USFBUNFOU Common problems with case reports t UJUMF JODMVEFT SFEVOEBOU XPSET F H ADBTF SFQPSU BOE SFWJFX PG UIF MJUFSBUVSF t DBTF JT OPU XPSUI SFQPSUJOH o POMZ TMJHIU WBSJBUJPO JO EJBHOPTUJD PS UIFSBQFVUJD BQQSPBDI t UIFSBQFVUJD BQQSPBDI XJUIPVU TUSPOH SBUJPOBMF BOE OP JNQBDU PO PVUDPNF t FYDFTTJWFMZ MPOH NBOVTDSJQU t FYDFTTJWFMZ DPNQMJDBUFE DBTF t MBDLT TDJFOUJÜD FWJEFODF t OP QSPPG PG EJBHOPTJT t OP BEEJUJPOBM PS JODSFNFOUBM LOPXMFEHF t PWFS HFOFSBMJTBUJPO t PWFS BNCJUJPVT DPODMVTJPO OPU TVQQPSUFE CZ FWJEFODF
SAJDVD The South African Journal of DIABETES & VASCULAR DISEASE
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Highly Effective 1,2 Low Risk of Hypoglycaemia and no Weight Gain 1-4 Proven Outcomes 1,5
For full prescribing information, refer to package insert approved by medicines regulatory authority. DIAMICRON 速 MR 60 mg Tablets. Gliclazide 60 mg. Reg. No. 43/21.2/0957. NAME AND BUSINESS ADDRESS OF THE HOLDER OF THE CERTIFICATE: SERVIER LABORATORIES SOUTH AFRICA (Pty) Ltd. Reg. No. 72/14307/07. Building Number 4, Country Club Estate, 21 Woodlands Drive, Woodmead 2191. PO Box 930, Rivonia 2128, Republic of South Africa. Tel: +27 (0) 861 700 900. Fax: +27(0)11 525 3401. References: 1. The ADVANCE Collaborative Group. N Engl J Med. 2008; 358: 2560-2572 2. SEMDSA Guidelines 2012 3. Al Sifri S et al. Int J Clin Pract. 2011;11 :1132-1140 8. 4. Aravind SR et al. Curr Med Res Opin. 2012;28:1-8. 5.Perkovic V et al. Kidney Int. 2013 Jan 9. Epub ahead of print.
A leading partner in the field of diabetic research www.servier.com
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Diabetes Personality LOVE AND PASSION MAKE ALL THE DIFFERENCE WHEN MANAGING PATIENTS WITH DIABETES S Afr J Diabetes Vasc Dis 2013; 10: 143–144
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r Ashley Murugan is this year’s winner of the Servier award for Community Involvement in Diabetes, presented each year at the Centre for Diabetes and Endocrinology’s (CDE’s) annual Postgraduate Forum in Diabetes Management. He describes himself as ‘shocked’ to have received the award, having opened his diabetes clinic only in 2011. ‘So receiving the Servier community award in 2013 is a huge achievement for me. When I first became involved in community work, my aim was to make a difference in people’s lives, not to be recognised or win an award of any kind. My work is motivated purely by love and passion. Winning the award was therefore totally unexpected. I also offer my heartfelt thanks and gratitude to all my staff members for their on-going effort and dedication.’ Dr Murugan is a general practitioner with a special interest in diabetes management. ‘It is well known that the management of diabetes in South Africa is a major health challenge. Since entering private practice in 2010, I’ve seen the prevalence of diabetes and its complications increase at an alarming rate, a phenomenon even more pronounced in rural communities where access to medical care and resources is limited. This prompted me to open my diabetes clinic, the Zululand Centre for Diabetes and Related Illnesses, in February 2011’, he says. Dr Murugan feels that the face of diabetes is constantly changing and that there are still massive gaps in many fundamental aspects of diabetes management. ‘It is well known that the diabetes epidemic is associated with long-term complications, including
nephropathy, retinopathy, neuropathy, cardiovascular disease, stroke and death. All of these can be minimised by timely and effective treatment of elevated blood pressure, lipids and blood glucose levels. Very importantly, individuals with undiagnosed type 2 diabetes are also at significantly higher risk for these complications.’ ‘Sadly, in South Africa a large proportion of people with diabetes are not routinely monitored either for the condition itself or its complications. This is especially true for people living in rural communities such as the one where I work, where the opportunity to commence early treatment is often missed. One way to address this is diabetes screening, which has become the cornerstone for early diagnosis within my clinical setting.’ Challenges and rewards It’s Dr Murugan’s experience that a substantial proportion of diabetic patients fail to comply with some or all aspects of diabetes management. ‘When it comes to assisting a patient better understand his/ her diagnosis while simultaneously enhancing compliance, I face major challenges on a daily basis. The diagnosis itself often carries significant emotional issues. In a newly diagnosed diabetic, much additional work may be required to address his/her perceptions of how the condition will place limitations on his/her life.’ ‘I often find that non-compliance is common in older patients (those aged above 55 years), who are asymptomatic at the time of diagnosis and have no apparent complications. In others, the absolute fear
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of the disease and its complications is often a trigger factor contributing to non-compliance. It is also imperative to acknowledge that very often patients have other priorities that they consider more important than diabetes, such as their family, an ill spouse, work stresses and financial issues.’ ‘Over the past two years, I have come to understand that every single person I see during a consultation has a whole lot more to him/her than is visible to me. In order to promote and foster compliance successfully, it is imperative to understand patients’ perceptions of compliance difficulties. The challenge lies in finding appropriate ways to enable them to open up and discuss their stresses and difficulties.’ What is the most satisfying and rewarding aspect of Dr Murugan’s work? ‘The smile on a patient’s face when he/she achieves milestones in his/her diabetes management that he/she never thought possible at the
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time of diagnosis, is satisfaction enough for me. It feels good to be instrumental in assisting diabetic individuals improve their knowledge, skills and confidence, thus enabling them to take control of their condition by integrating effective self-management skills into their daily lives. Helping to achieve positive outcomes like this motivates and drives me to continue with the community initiatives in which I am currently involved.’ ‘We have come a long way in diabetes management with regard to patient care’, he observes in conclusion. ‘Likewise, there have been some remarkable therapeutic interventions that enable us to manage our patients better. Hopefully, one day soon, there will be a cure for diabetes. But until then, all I can do is offer help and hope to individuals within the community in which I work.’ P Wagenaar
A diabetes event in the Uthulungu municipality on 24 October 2013.
