SARJ Vol 21, No 1 (2015)

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NUMBER 1

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MARCH 2015

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THE SOUTH AFRICAN

RESPIRATORY JOURNAL VOLUME 21 | NUMBER 1 | MARCH 2015

CONTENTS EDITORIAL 2

Obstructive sleep apnoea and cardiovascular disease in the developing world R Raine

ORIGINAL RESEARCH

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Assessment of risk of obstructive sleep apnoea syndrome among patients attending a medical outpatient clinic in a tertiary health facility in SouthWest Nigeria B Adeniyi, O Ilesanmi, A Adebayo, A Kareem, O Junaid, A Adeniji, G Erhabor

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EDITORIAL

Obstructive sleep apnoea and cardiovascular disease in the developing world Obstructive sleep apnoea (OSA) is a common condition, with studies from the USA suggesting that the prevalence is 4% in men and 2% in women.[1] The prevalence in other parts of the world is unknown but is likely to be similar.

The theory of epidemiological transition outlined by Omran[2] suggests there are three basic stages: pestilence and famine, receding pandemics, and degenerative and man-made disease. The developed world, in general, is in stage 3 with lifestyle changes (diet, reduced activity, smoking) resulting in atherosclerosis and death from cardiovascular disorders and other non-communicable diseases.

Improvements in availability of food, sanitation and healthcare in the developing world are leading to a move from pestilence and famine to an increased prevalence of non-communicable diseases, particularly diseases of the cardiovascular system. Cardiovascular disease accounts for approximately 30% of all deaths globally, 80% of these in low- and middle-income countries.[3] South Africa illustrates a blend of epidemiological stages – 67% of deaths in 2011 were a result of communicable diseases, 11% (38% of the non-communicable diseases) were due to cardiovascular disease.[4] OSA is strongly associated with a number of cardiovascular diseases. Hypertension, stroke, arrhythmias and heart failure are prominent among these. The Wisconsin Sleep Cohort followed 1 522 subjects and demonstrated greater mortality in those with severe OSA (19.1%) compared with those with none (4%). Cardiovascular mortality counted for 26% of deaths in those without OSA and 42% in those with severe OSA.[5] Similarly, Marin et al.[6] demonstrated a higher incidence of fatal cardiovascular events in those with untreated severe disease than those with mild disease (1.06 v. 0.55 events per 100 person years). Those patients with moderate or severe OSA who were treated with continuous positive airways pressure (CPAP) had rates of fatal and non-fatal cardiovascular events that were similar to those with no or mild disease.

Hypertension has the best documented association with OSA. Treatment with CPAP has a modest but significant effect on blood pressure, which is increased by better compliance with CPAP use for at least 4 hours per night,[7] although this effect is only seen in those who have symptoms of excessive sleepiness.[8] There is also evidence to suggest better outcomes after stroke and improved arrhythmia control, particularly atrial fibrillation, when OSA is diagnosed and treated.[9,10] The article in this journal by Adeninyi et al. is important as it highlights the high prevalence of symptoms typical of OSA in medical

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patients in a developing country. Sleep problems have been harshly dealt with and largely ignored in developing countries to date. The transition from diseases of pestilence and famine to increasing numbers of non-communicable diseases means that, as suggested by Gersh et al.,[11] increasing emphasis will have to be placed on simple measures such as avoiding smoking and obesity and increasing exercise. More complex measures such as the appropriate use of drugs and the recognition and management of OSA will become increasingly more important.

Richard Raine MB ChB, MMed (Med), FCP (SA) Respiratory Clinic, Department of Medicine, Groote Schuur Hospital and University of Cape Town

References

1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleepdisordered breathing among middle-aged adults. N Engl J Med 1993;328(17):12301235. [http://dx.doi.org/10.1056/NEJM199304293281704] 2. Omran AR. The epidemiologic transition: A theory of the epidemiology of population change. Milbank Mem Fund Q 1971;49(4):509-538.

3. Gaziano TA. Cardiovascular disease in the developing world and its cost-effective management. Circulation 2005;112(23):3547-3553. [http:dx.doi.org/10.1161/ CIRCULATIONAHA.105.591792] 4. World Health Organization. Noncommunicable diseases country profiles: South Africa 2011. http://www.who.int/nmh/countries/en/ (accessed 10 Feb 2014).

5. Young T, Finn L, Peppard PE, et al. Sleep disordered breathing and mortality: Eighteen-year follow-up of the Wisconsin sleep cohort. Sleep 2008;31(8):1071-1078.

6. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: An observational study. Lancet 2005;365(9464):1046-1053. [http://dx.doi.org/10.1016/S0140-6736(05)71141-7] 7. Sánchez-de-la-Torre M, Campos-Rodriguez F, Barbé F. Obstructive sleep apnoea and cardiovascular disease. Lancet Respir Med 2013;1(1):61-72 [http://dx.doi. org/10.1016/S2213-2600(12)70051-6].

8. Bratton DJ, Stradling JR, Barbé F, Kohler M. Effect of CPAP on blood pressure in patients with minimally symptomatic obstructive sleep apnoea: A meta-analysis using individual patient data from four randomised controlled trials. Thorax 2014;69(12):1128-1135. [http://dx.doi.org/10.1136/thoraxjnl-2013-204993] 9. Johnson KG, Johnson DC. Frequency of sleep apnea in stroke and TIA patients: A meta-analysis. J Clin Sleep Med 2010;6(2):131-137.

10. Ng CY, Liu T, Shehata M, Stevens S, Chugh SS, Wang X. Meta-analysis of obstructive sleep apnea as predictor of atrial fibrillation recurrence after catheter ablation. Am J Cardiol 2011;108(1):47-51. [http://dx.doi.org/10.1016/j.amjcard.2011.02.343] 11. Gersh BJ, Sliwa K, Mayosi BM, Yusuf S. Novel therapeutic concepts: The epidemic of cardiovascular disease in the developing world: Global implications. Eur Heart J 2010;31(6):642-648. [http://dx.doi.org/10.1093/eurheartj/ehq030]

S Afr Resp J 2015;21(1):2. DOI:10.7196/SARJ.7739

ORIGINAL RESEARCH

Assessment of risk of obstructive sleep apnoea syndrome among patients attending a medical outpatient clinic in a tertiary health facility in South-West Nigeria B O Adeniyi,1 MB ChB, FWACP; O S Ilesanmi,2 MBBS, MBA, MSc, FWACP; A M Adebayo,3 MBBS, FWACP; A O Kareem,2 MB ChB; O A Junaid,1 MB BS; A O Adeniji,4 MBBS, FWACS; G E Erhabor,5 MBBS, FWACP, FCCP, FRCP (Edin), FRCP (Lond) Department of Medicine, Federal Medical Centre, Owo, Ondo State, Nigeria Department of Community Health, Federal Medical Centre, Owo, Ondo State, Nigeria 3 Department of Community Medicine, University College Hospital Ibadan, Oyo State, Nigeria 4 Department of ENT, Federal Medical Centre, Owo, Ondo State, Nigeria 5 Department of Medicine, Respiratory Unit, Obafemi Awolowo University, Ile-Ife, Osun State, Nigeria 1 2

Corresponding author: Bamidele Olaiya Adeniyi (delbis2003@yahoo.com)

Background. Obstructive sleep apnoea syndrome (OSAS) is associated with increased morbidity and mortality. However, there are few studies from Nigeria that have evaluated the prevalence of OSAS in medical outpatient clinics.

