Delayed appearance of pulmonary maturation markers is associated with poor glucose control in diabetic pregnancies.

Fetuses born after pregnancies complicated by diabetes display delayed pulmonary maturation as measured by the delayed appearance of biochemical indicators of pulmonary maturity (phosphatidylglycerol, lecithin/sphingomyelin ratio) and by the occurrence of hyaline membrane disease even in term gestations. We tested the hypothesis that poor maternal glycemic control is associated with delayed appearance of the biochemical markers of fetal pulmonary maturation. Consecutive diabetic pregnancies with documentation of maternal glycemic control and amniotic fluid analysis for PG were analyzed. Maternal glycemic control was defined as good if the mean blood glucose was < or = 5.8 mmol/L (105 mg/dl) and poor if > 5.8 mmol/L. The presence of amniotic fluid phosphatidylglycerol was considered an indicator of lung maturity. Hyaline membrane disease was defined by the criteria of Corbet et al. [J Pediatr 118:277-284, 1991]. A total of 621 diabetic pregnancies were analyzed (261 good glycemic control, 360 poor glycemic control). Phosphatidylglycerol was absent in 21% of good glycemic control vs. 31% of poor glycemic control pregnancies (P < 0.05). When stratified by gestational age, the risk of absence of phosphatidylglycerol was significantly higher in the poor glycemic control group (O.R. 1.83, 1.19-2.84). At 36-37.9 weeks, poor glycemic control pregnancies had significantly higher rates of absent phosphatidylglycerol (37% vs. 22%, O.R. 2.04, 1.1-3.9). All cases of hyaline membrane disease beyond 32 weeks gestation occurred in poor glycemic control pregnancies. There were no cases of hyaline membrane disease beyond 37.0 weeks gestation. We conclude that poorly controlled maternal glucose levels are associated with delayed appearance of phosphatidylglycerol in diabetic pregnancies. However, after 37.0 weeks of gestation, no significant neonatal pulmonary disease occurred.