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DIABETES NEWS
Diabetes News
Novo Nordisk Changing Diabetes® cycle relay
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lowing winds and pouring rain were no match for the 16 cyclists who departed from Johannesburg on Thursday morning 7 November with the intension of cycling 1 200 km to George in a bid to raise funds and awareness for diabetes. The 2013 Changing Diabetes cycle relay started at Novo Nordisk offices in Rivonia, Johannesburg, and the teams arrived in George 48 hours later. The four exciting teams that took part in this gruelling 48-hour, non-stop marathon included: Team Novo Nordisk (all with type 1 diabetes), representing the event’s sponsors; Team C4D (Cycle for Diabetes); Bonitas procycling team; and a celebrity team that was headed by legendary former Springbok, Joel Stransky and Genelle van der Riet, who came third in her category in this year’s Iron Man competition. Joel Stransky said at the finish ‘cycling isn’t just a thrilling sport, it is also an amazing way to help others’. That’s what the annual Changing Diabetes® cycle relay is all about. Every year in November, local and international teams, including many individuals living with both type 1 and type 2 diabetes, take this opportunity to give back to others through something they’re passionate about. The mission for this year’s challenge was to raise funds to ensure that children from disadvantaged communities in the Western Cape have reliable access to the diabetes medication they need; and the message? With appropriate treatment and lifestyle management, people living with this chronic
Dr Jacques van Staden with the kids that benefit from the money raised. They were at the finish of the 48-hour Changing Diabetes cycle relay.
condition can have long, active, engaged and healthy lives. Speaking at the Garden Route mall in George, Novo Nordisk marketing manager David Broomfield said ‘last year I flew to George but this year I decided to drive as part of the support team, and I must say, I have a new respect for these guys’. Broomfield was speaking before handing over a cheque to the tune of R130 000.00 to the man behind the event and programme for the children, George general practitioner, Dr Jacques van Staden. Accepting the cheque, Dr van Staden said he established the C4D team when
he realised what a struggle it was for some of the families in his community to afford diabetes medication for their children. ‘While taking care of these children on a day-to-day basis, I know how important this medication and education is’, said van Staden. ‘In events like these, you know that at some point you’re going to suffer. You must just have the determination to get past that and keep going. It’s the result, for both yourself and others, that makes it all worthwhile.’ For further information about the Changing Diabetes® cycle relay, Novo Nordisk and diabetes, visit www.novonordisk.com/ www.facebook.com/ChangingDiabetesZA
Dr van Staden and the team.
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Novo Nordisk – Accu-Chek® Diabetes Update Symposium The journey towards glycaemic control: is it influenced by drug of choice or inertia?
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ovo Nordisk and Roche Diagnostics co-hosted the Diabetes Update Symposium, a satellite session affiliated to the August 2013 Centres for Diabetes and Endocrinology (CDE) meeting held in Boksburg. Novo Nordisk celebrated a milestone 90th birthday in 2013. In opening remarks, Dr Timmy Kedijang (general manager, Novo Nordisk SA) reaffirmed that as one of the first companies to produce insulin, Novo Nordisk remains committed to innovation in diabetes care in a socially, environmentally and financially sustainable manner.
