Endocrinology

Future work should focus on optimising the balance between OCS efficacy and safety

J Michael Ramsahai · Peter AB Wark

A 58-year-old woman was admitted with chronic lower limb ulcers

Alicia R Jones · Kavita Kumareswaran

To the Editor: Retinal screening is crucial to the prevention of vision loss from diabetic retinopathy. The recent National Eye Health Survey highlighted a gap in screening rates between Indigenous Australians (aged ≥ 40 years) and non-Indigenous Australians (aged ≥ 50 years),1 providing a foundation on which to target future eye health services. While acknowledging the budgetary and logistical constraints of such a large-scale study, we are concerned that another at-risk group — younger adults with type 2 diabetes who are aged 18–49 years — was not included in the National Eye Health Survey. The past two decades have seen a global increase in the incidence of type 2 diabetes in youth and young adults, with younger age being an independent risk factor for the development of diabetic retinopathy.2 In Australia, about 130 000 people with type 2 diabetes who are aged < 50 years are registered on the National Diabetes Services Scheme.3 However, there are no population-level data available regarding retinal screening rates in this age group. A decade ago, a survey of young Australian adults with type 2 diabetes (aged 16–35 years) reported a 55% retinal screening rate.4 Given the small, self-selected sample, this is likely an overestimate and compares unfavourably with the non-Indigenous rate of 78% reported for adults aged ≥ 50 years in the National Eye Health Survey.1Moreover, our qualitative research has shown that young adults aged 18–39 years who have type 2 diabetes face different psychosocial challenges and barriers to retinal screening compared with their older counterparts aged ≥ 40 years.5 Younger adults with type 2 diabetes require targeted, tailored intervention, which can only be provided if accurate, population-level data are available for this group. As Foreman and colleagues1 acknowledge, diabetic retinopathy is the leading cause of vision loss in working age adults — a situation with potential for considerable social and economic burden. The absence of current eye examination data for younger Australians with type 2 diabetes increases the risk that their needs will be neglected in future evidence-based policy and program delivery initiatives. We urge the Australian Government and other stakeholders to extend future population-level surveys (and other research and policy initiatives) to include all adults with diabetes.

Amelia J Lake · Jessica L Browne · Jane Speight

In reply

Joshua Foreman · Stuart Keel · Mohamed Dirani

To the Editor: We note with interest the recent review of challenges in the management of maturity onset diabetes of the young associated with glucokinase gene mutations (GCK-MODY).1 In Box 2, Bishay and Greenfield reported a prevalence of gestational diabetes mellitus (GDM) of 5–10%. Indeed, in 2010 we reported an estimated prevalence of 10–11% of GDM in south-western Sydney;2 however, the prevalence is now almost double that figure (18.5% of births at Bankstown-Lidcombe hospital in 2015). Bishay and Greenfield also summarised the findings of Chakera and colleagues3 for a population of predominantly European descent: A lower body mass index (BMI, < 25 kg/m2) and a fasting glucose level greater than or equal to 5.5 mmol/L have sensitivity and specificity of 68% and 96%, respectively. It is estimated that among lean women with mild fasting hyperglycaemia, the number of women needed to test is 2.7 to detect a single case of GCK-MODY.1 In contrast, in our recent study of women with GDM, we found that at least 8.1 women would need to be tested to identify one case of GCK-MODY.4 Given our interest in the management of women with GDM, we sought to determine whether these criteria were applicable in a large multi-ethnic cohort of women with GDM. Analysing de-identified, prospectively collected data from all women with GDM in our ethnically diverse population, diagnosed using the Australasian Diabetes in Pregnancy Society (1998) criteria at our institution between 1993 and 2013, we categorised the women into two groups: those with body mass index ≤ 21 kg/m2 (group A1) and those with body mass index > 21 kg/m2 and < 25 kg/m2 (group A2). We collected complete data, including post-partum oral glucose tolerance test results, for 171 women (54, group A1; 117, group A2). The oral glucose tolerance test and post-partum glycated haemoglobin results identified few women (< 14%) in either group who still had possible GCK-MODY. Testing all 171 of these women in pregnancy would have been a costly exercise with a low yield. In testing data in different ethnic groups, we therefore recommend caution regarding the number suggested by Chakera and colleagues.

Jeff R Flack · Glynis P Ross · N Wah Cheung

In reply

Ramy H Bishay · Jerry R Greenfield

To the Editor:We read with interest the excellent review by Scott and colleagues1 on the contribution of sarcopenia to type 2 diabetes in the ageing Australian population. In a prospective Australian cohort of community-dwelling men, we recently found that muscle grip strength and muscle quality, but not muscle mass, were associated with incident type 2 diabetes at 5 years follow-up.2 These associations were not mediated by serum interleukin 6 or tumour necrosis alpha. As we did not examine sarcopenia, nor appendicular lean mass adjusted for body mass index (ALM-BMI), we have undertaken further analysis in 1180 participants with valid sarcopenia data. Their mean age was 56.9 years (standard deviation [SD] ± 10.9), mean ALM-BMI at baseline was 0.950 (SD ± 0.135) and mean peak hand grip strength at baseline was 48.7 kg (SD ± 9.9 kg). At 5 years follow-up, incident type 2 diabetes occurred in 119 participants (10.1%). Baseline ALM-BMI of less than 0.789 occurred in 9.2% of patients (n = 109) and baseline grip strength of less than 26 kg occurred in 1.4% of patients (n = 16), thus only six participants (0.5%) had sarcopenia as defined by the Foundation for the National Institutes of Health Biomarkers Consortium Sarcopenia Project (both ALM-BMI < 0.789 and peak hand grip strength < 26 kg).3 Hence, in our middle-aged Australian cohort of men, the prevalence of sarcopenia was very low. Moreover, while there was an unadjusted association between baseline ALM-BMI of less than 0.789 and incident type 2 diabetes (odds ratio [OR] 2.54; 95% CI, 1.49–4.17; P < 0.001), this attenuated to non-significance after adjustment for age, subcohort, income, fasting plasma glucose, physical activity, family history of diabetes, triglycerides and hypertension (OR 1.73; 95% CI, 0.95–3.05; P = 0.06). However, when analysing ALM-BMI as a continuous variable, the adjusted association was significant (OR per 0.1 unit decrease: 1.33; 95% CI, 1.13–1.58; P < 0.001). Overt sarcopenia may not have a large contribution to type 2 diabetes in community-dwelling Australians. Rather, reduction of skeletal muscle strength, ALM-BMI and muscle quality across the spectrum of healthy values may have greater population level significance. Our previous population-attributable fraction calculations suggest that a substantial proportion of incident type 2 diabetes may be prevented if muscle strength in the Australian community was generally increased.2

Joule J Li · Jonathan W Newbury · Robert J Adams

In reply

David Scott · Barbora de Courten · Peter R Ebeling