Piper J M, Langer O
Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio 78284-7836.
Eur J Obstet Gynecol Reprod Biol. 1993 Sep;51(1):15-9. doi: 10.1016/0028-2243(93)90185-f.
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.