The dilemma of positioning incretins in type 2 diabetes Dr Aslam Amod, endocrinologist Pharmacological options for the management of diabetes have increased significantly during recent years, with the development of new drug classes and the registration of many individual agents within these classes. An existing evidence base for treatment options places metformin for use in first-line therapy and the addition of sulfonylureas (SUs) for use in second-line therapy. Classes with an evidence base for use as both second- and third-line therapy are insulin, DPP-4 inhibitors, GLP-1 agonists, alpha glucosidase inhibitors and TZD. A conundrum is thus placed in the hands of the treating practitioner, as this evidence base furnishes 50 possible therapy combinations between classes and 1 440 therapy combinations between individual agents. Recently updated guidelines from the ADA, EASD and AACE/ACE all provide multiple therapy options. This is of little assistance to practitioners who are not diabetologists. The 2012 SEMDSA treatment algorithm for type 2 diabetes offers a narrower range of preferred therapies, with alternative therapies for special circumstances. Dr Amod outlined an ideal diabetes therapy, his ‘utopiglutide’, as being strong in glycaemic control, with established reductions in microvascular, macrovascular and mortality outcomes. The therapy
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would result in no hypoglycaemia or side effects, weight loss (or no weight gain) and other non-glycaemic benefits. This therapy would also be affordable, with high patient acceptability. Dr Amod went on to contextualise the well-validated and newer therapeutic options in attaining a balance between the benefits of glycaemic control and improved outcomes against the disadvantages of hypoglycaemia, weight gain and side effects. Metformin should be the cornerstone of therapy. Extensive experience and data show a strong glycaemic effect, with macrovascular benefit. UKPDS data indicate a mortality risk reduction of 40%. Metformin is safe, weight neutral/beneficial and has high patient acceptability. Of importance, metformin is inexpensive, with many affordable generics available. However, metformin displays no microvascular benefits, gastrointestinal intolerance is experienced in 10 to 30% of patients, and currently there are concerns of increased mortality when used in combination with SUs. Metformin is the preferred first-line therapy as per the 2012 SEMDSA guidelines. Should the patient prove intolerant, he/she could try the extended-release formulation. If intolerance remains an issue, it can be replaced with any of the following: gliclazide or glimepiride, a DPP-4 inhibitor, acarbose or a GLP-1A injectable. Upon metformin failure, the preferred SEMDSA recommendation entails adding an SU to current metformin therapy. It is a common perception that SUs are not safe, with a propensity to weight gain, risk of hypoglycaemia and increased cardiovascular events. The second-generation SUs (gliclazide, glimepiride and glipizide) are newer and safer options. These have a strong glycaemic effect with reduced microvascular and mortality outcomes, have high patient acceptability, and are inexpensive. Gliclazide provides better results for hypoglycaemia (GUIDE study) and is weight neutral (ADVANCE study). Gliclazide is also the only SU that is not associated with an increased cardiovascular risk.
In patients with renal concerns, glibenclamide is the most dangerous and should not be used where the glomerular filtration rate (eGFR) is < 60 ml/min. Dr Amod suggests gliclazide or glimepiride as the SU of choice, based on efficacy, safety, evidencebased outcomes and cost. Acarbose or an incretin should be used in lieu of an SU in cases where frequent or severe hypoglycaemia occurs, circumstances exist wherein the risk of severe hypoglycaemia and its consequences would be significant and/or catastrophic (e.g. workers with frequent rotating shifts or heavy machinery operators), or weight gain has occurred and carries unacceptable obesity-related morbidity risks. Upon failure of second-line therapy, Dr Amod recommends the addition of basal insulin to the existing therapy. Insulin is strong in glycaemic benefit, as well as microvascular, macrovascular and mortality benefit. However, high rates of hypoglycaemia and weight gain result in very low patient acceptability. Acarbose or an incretin should be used in lieu of insulin for the same reasons mentioned with SU substitution. Other circumstances where insulin therapy may not be desirable include insulin allergy, as well as failure or inability to master injections or self-titration. DPP-4 inhibitors have a moderate glycaemic effect, with the advantages of low rates of hypoglycaemia and being weight neutral. Adverse events are similar to placebo; however renal, hepatic and dermatological concerns have been raised. DPP-4 inhibitors are expensive, although patient acceptability is high. GLP-1A shows strong glycaemic benefit, but there are currently no benefit data for microvascular, macrovascular and mortality outcomes. There are low rates of hypoglycaemia, unless used in combination with an SU, and the weight benefit is variable with a mean weight loss of 2.5–3.5 kg. Side effects of GLP-1A are predominantly gastrointestinal. These agents are very expensive, with variable patient acceptability. Concerns have been raised surrounding increased risk of pancreatitis and pancreatic cancer with the use of DPP-4 inhibitors
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and GLP-1A. An ADA/EASD/IDF statement released 28 June 2013 found that there is insufficient information to modify current treatment recommendations for GLP-1A.
Initiating insulin in the world of incretins: when is the right time? Prof Stefano Del Prato, Department of Endocrinology and Metabolism, University of Pisa, Italy Insulin, if used in the proper manner, should allow for best HbA1c control in hypothetical situations; yet defining the right time to initiate insulin therapy poses great difficulty. Prof Del Prato questioned whether insulin therapy is already inappropriately delayed. Clinical inertia is a major contributor to this delay, due to an unbalanced assessment of hypoglycaemia, weight gain, chronic hyperinsulinaemia and limited understanding of the role functional beta-cell mass loss plays in disease progression. Another confounding factor is physician concerns and underestimation of the patient’s tolerance for regular testing and injections. Translating these considerations into the real-world setting, Prof Del Prato presented results from the A1chieve study. This global cohort of more than 66 000 participants saw approximately 45 000 patients initiated on insulin during the course of the study. In terms of glycaemic efficacy, a reduction in HbA1c level of 2.1% was seen from baseline to 24 weeks, with 30–35% of patients achieving target at 24 weeks. There was no significant difference in hypoglycaemia between baseline and 24 weeks, and a weight gain of 100 g was seen over this period. Weight gain was dependant on the type of insulin used. Insulin detemir was equated with an increased weight-loss trend, whereas the other insulin formulations were associated with weight gain. In terms of self-assessed quality of life, a significant improvement was reported over the study period. Prof Del Prato considered criteria for selection of insulin or a GLP-1A as potential treatment in the patient failing metformin. Insulin is the therapy of choice in those with high HbA1c levels; in the patient with a focus on body weight reduction, a GLP-1A is more appropriate. There may, however, be some logic in combining the two agents, as there are many synergies between the function of insulin and the GLP-1 receptor agonists. The primary effect
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of decreased fasting glucose is gained from both agents. Decreased inter-prandial glucose is seen with basal insulin; and GLP-1A use effects decreased fasting glucose. Mechanisms of action shared by both agents include decreased hepatic glucose production and decreased glucagon secretion. Other mechanisms of basal insulin are increased insulin concentration and increased non-glucosedependant endogenous insulin; whereas GLP-1A has the benefit of increased glucosedependant insulin secretion and increased satiety, with decreased food intake and delayed gastric emptying. In his closing statements, some indications for initiation of insulin were considered. ‘If the patient is symptomatic at the time of diagnosis, initiate with insulin therapy. When HbA1c level is under control, with improved well-being of the patient, halt the insulin and introduce a different agent. Then, as disease progression occurs, insulin can be reinitiated in the patient with improved expectations and experience.’
