Pre-gestational diabetes and the risks of fetal and infant death in normally-formed offspring

Tennant, PWG; Glinianaia, SV; Bilous, RW; Rankin, J; Bell, R

doi:10.1136/archdischild-2013-303966.298

Pre-gestational diabetes and the risks of fetal and infant death in normally-formed offspring

Lookup NU author(s): Peter Tennant, Dr Svetlana Glinianaia, Professor Rudy Bilous, Professor Judith Rankin ORCiD, Dr Ruth Bell

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Abstract

Background: Pre-gestational diabetes is associated with substantially increased risks of congenital anomalies, but the impact on normally-formed offspring is less well explored. This study explored the risks of fetal and infant death, examining the influence of HbA1c, in normally-formed offspring of women with pre-gestational diabetes. Methods: All normally-formed singleton pregnancies in Northern England delivered during 1996–2008 were identified from the Northern Diabetes in Pregnancy Survey. Fetal (≥20 weeks gestation) and infant deaths were identified from the Northern Perinatal Morbidity and Mortality Survey. Relative risks were estimated by comparing the prevalence rates between those with and without diabetes. The associations between peri-conception and third trimester HbA1c with each outcome were examined by logistic regression. Results: 400,158 normally-formed singletons were registered during the study period, including 1548 in women with pre-gestational diabetes. There were 46 fetal and 10 infant deaths following pregnancies in women with diabetes. The relative risks of fetal and infant death associated with pre-gestational diabetes were 4.54 (95%CI: 3.41–6.05, p < 0.0001) and 1.82 (95%CI: 0.98–3.38, p = 0.06) respectively. The odds of a fetal or infant death increased by 19% (OR = 1.19, 95%CI: 1.02–1.39, p = 0.02) and 42% (OR = 1.42, 95%CI: 1.09–1.85, p = 0.01) respectively for each percentage increase in peri-conception HbA1c, although third trimester HbA1c was a stronger predictor of late fetal death (OR = 1.67, 95%CI: 1.25–2.24, p = 0.001). Conclusions: Pre-gestational diabetes is associated with a substantially increased risk of fetal death in normally-formed offspring. The effect is largely moderated by glycaemic control, with increasing HbA1c conferring higher risks of both fetal and infant death.