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Effect of maternal-fetal disorders on lung maturation. I. Diabetes mellitus
Insights
Maternal diabetes does not significantly impact fetal lung maturity. Amniotic fluid analysis showed similar lecithin phosphorus levels in diabetic and healthy pregnancies, suggesting improved diabetic control normalizes the fetal environment.
Area of Science:
- Obstetrics and Gynecology
- Perinatology
- Endocrinology
Background:
- Fetal lung maturity is crucial for neonatal survival.
- Maternal diabetes historically raised concerns about delayed fetal lung maturation.
Purpose of the Study:
- To investigate the influence of maternal diabetes on fetal lung maturation.
- To compare amniotic fluid lecithin phosphorus levels between diabetic and healthy pregnancies.
Main Methods:
- Amniotic fluid samples were collected from 287 healthy and 198 diabetic women.
- Lecithin phosphorus concentration was analyzed in relation to gestational age.
- Diabetic patients were matched with control subjects based on race, infant sex, and gestational age.
Main Results:
- No statistically significant differences were found in regression lines of lecithin phosphorus concentration versus gestational age between diabetic and control groups.
- Matched analysis also revealed no significant differences between diabetic and control subjects.
- The proportion of mature lecithin phosphorus concentrations did not differ between diabetic and normal women.
Conclusions:
- Maternal diabetes, particularly with improved control, does not appear to negatively affect fetal lung maturation.
- Normalization of the fetal metabolic environment due to better diabetic management may explain these findings.
- This suggests a reduced risk of respiratory distress syndrome in neonates from well-controlled diabetic pregnancies.
Abstract:
Amniotic fluid for fetal lung maturity studies was obtained from 287 healthy and 198 diabetic women. Classes of diabetes were as follows: Class A, 111; Class B, 58; Class C, 13; Class D, 11; Class F, 4; and Class R, 1. The regression lines representing the relationship of amniotic fluid lecithin phosphorus concentration to gestational age at amniocentesis in each of the groups of diabetic patients were not statistically different from those of the control subjects. Each of the diabetic patients was then matched with a control subject of the same race, sex of newborn infant, and gestational age at amniocentesis. The regression lines of the nonhypertensive, hypertensive, and all diabetics were not different from those of their respective matched control subjects. Also there was no difference in the proportion of mature lecithin phosphorus concentrations at different weeks between diabetic and normal women. The absence of a significant influence of diabetes on fetal lung maturation is probably due to improvement in diabetic control resulting in normalization of the fetal metabolic environment.