Minimising adverse treatment outcomes: weight, hypoglycaemia and treatment adherence Prof Stefano Del Prato, Department of Endocrinology and Metabolism, University of Pisa, Italy Prof Del Prato opened his second presentation with the thought that a conservative approach to management of diabetes leads to clinical inertia. In support of this statement, he illustrated a typical timeline of the diabetic patient between diagnosis and pro-active HbA1c control: diet and exercise are therapy of choice for the initial two-and-a-half years. During this time, the HbA1c level increases and the patient is initiated on an oral agent as monotherapy. Glycaemic control worsens and the oral agent dose is up- titrated, until the addition of a second oral agent is required in combination therapy. Upon failure of combination therapy, basal insulin is added to the regimen. The average time period between diagnosis and insulin initiation is eight years, representing an eight-year period of avoidable glycaemic burden. Furthermore, insulin initiation at this late stage of disease progression generally has a high rate of complications, with 30% of patients displaying prior cardiovascular disease by this stage.
A proactive approach to diabetes management is recommended by Prof Del Prato, whereby individual targets are set at diagnosis and reacted to if not achieved. In this manner, long-term outcomes are improved, with fewer complications. Insulin should be considered an interventional option throughout the timeline of diabetes disease progression, and Prof Del Prato questioned why it is not being more commonly used. Concerns surrounding insulin use are hypoglycaemia, weight gain and adherence to therapy. In terms of hypoglycaemia, the peak plasma concentration of insulin detemir is preferable to that of NPH insulin, with the advantage of fewer overall and nocturnal hypoglycaemic events. ‘Weight worry’ is a common psychological barrier preventing initiation of insulin therapy. It has been postulated that with insulin use, a 1% decrease in HbA1c level equates to a weight gain of 2 kg. Insulin glargine has a neutral effect on body weight. Insulin detemir activates cerebrocortical β-activity in overweight humans and may therefore have some potential to condition appetite. Data from A1chieve suggest that switching to insulin detemir from NPH insulin or glargine is associated with a greater reduction in HbA1c level, as well as a greater proportion of patients achieving target. The switch to detemir also resulted in small weight loss. Adherence is a considerable problem in the management of type 2 diabetes, with approximately twothirds of patients taking < 80% of doses. It is postulated that a 10% improvement in adherence translates to an additional 0.15% reduction in HbA1c level. Minimising hypoglycaemia and weight gain are effective measures to improve adherence.
Hypoglycaemia: diving, driving and flying Dr Angela Murphy, endocrinologist Presenting existing data on the effects of hypoglycaemia on driving, diving and flying, Dr Murphy drew the following conclusions. Hypoglycaemia does affect driving performance, with a trend that diabetic patients have increased risk for motor vehicle accidents, but accidents caused directly by diabetics are rare. Generally, there are no restrictions placed on the driving of private vehicles. However, requirements for commercial driving include a 24-month review to establish that no hypoglycaemia has
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occurred, there is regular monitoring, with an understanding of the risks of hypoglycaemia, and that there are no other dangerous co-morbidities. It is recommended that drivers test their blood glucose levels prior to departure and not drive if it is < 4.0 mmol/l. Driving is not recommended for 45â&#x20AC;&#x201C;60 minutes following non-severe hypoglycaemia. Flying may affect blood sugar levels due to changes in time zones. Flying east shortens the day and may require less insulin, with a possible risk of hypoglycaemia. The patient flying west has a longer day that may require more insulin, with a possible risk of
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hyperglycaemia. Insulin pump function may be affected by changes in altitude; a pressurised cabin may slightly increase insulin delivery, with a slight decrease in delivery upon descent. The South African Civil Aviation Authority has an extensive diabetes mellitus protocol for pilots. See http://www. caa.co.za/resource%20center/ASO/Avmed/ Docs/Diabetes%20protocol.pdf. Diving poses unique challenges to the diabetic patient. The diving environment implies an inability to rest, eat or drink in cold conditions. There are also the dangers of decompression and diagnostic confusion. However, there are no data to suggest that
diving is more hazardous in the patient with diabetes. Guidelines from various diving organisations (e.g. DAN, PADI) recommend waiting three months after initiation of or changes to medication and waiting one year after a severe hyper/hypoglycaemic incident that required assistance. The scope of diving should be to a depth of less than 30 m with a duration of less than one hour. Patients should avoid long, hard, cold dives and wrecks and caves. The dive buddy should be educated about diabetes, but not have diabetes him/herself. G Hardy
Sponsored by Novo Nordisk
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CDE WATCH SUMMARIES
2013 UPDATE FROM THE CENTRES FOR DIABETES AND ENDOCRINOLOGY 15th Postgraduate Forum in Diabetes Management Contributor: P Wagenaar
