Despite growing knowledge of the pathophysiology leading to the development of preeclampsia (PreE) and diabetes mellitus (DM), the interaction between the two disease processes needs to be further examined. This study compared normal pregnancies to those complicated with preE, gestational diabetes mellitus (GDM), and/or pre-existing diabetes in order to assess the effects of elevated glucose on placental development and its potential role in the pathogenesis of preE.
The chart review was performed in an IRB approved retrospective cross-sectional study of live born singleton deliveries. A total 621 subjects were randomly selected from deliveries occurring between 2008 to 2011 at Baylor Scott & White Memorial hospital. Statistical analysis was performed using Duncan's post-hoc test and ANOVA.
Patients who developed preE had higher systolic and diastolic blood pressures than those who did not develop preE (p<0.05). Patients with either pre-existing diabetes or GDM were older. There was no difference among groups for gravidity (p=0.21) with an average gravidity of 2.7 (1.8SD) for 621 subjects and a range of 1 to 14 pregnancies. Patients with preE delivered earlier in pregnancy than those without preE regardless of diabetes status. However, those with preE and pre-existing diabetes delivered significantly earlier at 35.0+/−0.4 than the other two preE groups (*p<0.05 for each), suggesting more severe condition. Additionally, patients with pre-existing diabetes who developed preE delivered smaller babies than those with pre-existing diabetes without preE (1.00±0.03, p<0.05 for each). However, the development of GDM did not result in smaller babies for those pregnancies with preE.
The development of preE in those with pre-existing diabetes led to growth restriction and more severe disease as evidenced by lower birth weights and earlier gestational ages at delivery. These differences were not seen in GDM pregnancies. This supports the concept that elevated glucose levels during placental development in the first trimester may alter the placenta and lead to restriction later in pregnancy when a second stimulus triggers preE.