Objective. To determine the degree of the risk of OSAS among patients attending the medical outpatient clinic of the Federal Medical Centre, Owo, South-West Nigeria.

Methods. A cross-sectional survey was conducted among 208 medical outpatients using the Berlin questionnaire and the Epworth sleepiness scale (ESS).

Results. The mean (standard deviation) age of participants was 53.8 (16.5) years, 110 (52.9%) were female, and 73.1% of participants had a high likelihood of sleep-disordered breathing (HSDB). Subjects with a high body mass index (BMI) were more likely to have sleep -disordered breathing when compared with those with a normal BMI (26 (96.3%) v. 7 (29.2%), p<0.001). The respondents with multiple primary morbidities were about 24 times more likely to have HSDB compared with respondents with a single morbidity (p=0.009). The odds of having HSDB was 16 times greater in those with hypertension compared with patients with asthma (odds ratio 16, 95% confidence interval 3 - 83, p=0.001). The Berlin questionnaire and the ESS were useful screening tools in the Nigerian setting.

Conclusion. In resource-poor settings in Africa, where there is an emphasis on screening and treating diseases of poverty, patients with medical conditions such as high BMI and hypertension should be screened for OSAS. S Afr Resp J 2015;21(1):3-7. DOI:10.7196/SARJ.7740

Obstructive sleep apnoea syndrome (OSAS) is increasingly becoming a disease of public health importance in Nigeria and Africa with longterm negative effects. It is a chronic illness that results from partial or complete collapse of the airway during sleep, and loud snoring is a common complaint by the patients or their partners. [1,2] Some of the most common manifestations of OSAS include loud snoring, excessive daytime sleepiness (EDS) and breathing pauses during sleep. It is gradual in onset and the associated symptoms are mostly unrecognised by patients.[3] OSAS contributes to long-term clinical consequences such as hypertension, cardiovascular disease and abnormalities in glucose metabolism.[4-6] The prevalence of snoring among adults varies in different parts of the world from 19.3% to 52.3%, while the risk of OSAS ranges from 16.8% to 33.3%. [7-9] The prevalence of clinically suspected OSAS in a study done in Abuja, Nigeria was low at 1%.[9] However, with increasing westernisation of diet, obesity, tendencies towards

sedentary lifestyles and increasing prevalence of diabetes mellitus (DM) and hypertension, OSAS is becoming an increasing problem.

The laboratory overnight polysomnography (PSG) is the gold standard for diagnosis of OSAS but this is expensive and not commonly available. Resource constraints mean that many patients with a history of snoring or other symptoms of OSAS cannot easily be diagnosed in countries such as Nigeria.[10-14] The practical assessment of patients at high risk of developing sleep-disordered breathing and OSAS includes use of validated questionnaires such as the Epworth Sleepiness Scale (ESS), the STOPBANG questionnaire, the Cleveland Sleep Habits Questionnaire and the Berlin questionnaire. These assessments are widely used to estimate and evaluate the likelihood of sleep-disordered breathing. Identifying those who are at risk of OSAS will help to determine who may require subsequent evaluation with more comprehensive tests.[10,15-18] The majority of patients affected by OSAS are undiagnosed, and many physicians do not actively screen for this condition when evaluating other medical conditions that are associated with OSAS.[19]

SARJ VOL. 21 NO. 1 2015

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ORIGINAL RESEARCH This study was aimed at determining the risk of OSAS among patients attending a medical outpatient clinic in a tertiary health facility using the Berlin questionnaire and the ESS.

Methods

Study area Owo is an ancient city located in the Owo local government area of Ondo State, South-West Nigeria. Agriculture (including fishing) constitutes the main occupation of the people. It is located about 350 km from Lagos State and 50 km from Akure, the state capital. The Federal Medical Centre (FMC) in Owo was a general hospital taken over by the Federal Government of Nigeria in 1989 and redesignated FMC with the aim of providing tertiary services in Ondo State. It is a 250-bed hospital with a staff of 1 200, of which doctors and nurses constitute about 500. It is the only tertiary hospital in Ondo state and provides primary, secondary and tertiary levels of care.

Study design This was a descriptive cross-sectional study of adults attending the medical outpatient clinic of FMC, Owo. Study population The population sampled for this study included patients with common conditions attending the medical outpatient clinic, which was largely made up of patients with hypertension, DM, asthma and tuberculosis.

Sample size determination The required sample size for this study was calculated using standard formulae for calculating minimum sample size for descriptive cross-sectional study.

Minimum sample size = Zα2pq/d2.

Zα 2 is the standard normal deviate corresponding to level of significance (usually 5%). This was 1.96. p is the prevalence of outcome of interest.

A prevalence of high risk OSAS of 17.4% was used.[15] q is 1 – p. d is the level of precision (0.05 was used).

This sample size was calculated to be 220.

However, only 208 patients were seen during the study period.

Sampling method Consecutive patients who were not previously

4 SARJ VOL. 21 NO. 1 2015

diagnosed with OSAS or sleep-disordered breathing were eligible for recruitment. Since the estimated minimum sample size was 220 subjects, and the clinic recorded an average of 80 patients per month, the study lasted from January to March 2014.

A semi-structured self-administered questionnaire was used for data collection.

Medical doctors attending to patients at the outpatient clinic participated in questionnaire administration. The questionnaire was categorised into three sections using the objectives of the study as criteria: section A – sociodemographic characteristics; section B – ESS; section C – Berlin questionnaire for sleep evaluation.

ESS score <11 was categorised as normal, while a score ≥11 suggested EDS. Berlin questionnaire scores ranged from 0 to 3, respondents with a score of 3 were categorised as having a high likelihood of sleep-disordered breathing (HSDB) while those scoring less were categorised as having a low likelihood of sleep-disordered breathing (LSDB). The patients’ bed partner, when available, was asked about the presence of snoring, and the patients themselves were asked when there was no one who accompanied them to the hospital, or when those who accompanied them did not have such information.

Data analysis The data obtained were analysed using the Statistical Package for Social Sciences (SPSS) for Windows evaluation version 21 (International Business Machines Corporation, USA). Data were presented using tables. Association between variables was assessed with χ2 test. Bivariate logistic regression analysis was used to determine predictors of high likelihood of sleepdisordered breathing. Level of significance was set at p=0.05%.

Consent Permission to conduct the study was sought from each respondent before conducting the interview and a high level of privacy was ensured. Respondents were adequately informed that they had the right to decline participation or to withdraw from the study at any point in time. In addition, respondents were informed that refusal to participate in the study or withdrawal from it would not result in any penalty.