Insulin: friend or foe? Dr Aslam Amod, endocrinologist, Centre for Diabetes, Endocrinology and Metabolic Disease, Life Healthcare Chatsmed Garden Hospital, Durban Insulin can be a friend. It can protect and save lives, but it can cause harm and even kill. This was Dr Aslam Amod’s cautionary message to delegates at the 15th CDE postgraduate forum in diabetes management, which took place at the Birchwood Hotel and Conference Centre, Boksburg, in August. There is no disputing that the discovery of insulin has changed the lives of type 1 diabetes patients forever. ‘It was one of the most dramatic moments in medicine, and for type 1 diabetes patients, insulin therapy remains the only available option. It is to all intents and purposes, hormone replacement therapy with numerous benefits, including near normalisation of metabolism and improved long-term survival. But type 2 diabetes is another animal entirely and different for different people.’ Ascertaining the role of insulin in type 2 diabetes begs the questions, ‘Why, when and in whom? Should it be introduced at diagnosis, as an early elective option or as a last resort? How does it compare with other therapies in respect of benefit and risk, both glucose related and non-glucose related? Based on pathophysiology, can we define specific subgroups and disease stages where it is indicated?’ The profound heterogeneity of type 2 diabetes makes answering those questions a challenge. ‘Reality and randomised controlled trials are very different from each other’, said Dr Amod. ‘Yet all diabetes patients are lumped together, despite a multitude of different disease pathways, discordant expert opinion and a lack of simple measures of beta-cell function.’
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August 2013
Turning to the evidence base, Dr Amod cited the 1978 UGDP study, which showed no difference in fatal cardiac events after 14 years in insulinised versus non-insulinised patients. ‘The Kumamoto study found that while insulin had a beneficial effect on microvascular complications, it had no effect on macrovascular parameters. This was borne out by the UKPDS, which again found only microvascular benefit, but no macrovascular or mortality benefit. Insulin was not superior to the sulphonylureas in this study. The DIGAMI-2 study, which focused on the prevention of secondary complications following acute myocardial infarction (MI), found that insulin actually increased the risk of stroke and re-infarction. The ACCORD study showed that insulin had no effect on rates of major cardiovascular events, death or microvascular complications. In the VADT studies, insulin was associated with increased mortality and no significant reduction in cardiovascular events, while ORIGIN showed no difference between standard care and early insulin therapy. ‘This means that in 2013, we have no formal evidence base that insulin improves the long-term prognosis of patients with type 2 diabetes compared to other therapies’, continued Dr Amod. ‘The glucose hypothesis central to type 1 diabetes is not upheld when we look at the cardiovascular
disease and mortality associated with type 2 diabetes. Many alternative treatments are available and the long-term survival improvement we see is not due to insulin. There is no evidence that it preserves betacell function and it is associated with only partial normalisation of metabolism.’ Further to the UKPDS finding that intensive glucose-lowering in the early stages of type 2 diabetes has a long-term ‘legacy effect’, the use of insulin has increased dramatically. ‘But there have been no improvements in HbA1c levels, and in fact HbA1c levels are worse with insulin than with other therapies. Given the absence of benefit, it begs the question, “Can insulin be harmful?” Epidemiologically it has traditionally been associated with a two- to three-fold greater mortality rate than other therapies, and recent surveys suggest that patients on insulin have a worse prognosis. In terms of pathophysiology, endogenous and exogenous insulin are different, with the latter carrying a much higher peripheral:portal gradient risk. “Lean and thirsty” patients will do well, but the “obese and hungry” will not. Many of the latter just continue to put on weight, something known as the “insulin sink syndrome”.’ Insulin has been shown to be pro-atherogenic in vitro, which might explain the absence of microvascular benefit. No randomised, controlled trials have shown car-
TABLE OF CONTENTS Insulin: friend or foe?................................................................................................................................ 145 Novel and emerging basal insulin preparations.......................................................................................... 146 Diabetic nephropathy: countdown to disaster? The Ascending Star lecture................................................ 146 Neuropathy: a diagnosis?.......................................................................................................................... 147 The debate renewed… Is bariatric surgery a ‘cure’ for diabetes?............................................................... 147
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diovascular benefits for insulin, while the weight gain associated with intensive insulin therapy has a greater negative impact on patient longevity than diabetes itself. In addition, insulin increases the risk of severe hypoglycaemic episodes three-fold, and severe hypoglycaemia is a stronger risk factor for a cardiovascular event than a previous MI. ‘Insulin can transform well-selected patients, but how do you select them, given that there is no one set of criteria? In the absence of these, all insulin use must be empirical. It has not been shown to improve prognosis and the case for early elective insulin therapy is not established. We also need to move away from looking at it as the “ultimate treatment” and must never stop thinking about the bigger picture when it comes to diabetes management. Patients on insulin might not need to remain on it forever’, he concluded. ‘Whether insulin is a friend or foe in type 2 diabetes ultimately lies with clinicians and individual patients and will depend on multiple factors. Individualisation of treatment remains key.’
