OBJECTIVETo investigate the clinical significance of falling insulin requirements in women with preexisting or overt diabetes in pregnancy.
RESEARCH DESIGN AND METHODSA retrospective review of 139 pregnancies was conducted in women, with preexisting diabetes, delivering between January 2010 and January 2013. Women with falling insulin requirements of 15% or more from the peak total daily dose in late pregnancy were considered case subjects (n = 35). The primary outcome consisted of a composite of clinical markers of placental dysfunction, including preeclampsia, small for gestational age (SGA, £5th percentile for gestational age), stillbirth (>20 weeks), and premature delivery (£30 weeks).
RESULTSA total of 25.2% of women had >15% fall in insulin requirements with nulliparity as the only predictor at baseline (odds ratio [OR] 2.5 [95% CI 1.1-5.7], P = 0.03). Falling insulin requirements were associated with an increased risk of preeclampsia (OR 3.5 [1.1-10.7], P < 0.05) and the composite of clinical markers of placental dysfunction (4.4 [1.73-11.26], P = 0.002). Although falling insulin requirements were associated with higher rates of SGA (3.4 [1.0-11.3], P = 0.048), they were not associated with other adverse neonatal outcomes. However, there was a higher incidence of neonatal intensive care unit admission (15.5 [3.1-77.6], P = 0.001) and earlier delivery in this group (median 37.7 weeks ], P = 0.014).
CONCLUSIONSFalling insulin requirements, in women with preexisting diabetes, are associated with an increased risk of complications related to placental dysfunction. Further prospective studies are needed to guide clinical management.Falling insulin requirements in late pregnancy are thought to signify feto-placental compromise, often prompting admission to hospital for maternal and fetal monitoring as well as emergency delivery in some cases (1). Most women with preexisting diabetes experience an increase in insulin requirements during the second half of pregnancy (2) to maintain euglycemia, in light of a 50-70% rise in insulin resistance (3). Because insulin resistance is driven by placental-mediated hormone production, including human placental lactogen (hPL), cortisol, and progesterone