Results

There were 208 respondents, mean age (standard deviation (SD)) was 53.8 (16.5) years, 98 (47.1%) males and 110 (52.9%) were females. The most common diagnosis was hypertension in 66 (38.2%). The sociodemographic characteristics and primary diagnoses of the respondents are summarised in Table 1. The Berlin questionnaire showed that 152 (73.1%) had HSDB. Only 39 (18.8%) had EDS using the ESS as shown in Table 2. Twenty-seven of the respondents (13%) were obese and 54 (26%) were overweight.

Among respondents aged <44 years, more than half (36 (62.1%)) had a LSDB compared with 22 (37.9%) who had HSDB (p<0.001). Increasing body mass index (BMI) was associated with an increasing HSDB; respondents who were obese (26 (96.3%)) Table 1. Sociodemographic characteristics and primary diagnosis of respondents Variables

n (%)

Age (years) <44

58 (27.9)

44 - 64

87 (41.8)

≥65

63 (30.3)

Sex Male

98 (47.1)

Female

110 (52.9)

Primary diagnosis (N=173) Pulmonary tuberculosis

41 (23.7)

Hypertension

66 (38.2)

DM

16 (9.2)

Hypertension and DM

34 (19.7)

Asthma

16 (9.2)

Table 2. Sleep evaluation of respondents using Berlin questionnaire and the Epworth sleepiness scale Tool used

n (%)

Berlin sleep evaluation LSDB

56 (26.9)

HSDB

152 (73.1)

ESS Normal <11

169 (81.3)

EDS ≥11

39 (18.8)

LSDB = low likelihood of sleep-disordered breathing; HSDB = high likelihood of sleep-disordered breathing; EDS = excessive daytime sleepiness.

ORIGINAL RESEARCH had HSDB compared with the underweight resp ondents (7 (29.2%), p<0.001).

Table 3 shows the association between sociodemographic characteristics of the respondents and sleep-disordered breathing.

Table 4 shows the association between primary diagnosis and sleep-disordered bre at hing in resp ondents. Among respondents with multiple primary morbidity, 33(97.1%) had HSDB compared with 103 (74.1%) of respondents with single morbidity (p=0.003). Of the hypertensive respondents, 63 (95.5%) had HSDB while only 3 (4.5%) had LSDB (p<0.001).

The predictors of HSDB are shown in Table 5. Respondents aged 44 - 64 years were about 6 times more likely to have HSDB compared with those <44 years (odds ratio (OR) 5.6, 95% confidence interval (CI) 1.5 20.7, p=0.009).

The likelihood of having HSDB increased with increasing BMI (OR 4.9, 95% CI 1.1 21.9, p=0.037) in those with normal BMI (OR 13.3, 95% CI 2.2 - 81.0, p=0.005) in overweight and markedly increased in obese respondents (OR 17.56, 95% CI 1.4 215.5, p=0.025) compared with those with underweight BMI. The respondents with multiple primary morbidities were about 24 times more likely to have HSDB compared with respondents having single morbidity (OR 23.7, 95% CI 2.2 - 255.73, p=0.009).

The probability of having HSDB was much greater in respondents with hypertension compared with those with asthma (OR 15.6, CI 2.95 - 82.8, p=0.001).

Discussion

OSAS is diagnosed using the standard laboratory overnight PSG, which is not commonly available, and is expensive and time and personnel intensive. This has led to OSAS being underdiagnosed, making accurate quantification of the health burden of untreated OSAS difficult, thus contributing to the occurrence of complications of OSAS, especially cardiovascular morbidities.[10-13] The provision of validated questionnaires such as the Berlin questionnaire and the ESS thus serve as surrogates to identify patients with HSDB.[10,16-18] The major finding of this study was that a significant number of patients who were being managed for chronic medical diseases in our tertiary hospital were at high risk of having OSAS. It was observed that most

Table 3. Association between sociodemographic characteristics of respondents and sleep-disordered breathing Sleep-disordered breathing Variables

LSDB n (%)

HSDB n (%)

χ2

p-value

36 (62.1)

22 (37.9)

0.505

<0.001

0.256

0.613

0.387

<0.001

Age group in years <44 45 - 64

11 (12.6)

76 (87.4)

≥65

9 (14.3)

54 (85.7)

Male

28 (28.6)

70 (71.4)

Female

28 (25.5)

82(74.5)

Underweight

17 (70.8)

7 (29.2)

Normal

31 (30.4)

71 (69.6)

Sex

BMI

Overweight

6 (11.1)

48 (88.9)

Obese

1 (3.7)

26 (96.3)

Table 4. Association between primary diagnosis and sleep-disordered breathing in respondents Sleep-disordered breathing LSDB n (%)

HSDB n (%)

χ2

p-value

Single

36 (25.9)

103 (74.1)

8.564

0.003

Multiple

1 (2.9)

33 (97.1)

Pulmonary tuberculosis

22 (53.7)

19 (46.3)

51.269

<0.001

Hypertension

3 (4.5)

63 (95.5)

DM

3 (18.8)

13 (81.3)

Hypertension and DM

1 (2.9)

33 (97.1)

Asthma

8 (50.0)

8 (50.0)

Non-excessive <11

44 (26.0)

125 (74.0)

0.361

0.548

EDS≥11

12 (30.8)

27 (69.2)

Variables Number of primary morbidities

Primary diagnosis

Daytime sleepiness

clinicians did not ask questions regarding snoring or EDS while attending to patients in the Medical Outpatients Department.[20] In agreement with our findings, a study carried out at the university of Benin Teaching Hospital, Nigeria, showed that among a total of 102 medical outpatients with a mean age (SD) of 55.1 (13.6) years, the prevalence of OSAS risk among the respondents who were positive according to the Berlin questionnaire was 67 (65.7%). The study also observed a statistically significant association between age group in years (p=0.01), BMI (p<0.001), type of primary diagnosis (p<0.001), and Berlin risk of OSAS.[20]

Our study showed a potentially high prevalence of OSAS among patients with chronic medical diseases as depicted by HSDB in the middle-aged and elderly groups using the Berlin questionnaire.

