Decreased prostacyclin production in the infant of the diabetic mother.

Maternal diabetes mellitus is recognized to be a predisposing factor to thrombosis in the neonate. In the adult with diabetes, abnormalities in the metabolism of AA by the platelet and vessel wall occur, which result in an increase in proaggregatory platelet thromboxane A2. A decrease in antiaggregatory vascular PGI2 has been demonstrated in the diabetic rat, although conclusive proof of a similar abnormality is lacking in humans. We evaluated vascular AA metabolism in 10 IDM (groups II and III comparison to 20 control neonates of gestational ages 32 to 40 weeks (group I). Mean uptakes of labeled AA into vascular tissue of both controls and IDM were similar. The conversion of [14C] AA to 6-keto-PGF1 alpha was not dependent on gestational age (r = 0.223) in the control neonates, with a mean value of 5.2% +/- 1.3 (1 S.D.). A marked decrease (p less than 0.001) in 6-keto-PGF1 alpha formation to 1.7% +/- 0.3 was found in the group II IDM of mothers with poor diabetic control (HbA1c = 9.3% +/- 0.5). In the group III neonates whose mothers had normal HBA1c levels (6.1% +/- 0.9), 6-keto-PGF1 alpha production was normal at 4.9% +/- 0.8. Although no correlation between maternal fasting blood glucose and neonatal 6-keto-PGF1 alpha was demonstrable, a significant inverse correlation (r = 0.872; p less than 0.02) was observed between maternal HbA1c levels and the conversion of AA to 6-keto-PGF1 alpha in the vascular tissues of the IDM. It appear possible that abnormalities in platelet-vascular AA metabolism may play an etiologic role in the vascular complications present in some IDM.