Numerical data were compared using a two-sample Wilcoxon rank-sum test, and categorical data were compared using a Pearson Chi-square test with test for trend, as appropriate. The associations between the combination of GDM and obesity and the indicators of abnormal fetal growth were modelled using log-binomial regression to obtain adjusted relative risks. The relative risk of AC in the top decile at 28wkGA associated with subsequent GDM was estimated in the whole study group and stratified by maternal obesity, the treatment used, the diagnostic criteria employed, and confined to women with a normal post-partum OGTT. Non-linearity was assessed using fractional polynomials and interactions were tested using the likelihood ratio test. Missing covariate data were imputed using chained equations. All analyses were adjusted for the year of the 28 wkGA scan to take into account any temporal changes in the incidence, screening, diagnosis or treatment of GDM. Analyses were performed with and without adjustment for maternal age, height, ethnicity, weight gain and BMI, as appropriate. Finally, the relative risk of at birth associated with the indicators of abnormal fetal growth was estimated in the group of women who were obese and/or had GDM diagnosed at ≥28 wGA. All analyses used Stata version 14.0. Results Among 4,512 recruited women, a total of 4,305 attended for their 28 wkGA scan (see Sovio et al,10 for flow diagram). Of these, 7 withdrew, 6 failed to attend their 20 wkGA scan, 188 delivered elsewhere, 14 women had pre-existing diabetes, 17 women had GDM diagnosed prior to 28 wkGA and 7 women had missing data on GDM or BMI. A total of 236 (5.5%) of these women had one or more of the exclusion criteria, leaving a study group of 4,069 among whom 171 (4.2%) had a diagnosis of
GDM ≥28 wkGA. Women who subsequently developed GDM were older, shorter, more likely to be obese, gained slightly less weight, and were more likely to have induced labour and caesarean delivery (Table 1). Their babies were born slightly smaller, but had higher birth weight z scores and a higher proportion of them were . At 20 wkGA, there were no significant differences in fetal biometry associated with subsequent GDM, however, the risks of AC >90th and HC:AC ratio <10th percentile were increased in fetuses of obese mothers (Table 2). At 28 wkGA, subsequent GDM and maternal obesity were each associated with an approximate 2-fold risk of AC >90th and a 1.5 to 2-fold risk of HC:AC ratio <10th percentile. The effects of obesity and subsequent GDM were additive: the combination was associated with an almost 5-fold risk of AC >90th and an almost 3-fold risk of HC:AC ratio <10th percentile at 28 wkGA. Subsequent GDM and maternal obesity were each associated with an increased risk of AC growth velocity >90th percentile, and the combination was associated with an almost 3-fold risk. There were no interactions between the two exposures, or between either exposure and any of the maternal covariates in their associations with fetal biometry (all P>0.05). The relative risk of AC >90th percentile associated with subsequent GDM was similar when stratified by maternal obesity, the treatment used, the diagnostic criteria employed, and when the analysis was confined to women with a normal OGTT (Figure 1). Ultrasonic fetal biometry at 28 weeks identified pregnancies at increased risk of a infant at delivery among the 672 women who were obese and/or had a diagnosis of