However, the prevalence was low with the ESS. This may underscore the fact that the Berlin questionnaire has been documented to be clinically more sensitive and correlates significantly with the presence of OSAS among various populations.[10] The ESS has been documented to be more specific even though it is less sensitive than the Berlin questionnaire.[21] Another study carried out

SARJ VOL. 21 NO. 1 2015

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ORIGINAL RESEARCH

Table 5. Predictors of HSDB Variables

Odds ratio

95% CI

p-value

Age group in years <44

1

44 - 64

5.628

1.530 - 20.706

0.009*

â&#x2030;Ľ65

3.172

0.879 - 11.439

0.078

BMI Underweight

1

Normal

4.902

1.099 - 21.863

0.037*

Overweight

13.333

2.197 - 80.906

0.005*

Obese

17.554

1.430 - 215.480

0.025

Number of primary morbidities Single

1

Multiple

23.698

2.196 - 255.723

0.009*

Pulmonary tuberculosis

1.071

0.266 - 4.309

0.923

Hypertension

15.623

2.949 - 82.763

0.001*

DM

2.368

0.369 - 15.185

0.363

Asthma

1

Primary diagnosis

* p<0.05 is significant.

using the STOPBANG questionnaire in a tertiary facility in Lagos, Nigeria, showed that 36.3% of the respondents had a high risk of OSAS while 24.4% had EDS using the ESS.[22] The seemingly lower value that was observed in the Lagos study compared with ours may be explained by the heterogeneity of the patients used for their study, since recruitment was done from both medical and surgical departments while ours focused strictly on those with medical conditions.

There appeared to be a significant increased risk of OSAS among middle-aged respondents when compared with those who were elderly.

Increasing BMI was associated with higher risk of OSAS in this study; there was a strong positive association between them, with a gradual increase from respondents that were underweight to those that were obese. This has also been documented by several other studies.[9,23,24] The significant association between respondents who were hypertensive and at high risk of OSAS could result from the higher percentage of this condition among those who were overweight and obese, compared with those with normal BMI, leading to increased risk of cardiovascular diseases. Of note also is the fact that those

6 SARJ VOL. 21 NO. 1 2015

with multiple morbidities had a higher risk of OSAS compared with those with a single morbidity. Hypertension and DM combined constituted the highest risk, possibly resulting from the synergistic effect of these two conditions and their associations with obesity in the so-called metabolic syndrome. Asthma constituted the lowest risk as observed in this study. However, the percentage of those who were asthmatic among the respondents was small and may account for the low risk identified.

Several studies have described the increase in statistical significance of EDS and the risk of OSAS.[22,24] Although there was a positive association between EDS (as measured by the ESS) and the risk of sleep apnoea (as assessed by the Berlin questionnaire), it was not significant in our study. This may result from the limitations of the instruments used in this study and the subjective nature of the responses obtained. An objective assessment of overnight pulse oximetry or PSG, which could be more informative, was not done in this study due to lack of availability and the huge cost implications.

Our study has shown a considerable risk of OSAS among patients attending the Medical Outpatients Department and its association with other health-related factors.

In conclusion, the risk of OSAS increased with increased BMI. Hypertension and the presence of multiple comorbid conditions also increased the risk of OSAS. It is important that healthcare providers make efforts to screen all patients for OSAS using the available screening questionnaires designed for this purpose, and to ensure the prompt and comprehensive treatment of comorbidities. Increased awareness should be created among the healthcare workers with a view to asking questions regarding snoring and a tendency to fall asleep during the day. Attention should also be paid to preventive strategies, including lifestyle modifications.

Like other descriptive cross-sectional studies, recall bias of snoring while asleep or during daytime, especially when the respondent is not staying in the same room with the spouse, is a possible limitation. This limitation is minimised by the short recall period in the assessment tools. There is also the possibility of the respondents denying sleeping, either at work or while driving, for fear of losing their jobs.

We conclude that there is an urgent need for sleep laboratories in Nigeria so that patients with a high risk of OSAS can easily be referred for further evaluation.

References

1. Punjabi NM. The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc 2008;5(2):136-143. [http://dx.doi.org/10.1513/pats.200709-155MG] 2. American Academy of Sleep Medicine. International Classification of Sleep Disorders, Third Edition (ICSD-3). Rochester, USA; 2014.

3. Akintunde AA, Okunola OO, Oluyombo R, Oladosu YO, Opadijo OG. Snoring and obstructive sleep apnea syndrome among hypertensive Nigerians: Prevalence and clinical correlates. Pan Afr Med J 2012;11:75.

4. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342(19):1378-1384. [http://dx.doi.org/10.1056/ NEJM200005113421901] 5. Peker Y, Carlson J, Hedner J. Increased incidence of coronary artery disease in sleep apnoea: A long-term follow-up. Eur Respir J 2006;28(3):596-602. [http:// dx.doi.org/10.1183/09031936.06.00107805] 6. Punjabi NM, Polotsky VY. Disorders of glucose metabolism in sleep apnea. J Appl Physiol 2005;99(5):1998-2007. [http://dx.doi.org/10.1152/ japplphysiol.00695.2005] 7. Khassawneh B, Ghazzawi M, Khader Y, et al. Symptoms and risk of obstructive sleep apnea in primary care patients in Jordan. Sleep Breath 2009;13(3):227-232. [http://dx.doi.org/10.1007/s11325-008-0240-4] 8. BaHammam AS, Alrajeh MS, Al-Jahdali HH, BinSaeed AA. Prevalence of symptoms and risk of sleep apnea in middle-aged Saudi males in primary care. Saudi Med J 2008;29(3):423-426.

ORIGINAL RESEARCH 9. Adewole OO, Adeyemo H, Ayeni F, et al. Prevalence and correlates of snoring among adults in Nigeria. Afr Health Sci 2008;8(2):108-113.

10. Abrishami A, Khajehdehi A, Chung F. A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth 2010;57(5):423-438. [http://dx.doi. org/10.1007/s12630-010-9280-x] 11. Senn O, Brack T, Russi EW, Bloch KE. A continuous positive airway pressure trial as a novel approach to the diagnosis of the obstructive sleep apnea syndrome. Chest 2006;129(1):67-75. [http://dx.doi.org/10.1378/chest.129.1.67] 12. Practice parameters for the indications for polysomnography and related procedures.

Polysomnography Task Force, American Sleep Disorders Association Standards of Practice Committee. Sleep 1997;20(6):406-422.

13. Pagel JF. Obstructive sleep apnea (OSA) in primary care: Evidence-based practice. J Am Board Fam Med 2007;20(4):392-398. [http://dx.doi.org/10.3122/ jabfm.2007.04.060201] 14. Young T, Evans L, Finn L, Palta M. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep 1997;20(9):705-706.

15. Sogebi OA, Ogunwale A. Risk factors of obstructive sleep apnea among Nigerian outpatients. Braz J Otorhinolaryngol 2012;78(6):27-33.

16. Hrubos-Strøm H, Randby A, Namtvedt SK, et al. A Norwegian population-based study on the risk and prevalence of obstructive sleep apnea. The Akershus Sleep Apnea Project (ASAP). J Sleep Res 2011;20(1 Pt 2):162-170. [http://dx.doi.org/10.1111/ j.1365-2869.2010.00861.x]

17. Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire; a tool to screen patients with obstructive sleep apnea. Anesthesiology 2008;108(5):812-821. [http://dx.doi. org/10.1097/ALN.0b013e31816d83e4] 18. Netzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med 1999;131(7):485-491.

19. Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 1999;22(5):667-689.

20. Aigbokhaode A, Isara A. Obstructive sleep apnoea risk in patients attending medical outpatient clinics in University of Benin Teaching Hospital, Benin City, Nigeria. S Afr Respir J 2014;20(2):32-35.

