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Is lung maturation related to fetal growth in diabetic or hypertensive pregnancies?
1Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio 78284-7836.
Insights
Maternal diabetes or hypertension does not alter fetal pulmonary maturity timing in infants with abnormal growth. Macrosomic or growth-retarded infants show similar lung development rates compared to controls.
Area of Science:
- Perinatology
- Neonatology
- Obstetrics
Background:
- Maternal diabetes and hypertension can cause abnormal fetal growth, including macrosomia and growth retardation.
- The impact of these conditions on fetal pulmonary maturity timing is not fully understood.
- Pulmonary maturity is crucial for neonatal respiratory adaptation after birth.
Purpose of the Study:
- To investigate if maternal diabetes or hypertension affects fetal pulmonary maturity timing in infants with abnormal growth.
- To compare pulmonary maturity rates in infants with macrosomia or growth retardation versus those with normal growth.
- To determine if abnormal fetal growth secondary to maternal disease alters lung development trajectories.
Main Methods:
- Study included 874 women undergoing fetal pulmonary maturity testing.
- Infants were categorized by birth weight: small for gestational age (SGA), appropriate for gestational age (AGA), and large for gestational age (LGA).
- Pulmonary maturity was assessed using phosphatidylglycerol (PG) and lecithin/sphingomyelin (L/S) ratio.
Main Results:
- Pulmonary maturity rates (PG and L/S) did not differ between term large for gestational age (LGA) infants of diabetic mothers and controls.
- No significant differences in maturity rates were observed when comparing phosphatidylglycerol (PG) alone across study groups.
- Gestational age breakdown showed no significant variations in maturity rates between maternal disease and fetal size groups.
Conclusions:
- Macrosomic infants of diabetic mothers and growth-retarded infants of hypertensive mothers exhibit normal fetal pulmonary maturation timing.
- Maternal diabetes and hypertension, when leading to abnormal fetal growth, do not appear to delay or accelerate lung development.
- Fetal pulmonary maturity timing is consistent across groups, regardless of maternal disease status or fetal growth patterns.
Abstract:
The purpose of this study was to determine whether infants sufficiently affected by maternal diabetes or hypertension to exhibit abnormal growth (macrosomia, growth retardation) would also display significant alteration in timing of pulmonary maturity (delay or acceleration, respectively). We studied 874 consecutive women with fetal pulmonary maturity testing prior to delivery. Patients were stratified by birth weight into fetal size categories (small for gestational age [SGA], appropriate for gestational age [AGA], large for gestational age [LGA]). Cases were compared based on maternal disease, fetal size categories and pulmonary maturity testing results. Pulmonary maturity rates based on both phosphatidylglycerol (PG) and lecithin/sphingomyelin ratio (L/S) did not differ between term LGA infants of diabetic mothers (97%) and term LGA (80%) or AGA (97%) infants of non-diabetic, non-hypertensive mothers. When compared based on PG alone, there was no difference between the rate of positive PG in term AGA infants of non-hypertensive, non-diabetic mothers (75%) and that seen in the other pregnancy groups (33-80%). Breakdown by gestational age revealed no significant differences in maturity rates between the study groups. Macrosomic diabetic infants and growth-retarded hypertensive infants are no different from controls in their timing of fetal pulmonary maturation.