Novel and emerging basal insulin preparations Dr Stan Landau, specialist physician, Centre for Diabetes and Endocrinology, Johannesburg Basal insulins form the backbone of insulin therapy in type 2 diabetes and their use has increased dramatically in recent years. Though well tolerated, safe and easy to administer, those currently available still have limitations and even in the era of the analogues, glargine and detemir, only 41% of patients achieve HbA1c levels below 7%. In addition, neither agent provides full 24-hour peakless insulin cover, neither has eliminated the risk of nocturnal hypoglycaemia, and successful treatment still requires careful individual titration, given persistent intra-patient variability. ‘We need to improve glycaemic control. Hypoglycaemia, which is an insulin problem, limits our treatment mandate and simply putting patients on insulin does not automatically equate to an improvement in glycaemic control. Hypoglycaemia is associated with worse cardiovascular outcomes and hypoglycaemic episodes are dangerous even in low-risk patients. Ideally, we need an insulin with a flat action profile, reduced or
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no variability in its glucose-lowering effect, reduced risk of hypoglycaemia and a longer duration of action’, observed Dr Landau. Several new agents not yet available in South Africa show some promise in this regard. ‘Insulin degludec is an analogue with an exceptionally flat and stable 24-hour profile that, irrespective of dose, is gradually delivered into the peripheral system in a sustained manner. Its HbA1c outcomes are equivalent to glargine, against which it has been compared in non-inferiority trials. Amendments to the insulin molecule allow it to be used flexibly, so the timing of doses is less critical than with glargine and detemir. Intervals of between eight and 40 hours have been observed in trials involving both type 1 and type 2 diabetes patients. This is an advantageous development for people with diabetes who do shift work, travel frequently or who are in institutional care. In addition, it is one of only two basal insulins that can be co-formulated with aspart or GLP-1.’ In respect of safety, data show it to be safe in both chronic kidney disease and liver disease. There are no tolerability issues, it is effective across different ethnic profiles and is not affected by body mass index (BMI) or duration of diabetes. A major benefit is that it lowers nocturnal hypoglycaemia. Lilly basal insulin LY2605541 is the second long-acting basal insulin. It has a preferential hepatic mode of action and weight loss may be a reasonable expectation. Dr Landau cautioned, however, that most of the data so far are animal data and current knowledge is largely abstract. ‘There are no data in individuals with type 2 diabetes; only healthy volunteers, and it is not without concerns. Phase 2 data have indicated that it may raise triglyceride levels and cause deranged hepatic function.’ Other agents are on the way too, including insulin glargine U3000, which also diminishes nocturnal hypoglycaemia, FT-105 and the so-called ‘smart insulins’, which comprise glucose-responsive molecules with attached insulin. Despite their promise, Dr Landau feels that modern insulins require ‘deconstruction’ and that it is mainly secondary outcomes that differentiate the newcomers from what’s currently available. ‘Everything depends on how we use the material, not the material itself and new is not necessarily superior. Insulin isn’t always what it seems and control is worsening despite increased insulin usage. Changing a patient’s brand of insulin is only one consideration when
one is trying to prevent hypoglycaemia’, he concluded.
Diabetic nephropathy: countdown to disaster? The Ascending Star lecture Dr Julien Trokis, Diabetes Care Centre, Stellenryk Diabetes is the most common cause of end-stage renal disease (ESRD). Chronic kidney disease (CKD) is underdiagnosed and undertreated and opportunities for early intervention are often missed due to lack of awareness. Various modifiable risk factors can be addressed: these include hypertension, lipids, smoking and obesity. The financial burden is considerable and in 2007, dialysis cost the USA US$35.3 billion. ‘Diabetes patients with CKD cost three times as much to treat as those without. The life expectancy of patients receiving treatment for ESRD is considerably reduced, with only 51% still alive after three years’, said Dr Trokis. Abnormal albuminuria is the most powerful risk factor for decline in glomerular filtration rate (GFR). It heralds the onset of worsening function, together with raised cardiovascular and all-cause mortality risk, with the former surpassing the latter at all stages. ‘While microalbuminuria is reversible, when macroalbuminuria is present, we can only slow disease progression’, warned Dr Trokis. ‘As GFR drops, cardiovascular risk climbs. Cardiovascular mortality is the hidden danger beneath the surface of CKD.’ Undiagnosed CKD is common in diabetes and a failure to screen patients is an important factor. ‘We therefore need to screen more actively. Guidelines recommend annual screening for microalbuminuria, starting at diagnosis in type 2 diabetes patients, and five years after diagnosis in type 1 patients. Serum creatinine levels should be measured at least annually and used to estimate GFR.’ Healthcare professionals need to be aware that there is sometimes discordance between GFR and albuminuria and that both albuminuria and retinopathy may be absent in diabetes patients with CKD. ‘We need to shatter the myth that we can always rely on the presence of one of them to raise our suspicion that nephropathy may be present.’ Various studies have shown that intensive glycaemic control reduces the incidence and rate of progression of diabetic nephrop-
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athy. However, these effects are seen mainly in incipient rather than overt disease. ‘In the latter, blood pressure control is the key concern, delaying progression and having a beneficial effect on kidney function.’ Renin–angiotensin system (RAS) blockade is the mainstay of blood pressure treatment in CKD patients, with angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reducing proteinuria and slowing disease progression. Thiazide diuretics have a lower efficacy in the kidney-impaired and loop diuretics are preferred in the context of proteinuria and ESRD. Statins can significantly improve GFR or delay its decline in type 2 diabetes, but need to be initiated early as they have little effect when kidney impairment is advanced. Renal anaemia affects 20% of diabetes patients with stage three CKD. It worsens with disease progression, and low haemoglobin levels increase the risk of all-cause mortality. Patients need to be screened for anaemia. Erythropoietin-stimulating agents may be indicated, but need to be used with caution as they do carry risk. Abnormalities in bone mineral metabolism should also be addressed. Lifestyle measures should not be underestimated. ‘Smoking promotes the onset and progression of diabetic kidney disease, while cessation reduces cardiovascular risk and prevents the progression of early CKD. Weight loss reduces proteinuria and microalbuminuria, and improves glycaemic control. While there are less robust data for dietary modification, protein restriction is recommended. Exercise has been shown to attenuate disease progression in animal models and may therefore be of benefit.’ Summing up, Dr Trokis underscored that timeous nephrology referral reduces cost, hospitalisation and mortality. ‘We have the knowledge and means to prevent unnecessary deaths. Screen routinely and actively. Be aware of exceptions to stereotypes. Consider non-diabetic causes of kidney disease. Maintain glycaemic and lipid targets early, and never accept “almost there” blood pressures.’