21. El-Sayed I. Comparison of four sleep questionnaires for screening obstructive sleep apnoea. Egyptian Journal of Chest Diseases and Tuberculosis 2012;61(4):433-441. [http://dx.doi.org/doi:10.1016/j.ejcdt.2012.07.003] 22. Ozoh OB, Okubadejo NU, Akinkugbe AO, et al. Prospective assessment of the risk of obstructive sleep apnea in patients attending a tertiary health facility in Sub-Saharan Africa. Pan Afr Med J 2014;17:302. [http://dx.doi.org/10.11604/pamj.2014.17.302.2898] 23. Hiestand DM, Britz P, Goldman M, Phillips B. Prevalence of symptoms and risk of sleep apnea in the US population: Results from the national sleep foundation: Sleep in America 2005 poll. Chest 2006;130(3):780-786. [http://dx.doi.org/10.1378/chest.130.3.780] 24. Sharma SK, Malik V, Vasudev C, et al. Prediction of obstructive sleep apnea in patients presenting to a tertiary care center. Sleep Breath 2006;10(3):147-154.

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South African Thoracic Society

ANNUAL CONFERENCE

7-10 August 2015 CAPE TOWN | South Africa

Further information available online:

www.satsconference2015.co.za For more details, please contact Deidre Raubenheimer: deidre.raubenheimer@uct.ac.za

SATS NEWS

2 March 2015 Dear Colleagues: This mail is to notify you of an important, innovative agreement that has been signed with the European Respiratory Society (ERS). In view of the fact that this is an agreement that carries major changes, and in particular benefits for SATS members, we would like to provide you with a short summary of the scope of this agreement.

As from 1 January 2015 SATS will have an institutional affiliation for all its active members, which means that any SATS member will automatically become an ERS partner with all its advantages and rights.

Self-evidently, SATS must disclose some of your personal data (name and email address) to the ERS for the sole purpose of creating a database of SATS members for the terms of this agreement. Should any SATS member wish to object to the disclosure of their data, or if now or later they do not wish to be an ERS member, they must send an email to sarj@iafrica.com indicating ‘OPT OUT SATS-ERS’ in the subject line and providing their name, surname, SATS member number and stating their wish not to be an ERS member and their right will be exercised.

Under no circumstances is it mandatory to join ERS, nor does it entail any detriment to the advantages of SATS membership. For the ERS, this new agreement means increasing the number of South African members from approximately 41 to the 150 currently made up by SATS. One of the key points of this agreement that we wish to stress is that this dual affiliation does not entail any increase in the annual fee for SATS membership, as it will be supported by SATS itself, provided that the SATS fees payments are up-to-date (i.e. you have to be a paid-up SATS member). It is also important to update your details with SATS.

The advantages of being an ERS member include: • ERS will provide electronic access to the European Respiratory Journal (ERJ) and to its other publications: European Respiratory Review (ERR), Breathe and ERS Monograph. It will also offer all its publications in a printed version to all interested members of SATS at a special price.

• ERS will distribute the ERS Weekly Bulletin.

• ERS and SATS will cooperate proactively to provide SATS members with access to the ERS educational services, both online and in person.

• ERS will start and finance a session’s programme at the ERS annual congress with the active participation of the SATS members and teachers.

• SATS members may take part in the constitutional meetings of the ERS; they may vote and be voted for. They can be elected for any post up to the Meeting Head without any restrictions owing to the habitual place of residence. They will also be entitled to any leadership position, including ERS President, provided that they have their main residence in Europe as specified in the Constitution and the ERS Articles of Association in its latest approved version.

• The members of the SATS Council Members and other SATS members may be considered for election as the prestigious Fellow of the ERS (FERS).

• SATS members may take part in the ERS workshops, courses and symposia.

From 1 January 2015 SATS members may vote and be voted for and they are granted all the rights and privileges detailed in the Constitution and the ERS Articles of Association in their latest approved version.

We hope this agreement proves very advantageous to SATS and is of mutual individual and corporate benefit.

Kind regards,

Dr Sabs Abdool-Gaffar SATS PRESIDENT S Afr Resp J 2015;21(1):9. DOI:10.7196/SARJ.7738

SARJ VOL. 21 NO. 1 2015

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IPSA NEWS It gives me great pleasure to report that the first implantations of lung volume reduction coils outside of the USA and Europe were performed in Cape Town in September 2014.

Dr Johan Theron (Panorama Hospital) and Prof. Koegelenberg (representing Stellenbosch University), in a private-public partnership, were trained and accredited by Pneumrx (Germany). The procedures (Fig. 1) were performed at Panorama Hospital and three

patients were successfully treated; Fig. 2 shows a successfully completed coil insertion. This was announced at a press conference on 10 March 2015 and received major local press coverage.

IPSA is currently in the process of negotiation with the medical aids and is trying to get more centres accredited (once the medical funders come on board). More information on the procedure can be found online at [https://www. youtube.com/watch?v=XxkWuvdIeRE] In an ongoing effort to teach interventional pulmonology to fellows, IPSA will hold a pre-

Fig. 1. The first procedure was performed on 16 September 2014 at Panorama Hospital, Cape Town.

congress workshop in August 2015 (SATS, Cape Town), focussing on bronchoscopy and endobronchial ultrasound. More information can be found online at [http:// www.satsconference2015.co.za/].

Prof. Coenraad FN Koegelenberg MB ChB, MMed (Int), FCP (SA), FRCP (UK), Cert Pulm (SA), PhD Division of Pulmonology, Department of Medicine, Stellenbosch University and Tygerberg Academic Hospital, Cape Town, South Africa S Afr Resp J 2015;21(1):11. DOI:10.7196/SARJ.7737

Fig. 2. A supine chest radiograph taken of one of the first two patients after her second procedure.

South African Thoracic Society

ANNUAL CONFERENCE

7-10 August 2015

FILLER

CAPE TOWN | South Africa

Further information available online: www.satsconference2015.co.za SARJ VOL. 21 NO. 1 2015 11 For more details, please contact Deidre Raubenheimer: deidre.raubenheimer@uct.ac.za

BREATH-TAKING NEWS

Clinical relevance of genomic signatures of type 2 inflammation in chronic obstructive pulmonary disease The Dutch hypothesis,[1] proposed by Dick Orie in 1961 at the University of Groningen, provides one of several biologically plausible explanations for the pathogenesis of chronic obstructive pulmonary disease (COPD). Clinical characteristics such as allergy and bronchial hyperresponsiveness that are commonly observed in individuals afflicted with asthma were viewed as likely determinants of COPD. Orie emphasised the interplay of host (genetics, allergy and airway hyperresponsiveness) and environmental (smoking, air pollution and infection) factors, as well as the importance of carefully phenotyping patients to discern the actual critical features of disease in individual patients.

