A review of maturity onset diabetes of the young (MODY) and challenges in the management of glucokinase-MODY

We thank Flack and colleagues for their detailed comments on our review.1 The prevalence of gestational diabetes mellitus (GDM) of 5–10% was based on a prospective study by Moses and colleagues using the Australasian Diabetes in Pregnancy Society criteria, which found a prevalence in Wollongong, New South Wales, of 8.6–10.5% (9.6% overall).2 Using the more recently adopted International Association of Diabetes and Pregnancy Study Groups diagnostic definition in the same study, the prevalence of GDM was 13.0%. However, the cohort primarily comprised Australian women of European descent and the data were likely influenced by the slightly older maternal age; therefore, it may not reflect the national prevalence of GDM. Although other studies have produced a similar figure (eg, 13.6%),3 data from the National Perinatal Data Collection provided by the Australian Institute of Health and Welfare indicated a prevalence of 4.8%.4 Therefore, a range of 5–10% was deemed an adequate approximation. We agree with Flack and colleagues that certain multi-ethnic populations (eg, Bankstown-Lidcombe) will have higher GDM prevalence rates.

The second comment related to the number of pregnant women with slim body habitus (body mass index, < 25 kg/m²) and isolated fasting hyperglycaemia (≥ 5.5 mmol/L) needed to test to yield one diagnosis of maturity onset diabetes of the young due to a glucokinase mutation (GCK-MODY). The figure of 2.7 derived from a study of primarily European women with a small (7%) ethnic minority.5 Although not representative of the multicultural Australian population, this study remains one of the largest population studies addressing GCK-MODY prevalence in pregnancy (n = 5500). Further, it is clear that the presence of a predominantly ethnic population, as noted from the authors’ cited studies (eg, Asian, Middle Eastern, Indian and Afro-Caribbean), may diminish the relative proportion of GDM secondary to GCK mutations, given the higher likelihood of insulin resistance in these populations. We agree that, in this context, the number needed to test may be much higher than 2.7; however, no large population-based Australian studies with confirmatory genetic testing were available at the time of writing.