Neuropathy: a diagnosis? Dr Brian Kramer, Centre for Diabetes and Endocrinology, Johannesburg When is neuropathy, neuropathy? ‘Currently it’s defined in terms of an alteration
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in morphology and function that results in a disturbance of the neurones, affecting the axon and myelin’, said Dr Kramer. Neuropathy is common in longstanding diabetes, with a lifetime risk of approximately 60%. The major consequences of neuropathy are foot ulcers and amputations. There is no universal consensus on what defines neuropathy and how to detect it and monitor its progress. Although hyperglycaemia plays an important role, the mechanism of neural damage remains poorly understood. As a result, it is difficult to develop and implement effective preventive and treatment strategies. ‘Where glycaemic exposure is concerned, a wellcontrolled patient may nonetheless develop neuropathy, and vice versa.’ There are various tools for detecting neuropathy, including screening/scoring systems and quality-of-life measures. ‘The monofilament test appears to be the best validated in respect of predicting future ulceration’, observed Dr Kramer. ‘While we have reasonable ways of detecting and scoring neuropathy and predicting risk, the question remains whether we’re diagnosing diabetic neuropathy or simply neuropathy occurring in a patient with diabetes but not necessarily caused by it’, concluded Dr Kramer. ‘The lack of specific tests to determine whether neuropathy is indeed caused by diabetes means that clinicians always need to bear other causes in mind and exclude these in patients with diabetes.’ The diagnosis of diabetic neuropathy is therefore one of exclusion. Those other possible causes include toxic neuropathy (caused by alcohol and drugs), systemic disease, malignancy, inflammatory/infective conditions, deficiency states and hereditary factors.
The debate renewed… Is bariatric surgery a ‘cure’ for diabetes? Drs Graham Ellis and Ray Moore went head to head on the subject, making persuasive cases for and against. However, the majority of the audience remained steadfast in their original views. Prior to the debate, 31% answered ‘yes’ to the question as opposed to 69% answering ‘no’. Afterwards, those figures had changed only slightly: to 34 and 66%, respectively.
Yes! Dr Graham Ellis, Helderberg Diabetes and Medical Clinic, Somerset West ‘If you want to lose your butt, bypass your gut’, quipped Dr Ellis. ‘We often treat glucose at the cost of obesity and most clinical trials ignore the obese diabetic patient; those with a BMI > 35–40 kg/m2. The data we use to extrapolate from may therefore not be appropriate to this group of patients with obesity-related co-morbidities.’ There is a correlation between weight loss and insulin sensitivity, although it is not a direct relationship. Bariatric surgery – biliopancreatic diversion (BPD) or Rouxen-Y – can improve insulin resistance by 50% and decrease BMI by 30%. Critically, the changes in sensitivity precede the actual weight loss. In a small group of patients, BPD is associated with complete restoration of the acute insulin response one month post surgery. ‘Cure’ is defined as remission that is partial, complete or prolonged. Partial remission requires an HbA1c level < 6.15 µg/dl and fasting plasma glucose (FPG) values between 5.6 and 7 mmol/l without pharmacotherapy for a year. The same is required for complete remission, except that FPG must be 5.6 mmol/l or lower. Prolonged remission is defined as complete remission sustained for five years. Laparoscopic banding has been associated with 73% remission at two years. For Roux-en-Y the figure is 75% and for BPD 95%. Bariatric surgery is also associated with a significant reduction in medication use, supporting the notion that it can ‘cure’ diabetes. And data show that it is well maintained and compares favourably with other interventions. But is normalising blood glucose sufficient, given that it is only a surrogate marker? Turning to other outcomes – mortality, microvascular complications and cardiovascular disease – Dr Ellis noted that medical therapy for weight loss may increase mortality, where lifestyle intervention usually produces only modest, shortterm results. ‘Indications are that bariatric surgery in the severely obese can reduce all-cause mortality by 21% at 16 years. Cardiovascular events and deaths are likewise reduced at 15 years post surgery. Preliminary evidence suggests that it improves retinopathy and nephropathy. There is therefore a growing body of data that it has a wide
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range of health benefits that go far beyond the cosmetic.’ In summary, Dr Ellis argued that bariatric surgery is highly effective, sustained in the majority of patients, and has benefits beyond glycaemic control, including mortality rate, blood pressure, hyperlipidaemia, obstructive sleep apnoea and improved quality of life. And even though it’s expensive, it might well be more cost effective than it appears at first glance. ‘We should be more interventionist than in the past’, he concluded. ‘Bariatric surgery is a cure for diabetes.’