It has since become clear that susceptibility to cigarette smoking, and hence COPD risk, is indeed conferred by pre-existing airway hyperresponsiveness and eosinophilia.[2] Tilley et al.[3] reported on a ‘COPD-like’ small airway epithelial transcriptome; by identifying differentially expressed genes they could classify clinically healthy smokers into subgroups with lesser and greater responses to cigarette smoking. Following these results, whole-genome gene expression profiling done on bronchial biopsies from COPD patients treated with inhaled corticosteroids (ICS) in the GLUCOLD study,[4] showed that gene expression in biological pathways of COPD is dynamic with treatment and reflects disease activity.

This was the background on which Christenson et al.[5] recently tested the hypothesis that COPD and asthma could share partially overlapping airway gene expression changes, reflecting shared processes that contribute to airflow obstruction. They compared disease-associated airway epithelial gene expression alterations in an asthma cohort and two COPD cohorts. A subphenotype (endotype) of asthma with increased airway Th2 inflammatory markers, the ‘Th2-high’ endotype, had higher IL-5 and IL-13 expression levels in bronchial biopsies, increased serum total IgE levels, greater blood and lung eosinophilia, increased airway hyperresponsiveness, and a better lung function (FEV1) response to ICS.[6] When evaluating this T helper type 2 (Th2) signature score (T2S) in two cohorts of steroid-naive COPD patients, there was significant gene expression overlap. Of the 200 genes most differentially expressed in asthma v. healthy control subjects, the expression of these genes in the COPD cohorts was enriched and associated with more severe airflow obstruction (p<0.001). A higher T2S score was associated with decreased lung function (p<0.001), but not asthma history, in both COPD cohorts. Higher T2S scores correlated with increased airway

12 SARJ VOL. 21 NO. 1 2015

wall eosinophil counts (p=0.003), blood eosinophil percentage (p=0.03), bronchodilator reversibility (p=0.01) and improvement in hyperinflation after corticosteroid treatment (p=0.019) in GLUCOLD.[4] Interestingly, from the same institute, Smolonska et al.[7] recently performed genome-wide association studies for both asthma and COPD and could find no common single nucleotide polymorphisms that reached genome-wide significance. They did, however, suggest that although inflammatory processes differ in asthma and COPD, they are both mediated by the NF-kB pathway, and could therefore be driven by the same underlying genes.

Half a century later, it would seem that the Dutch hypothesis may indeed hold true but only for a small subset of COPD and asthma patients who co-express similar gene expression alterations. The implications of this work are that genomics may lead the search to find biomarkers that will allow us to categorise patients with COPD into clearly defined clinical groups, and possibly even to novel therapeutics to improve the care of patients with COPD. Morné Vorster Pulmonology Fellow, Division of Pulmonology, Department of Medicine, Stellenbosch University, Tygerberg, Cape Town, South Africa

References

1. Orie NGM, Sluiter HJ, De Vries K, Tammeling GJ, Witkop J. The host factor in bronchitis. In: Orie NGM, Sluiter HJ, editors, Bronchitis. Assen, the Netherlands: Royal Van Gorcum; 1961. pp. 43-59.

2. Hospers JJ, Postma DS, Rijcken B, Weiss ST, Schouten JP. Histamine airway hyperresponsiveness and mortality from chronic obstructive pulmonary disease: A cohort study. Lancet 2000;356(9238):1313-1317. [http://dx.doi.org/10.1016/S01406736(00)02815-4] 3. Tilley AE, O’Connor TP, Hackett NR, et al. Biologic phenotyping of the human small airway epithelial response to cigarette smoking. PLoS One 2011;6(7):e22798. [http:// dx.doi.org/10.1371/journal.pone.0022798] 4. Van den Berge M, Steiling K, Timens W, et al. Airway gene expression in COPD is dynamic with inhaled corticosteroid treatment and reflects biological pathways associated with disease activity. Thorax 2014;69(1):14-23. [http://dx.doi.org/10.1136/ thoraxjnl-2012-202878] 5. Christenson SA, Steiling K, van den Berge M, et al. Asthma-COPD Overlap. Clinical relevance of genomic signatures of type 2 inflammation in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2015;191(7):758-766. [http://dx.doi. org/10.1164/rccm.201408-1458OC] 6. Bhakta NR, Solberg OD, Nguyen CP, et al. A qPCR-based metric of Th2 airway inflammation in asthma. Clin Transl Allergy 2013;3(1):24. [http://dx.doi. org/10.1186/2045-7022-3-24] 7. Smolonska J, Koppelman GH, Wijmenga C, et al. Common genes underlying asthma and COPD? Genome-wide analysis on the Dutch hypothesis. Eur Respir J 2014;44(4):860-872. [http://dx.doi.org/10.1183/09031936.00001914]

S Afr Resp J 2015;21(1):12. DOI:10.7196/SARJ.7736

WHO’S WHO IN SATS

Professor Refiloe Masekela MB BCh, MMed (Paeds) Pret., Dip Allerg (SA), Cert Pulm (SA) Paeds, FCCP, PhD

Professor Masekela obtained her undergraduate qualification at the University of the Witwaterstrand in 1997. She completed her internship and community service training at the Polokwane/Mankweng Hospital complex, after which she spent a year in the UK as a medical officer. In 2005 she undertook her paediatric specialist qualification at the University of Pretoria. She then went on to train as a subspecialist in Paediatric Pulmonology at the Catholic University in Leuven, Belgium and at the University of Pretoria, which she completed in 2007. She is a Fellow of the American College of Chest Physicians. She obtained her PhD in 2012 with a thesis titled ‘Chronic inflammatory lung disease in human immunodeficiency virus-infected children. Epidemiologic considerations, aetiological

determinants and the efficacy of low dose erythromycin in bronchiectasis.’

She recently joined the University of KwaZulu-Natal as the Head of Department of Paediatrics and Child Health.

Professor Masekela has a special interest in chronic lung disease (bronchiectasis) and cystic fibrosis in African children. Her research areas include cystic fibrosis bronchiectasis, non-cystic fibrosis bronchiectasis, pneumonia in HIV-infected children, childhood asthma and spirometry in African children.

She is passionate about education for doctors, students and the lay person about lung diseases, particularly asthma in children.

She has been a chairperson of the South African National Asthma Education Programme. She serves as an executive member on various boards, namely the South African Thoracic Society, National Asthma Education Program, Pan African Thoracic Society and the South African Cystic Fibrosis Association (Scientific Advisory Board).

Dr Medeshni Annamalai MB BCh (WITS), DCH (SA), DipAllerg (SA), DipHIVMan (SA), FCPaed, Cert Pulm(SA)

Dr Annamalai is a Paediatric Pulmonologist currently employed at Stanger Regional Hospital, KwaZulu-Natal. She has obtained a Diploma in Child Health, a Diploma in HIV Management and a Diploma in Allergy.

After her fellowship she worked at Edendale Hospital, KwaZulu-Natal, as a consultant for 3 years.

