Acceleration of fetal maturation by oxytocin-produced uterine contraction in pregnancies complicated with gestational diabetes mellitus: a preliminary report

Background: Prevention of the permanent sequelae of fetal hyperinsulinemia, namely hypertension and obesity, in infants born to mothers with gestational diabetes mellitus (GDM) has remained unresolved. Efforts to reduce fetal macrosomia by attempting to maintain blood sugar within a certain range have certainly failed. We have tried to eliminate fetal macrosomia by accelerating fetal maturation and delivery before the 36th week. Methods: Acceleration of fetal maturation was achieved by endogenous release of thyrotropin-releasing hormone brought about by periodic fluctuations in fetal oxygenation resulting from oxytocin-produced uterine contractions. Fifteen patients with GDM at 33-35 weeks, six of whom had previously given birth to a macrosomic fetus, agreed to participate in the study. Oxytocin was given for 6 h per day to produce regular contractions. In 13 patients it was given for 5 days, and in two patients for 7 days to reach a lecithin/sphingomyelin (L/S) ratio indicative of fetal maturity. Results: Eleven patients delivered vaginally after induction of labor and four delivered by Cesarean section. The mean Apgar score at 5 min was 9.13, and the mean birth weight was 2917 g (range 2100-3400 g). No newborn had respiratory difficulties, although four had short episodes of tachypnea. All were cared for in the regular nursery and all were discharged home with their mothers. Conclusion: Acceleration of fetal maturation, and delivery between 34 and 36 weeks, appears to be a promising means to reduce or even eliminate the permanent sequelae of fetal hyperinsulinemia in pregnancies complicated by GDM.