No! Dr Ray Moore, Umhlanga Centre for Diabetes and Endocrinology Bariatric surgery is not the answer to type 2 diabetes. On that point Dr Moore was adamant. ‘Not only will it leave you with a lighter wallet, but it carries a 5.5% risk of any complication and a 2.2% risk of a serious complication. It can even cause death.’
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The complications include stomal ulcer or stricture, wound infection, gastric ulceration, internal hernias, anastomotic leaks, small bowel or Roux loop obstruction and cholelithiasis. It is also associated with increased substance abuse. While smoking and alcohol intake are decreased at one month post surgery, they are increased at each successive visit, reaching significance at two years. ‘If you can no longer get pleasure from food, you’ll find it elsewhere.’ Various studies have shown too that only a relatively small proportion of those who undergo bariatric surgery achieve complete remission of their diabetes at five years and that there is also a relatively high rate of weight regain. So is there an alternative to bariatric surgery? Some investigators led by Prof Roy Taylor from Newcastle University, UK, have shown in a recent series of articles that rapid reversal of type 2 diabetes with a very low-calorie diet can be achieved in the same time frame as with bariatric surgery.
Using sophisticated MRI techniques, they showed that this reversal was associated with rapid reduction of the fatty infiltration of the liver and pancreas. ‘So weight loss from any cause sees a return towards normal functioning’, continued Dr Moore. ‘Even though, once established, type 2 diabetes seems inevitably progressive, it might just be a consequence of too much fat in the pancreas, while insulin resistance is the result of too much fat in the liver. ‘So who needs bariatric surgery? Why choose an expensive surgical option when a commercially available low-calorie diet can achieve the same result at a fraction of the cost, with no risk of the various complications mentioned earlier? Over and above everything else, bariatric surgery confers little or no long-term survival benefit. A diabetic patient should not qualify for bariatric surgery based on BMI alone. It should be reserved for only a highly selective group of patients.’
VOLUME 10 NUMBER 4 • NOVEMBER 2013
SCHEDULING STATUS: S3 PROPRIETARY NAME AND DOSAGE FORM: LANTUS 速 solution for injection. COMPOSITION: Each ml of the solution for injection contains 3.64 mg of the active ingredient insulin glargine, corresponding to 100 U human insulin, 2.7mg of the preservative metacresol and 0.0626mg of zinc chloride as stabiliser. 10ml vial contains 0.02mg polysorbate 20 as additional stabiliser. REGISTRATION NUMBER: 34/21.1/0248. NAME AND BUSINESS ADDRESS OF THE APPLICANT: sanofi -aventis south africa (pty) ltd, 2 Bond Street, Midrand, 1685. Tel: 011 256 3700. Reg. No. 1996/10381/07.
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References: 1. DeFronzo RA, Hissa MN, Garber AJ, et al. Once-daily saxagliptin added to metformin provides sustained glycaemic control and is well tolerated over 102 weeks in patients with T2D. Abstract. Presented at ADA 69th Scientific Session. New Orleans. 2009. 2. GĂśke B, Gallwitz B, Eriksson JG, et al. Saxagliptin vs. glipizide as add-on therapy in patients with type 2 diabetes mellitus inadequately controlled on metformin alone: long-term (52-week) extension of a 52-week randomised controlled trial. Int J Clin Pract 2013;doi: 10.1111/ijcp.12119. S3 ONGLYZAÂŽ 2.5 (Tablet) . Each ONGLYZAÂŽ 2.5 tablet contains saxagliptin hydrochloride equivalent to 2.5 mg saxagliptin free base. S3 ONGLYZAÂŽ 5 (Tablet). Each ONGLYZAÂŽ 5 tablet contains saxagliptin hydrochloride equivalent to 5 mg saxagliptin free base. Reg. No. ONGLYZAÂŽ 2.5 : 43/21.2/0608. Reg. No. ONGLYZAÂŽ 5 : 43/21.2/0609. ONGLYZAÂŽ is a registered trademark of Bristol-Myers Squibb. For full details relating to any information mentioned above please refer to the package insert. Bristol-Myers Squibb (Pty) Limited. Reg. No. 1956/001115/07. Woodmead North Office Park, 54 Maxwell Drive, Woodmead, 2191. PO Box 227, Sunninghill, 2157. Tel: (011) 808 5000. Fax: (011) 808 5301. AstraZeneca Pharmaceuticals (Pty) Ltd. Reg. No. 1992/005854/07. Building 2, Northdowns Office Park, 17 Georgian Crescent West, Bryanston, 2191. Private Bag X23, Bryanston, 2021. Tel: 011 797-6000. Fax: 011 797-6001. www.astrazeneca.co.za. Expiry Date: August 2015. Log No: ONG 09/13/004