In 2011 Dr Annamalai had the good fortune of joining The Gift of the Givers on a mission to Somalia. In 2012, she was the recipient of the Nycomed-Takaeda Pulmonology Scholarship. She completed her 2-year subspecialty in Paediatric Pulmonology at Inkosi Albert Luthuli Central Hospital under the University of KwaZulu-Natal.

She now focuses her attention on establishing a Respiratory Unit at Stanger Regional Hospital.

Visva Naidoo MB BCh, FCPaed (SA), Dip Allerg (SA), Cert Pulm (SA) Paed

Visva Naidoo is a Paediatric Pulmonologist providing a general paediatric and pulmonology service at King Edward VIII Hospital as well as supporting the paediatric pulmonology service at Inkosi Albert Luthuli Hospital. He has honorary lectureship status with the University of KwaZulu-Natal where he assists with both undergraduate and postgraduate training.

Visva’s undergraduate training was at the University of the Witwaterstrand. He qualified as a Specialist Paediatrician in 2008 after completing his registrarship through the University of KwaZulu-Natal.

He subsequently completed his Certificate in Paediatric Pulmonology in 2013.

He is a keen bedside clinician and enjoys teaching students and registrars.

SARJ VOL. 21 NO. 1 2015

13

CONGRESS AND CME EVENTS

14 SARJ VOL. 21 NO. 1 2015

PRODUCT NEWS

The COPD Assessment Test (CAT) The CAT has been designed to measure the impact of COPD* on a patient’s health by enabling them to describe their symptoms more accurately. This will improve communication with their doctor and give a better understanding of the disease’s true impact, allowing treatment to be better targeted and the patient’s care to be optimised.1,2 COPD limits airflow in the lungs causing breathing difficulties that affect patients’ health, quality of life and ultimately survival.

Over 210 million people worldwide have the condition3 and it causes around 250 deaths every hour, more than lung and breast cancer combined.4,5 However, partly due to difficulties in describing and assessing its full impact, it can be sub-optimally managed, causing patients to suffer increased symptoms, risk of hospitalisation and disability.6,7 The items that form the CAT, which is designed for patients to complete themselves, were identified following many interviews with patients coupled with rigorous scientific methodology. A wide range of international experts in COPD, patient groups and professional societies also played a key role in its development.1,2 The CAT, which was funded by GlaxoSmithKline (GSK), is freely available for use at: www.CATestonline.org.

References 1. Jones P, et al. Development and first validation of the COPD Assessment Test (CAT). Abstract 700144. Accepted for presentation at ERS 2009.

2. Jones P, et al. Development and first validation of the COPD Assessment Test. Eur Respir J 2009: 34:648-54.

3. The World Health Organization. Media Centre; Chronic obstructive pulmonary disease (COPD). (Last accessed 8 August 2009). http://www.who.int/ mediacentre/factsheets/fs315/en/).

4. The World Health Organization. The World Health Report 2002. Reducing risks, promoting healthy life. MDI.WHR.202.A. 5. Ferlay J, et al. GLOBOCAN 2002. Cancer Incidence, Mortality and Prevalence Worldwide. IARC CancerBase No.5, Version 2.0. IARCPress, Lyon, 2004.

6. Confronting COPD in America: Executive Summary; http://www.aarc.org/resources/confronting_copd/exesum.pdf; last accessed 130409.

7. Wilkinson T et al. Am J Respir Crit Care Med 2004;169;1298–1303

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South African Respiratory Journal Vol 20 No 4

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SARJ VOL. 21 NO. 1 2015

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PRODUCT NEWS

Bayer HealthCare Pharmaceuticals is excited to announce the launch of XARELTO® 15 and XARELTO® 20, in South Africa. Each XARELTO® 15 tablet contains 15 mg rivaroxaban and XARELTO® 20 tablet contains 20 mg rivaroxaban.

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116 SARJ VOL. 21 NO. 1 2015 16

South African Respiratory Journal Vol 20 No 4

South African Respiratory Journal Vol 20 No 4

INSTRUCTIONS TO AUTHORS

Author guidelines

The South African Respiratory Journal (SARJ) is the official journal of the South African Thoracic Society (SATS). The journal accepts submissions relating to both clinical and basic research in the respiratory field as well as state-of-the-art reviews on any topic related to the scope of the journal. It is important that authors comply with the format specified in these guidelines as failure to do so will result in delayed publication.

Submission of papers

The SARJ only accepts online submission of papers. Papers should be submitted through the SATS website, where there is a link for the SARJ. Authors may then submit their papers after registration with the Editorial Manager. The relevant links are provided on the SATS website (www.pulmonology.co.za).

As part of the submission process it will be necessary to provide a cover letter which should be used to explain why your manuscript should be published in the journal, to elaborate on any issues and to declare any potential competing interests. You will also be asked to provide the contact details (including email addresses) of potential peer reviewers for your manuscript. These should be experts in their field who will be able to provide an objective assessment of the manuscript. Any suggested peer reviewers should not have published with any of the authors of the manuscript within the past 5 years, should not be current collaborators and should not be members of the same research institution. Suggested reviewers will be considered alongside potential reviewers recommended by the Editor-in-Chief and/or Editorial Board members.

Types of manuscripts that will be accepted

Original articles should not exceed 3 500 words, although this may be reviewed on a case-by-case basis. References should preferably be limited to no more than 40. See document layout below for further details.

Brief reports: This should have an abstract of a maximum of 150 words, the total word content of the paper (excluding abstract and references) should be 1 500 words, with a maximum of 15 references.

The abstract should be structured in subheadings as outlined below.

This should contain a maximum of one table and one figure, i.e. a maximum of two inserts (or two figures/tables).

Case reports: A 50-word unstructured abstract is required.

Introduction, Methods/Results sections followed by a Discussion section. It should not exceed 800 words and should contain only one illustration or table and a maximum of five references. The key learning points should be provided in a table with bullet points – maximum 100 words.

Research letter: This should contain a 50-word unstructured abstract and may be divided into an Introduction, Methods/Results and a very brief Discussion section. The research letter should not exceed 800 words and a maximum of seven references. One insert (table or figure) is allowed.

Editorials may be solicited by the Editor, though contributors are invited to submit editorials or opinion pieces for consideration by the journal. These should normally not exceed 1 500 words.

Reviews: Contributors are encouraged to write to the Editor about

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possible papers to be considered for review, and where appropriate a review outline will be submitted to experts in the field for consideration before a full review is commissioned. It is expected that an author or authors have substantial experience and track record in the field that the review is about. Reviews should be a maximum of 3 500 words unless an alternative word limit has been arranged with the Editorin-Chief. Contributors are encouraged to include tables and figures in their reviews to keep to the maximum word count. Contributors are encouraged to submit pulmonary puzzles, which should not exceed a maximum of 800 words.

The journal welcomes comments and opinions about the published work, even if they are controversial and differ from the views of the author or the journal.

Authorship Manuscripts must be submitted by one of the authors of the manuscript and should not be submitted by anyone on their behalf.

