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Delayed appearance of pulmonary maturation markers is associated with poor glucose control in diabetic pregnancies
J M Piper1, E M Xenakis, O Langer
1Department of Obstetrics and Gynecology, University of Texas Health Science Center, San Antonio 78284-7836, USA.
Insights
Poor maternal glycemic control in diabetic pregnancies is linked to delayed fetal lung maturation, indicated by absent phosphatidylglycerol. However, lung disease risk diminishes after 37 weeks gestation.
Area of Science:
- Obstetrics and Gynecology
- Neonatology
- Endocrinology
Background:
- Diabetes in pregnancy can impair fetal pulmonary maturation.
- Delayed lung maturity increases the risk of respiratory distress in newborns.
Purpose of the Study:
- To investigate the association between maternal glycemic control and fetal lung maturity markers in diabetic pregnancies.
- To determine if poor glucose control correlates with delayed appearance of phosphatidylglycerol.
Main Methods:
- Analysis of 621 diabetic pregnancies with documented glycemic control and amniotic fluid phosphatidylglycerol (PG) levels.
- Maternal glycemic control classified as good (<= 5.8 mmol/L) or poor (> 5.8 mmol/L).
- Assessment of hyaline membrane disease occurrence based on established criteria.
Main Results:
- Phosphatidylglycerol was absent in 31% of poor glycemic control pregnancies versus 21% in good control pregnancies (P < 0.05).
- Poor glycemic control significantly increased the risk of absent PG, especially between 36-37.9 weeks gestation.
- All cases of hyaline membrane disease beyond 32 weeks occurred in the poorly controlled group, with none after 37 weeks.
Conclusions:
- Poor maternal glucose control is associated with delayed fetal lung maturation in diabetic pregnancies.
- While delayed PG appearance is noted, significant neonatal pulmonary disease was not observed after 37 weeks gestation.
Abstract:
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.