The submitting author takes responsibility for the article during submission and peer review. All named authors must consent to publication and confirmation of this consent should be noted in the cover letter.

Ethical approval SARJ publishes work subscribing to the highest ethical standards.

Any work involving human or animal subjects must be approved by the relevant institutional ethics committee. A statement to the effect that the work has been approved by the relevant ethical committee must be provided in the methods section of the paper.

Authors should provide evidence of Research Ethics Committee approval of the research where relevant. Authors must accept ethical responsibility for the work submitted to the journal and must agree to address ethical queries raised by the reviewers or the editor, should these arise.

Protection of patients’ rights to privacy Identifying information should not be published in written descriptions, photographs and pedigrees unless the information is essential for scientific purposes and the patient (or parent or guardian) gives informed written consent for publication.

Manuscript preparation

Manuscripts must be provided in UK English. There is a limit to the length of articles submitted and authors are encouraged to be concise.

There is no restriction on the number of figures or tables that can be included with each article online. However, authors should keep these to a minimum as appropriate.

It is important to note that the SARJ will not comprehensively edit submitted manuscripts for style or language and reviewers may advise rejection of a manuscript if it is compromised by grammatical errors. Qualification, affiliation and contact details of ALL authors must be provided in the manuscript and in the online submission process.

Abbreviations should be spelled out when first used and thereafter used consistently. Scientific measurements must be expressed in SI units except: blood pressure (mmHg) and haemoglobin (g/dl). Litres is denoted with an uppercase ‘L’ and ‘ml’ for millilitres.

INSTRUCTIONS TO AUTHORS

General formatting

The following file formats are acceptable for the main manuscript document: Microsoft Word, Rich text format (RTF) or Portable document format (PDF).

• Text should be single-spaced.

• Type in 12-point Times New Roman font.

• Text should not contain unnecessary formatting (type the text unjustified, without hyphenating words at line breaks and do not format the text in multiple columns).

• Use hard returns only to end headings and paragraphs, not to rearrange lines.

• Capitalise only the first word and proper nouns in the title.

• All pages should be numbered.

• Do not use lowercase letter ‘L’ (el) for ‘1’ (one) or ‘O’ for ‘0’.

• Be consistent with punctuation and only insert a single space between words and after punctuation.

• There should be no space between numbers and <, > and %.

Illustrations and tables

Acceptable file types (authors must be wary of image compression): EPS, PDF, TIFF, PNG and JPEG. Illustrations and graphs prepared in Microsoft PowerPoint or Excel are not acceptable.

It is the responsibility of the author/s to provide consent to republication obtained from the copyright holder for all tables or illustrations previously published elsewhere. Tables should be provided as ‘supplementary files’ and must be numbered in Arabic numerals (1, 2, 3...) and referred to in the text (e.g. ‘Table 1’).

Figures must be numbered in Arabic numerals and referred to in the text, e.g. ‘(Fig. 1)’. Figure legends should be listed at the end of the article. All illustrations/figures/graphs must be of high resolution/ quality: 300 dpi or more is preferable (a minimum of 250 dpi is required and images must not be resized to increase resolution. Unformatted and uncompressed images must not be embedded in the manuscript and must be attached as ‘supplementary files’ upon submission.

Document layout

Manuscripts submitted should include the following: • Title page • Abstract • Keywords • Introduction • Methods • Results • Discussion and Conclusions • List of abbreviations used • Conflict of interest • Authors’ contributions • Acknowledgements • References Title page The title page should provide the title of the article, list the full names, institutional addresses and email addresses for all authors and indicate the corresponding author. The title should include the study design and abbreviations should be avoided.

Abstract Please provide a structured abstract. This should not exceed 250 words and should be broken down into the following recommended headings: Objectives, Methods, Results and Conclusion. Please make sure that the conclusions in the abstract are backed up by the data presented in the abstract results section. Abbreviations should be avoided as far as possible and no references should be cited in the abstract.

Keywords Please provide 3 - 10 keywords representing the main content of the article.

Introduction This should be concise, reflect the underlying hypothesis or idea being tested, and in general should not exceed a maximum of 500 words.

Methods Authors should endeavour to keep this to a maximum of 600 words, depending on the type of article. It should include the design of the study, the setting, the type of participants/materials involved, a description of interventions and comparisons and the type of analysis used. Information about ethical approval and consent should also be detailed here.

Results The results and discussion may be combined into a single section or presented separately and may also be broken into subsections with short headings.

Discussion and conclusions This should state clearly the main conclusions of the research and give a clear explanation of their importance and relevance.

Conflict of interest All authors are required to declare all sources of support for the research and any association with a product or subject that may constitute conflict of interest. If the author does not have any conflict of interest to declare this should be stated (e.g. ‘The author(s) declare that they have no competing interests.’). Forms are available on the website and should be submitted via the Editorial Manager.

Authors’ contributions Authorship should be based on substantial contribution to: 1. conception, design, analysis and interpretation of data; 2. drafting or critical revision for important intellectual content; and 3. approval of the version to be published.

These conditions must all be met. All contributors who do not meet the criteria for authorship should be listed in an acknowledgements section.

Acknowledgements This section should be used to acknowledge anyone who contributed significantly towards the article but who does not meet the criteria for authorship. Permission to acknowledge from all those mentioned in the acknowledgements section should be obtained by the author/s.

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INSTRUCTIONS TO AUTHORS References Authors must verify references from the original sources. Only complete, correctly formatted reference lists will be accepted.

Reference lists must be generated manually and not with the use of reference manager software.

References should be inserted in the text as superscript numbers and all references (including URLs) should be listed consecutively at the end of the article in numerical order of appearance in the Vancouver style (not alphabetical order). Excessive referencing should be avoided. Unpublished data and personal communications should not be included in the reference list but may be included in the text and cited as unpublished data/personal communication provided the author has permission to do this.

For journal references, names and initials of all the authors should be included (if there are more than six authors, the first three names should be given followed by et al.), followed by the title of article, name

of journal (journal abbreviations follow Index Medicus/MEDLINE), year, volume, and first and last pages.

For example: 1. Tockman MS, Anthonisen MD, Wright EC. Airways obstructions and the risk of lung cancer. Ann Intern Med 1987;106:512-518.

For book references, the author(s) should be followed by the chapter title (if applicable), editor(s) (if applicable), book title, place of publication, publisher, year and page numbers.

For example: Colby VT, Carrington CB. Infiltrative lung disease.

In: Thurlbeck WM, editor. Pathology of the Lung. New York: Theime Medical Publishers, 1988.

Copyright notice

The SARJ reserves copyright of the material published. The SARJ does not hold itself responsible for statements made by the authors.

The South African Respiratory Journal PO Box 13725 Mowbray 7705 Any correspondence to the Editor should be sent to the same address or via email to: sarj@iafrica.com The website of The South African Thoracic Society can be found at www.pulmonology.co.za

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The South African Respiratory Journal acknowledges with thanks the invaluable sponsorship of the following companies: Aspen GSK Division Bayer Healthcare