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Alterations in Circulating Human Chorionic Gonadotropin Free -Subunit in Insulin-Dependent Diabetic Pregnancy: Correlation with Maternal Characteristics^*

Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine Cincinnati, Ohio 45267

Address all correspondence and requests for reprints to: Robert M. Cohen, M.D., Division of Endocrinology and Metabolism, University of Cincinnati College of Medicine, 231 Bethesda Avenue, ML 547, Cincinnati, Ohio 45267–0547.

Circulating concentrations of hCG free -subunit (hCG) increase throughout pregnancy. To address the hypothesis that maternal plasma hCG may reflect placental dysfunction and/or adverse perinatal outcome during insulin-dependent diabetic pregnancy, hCG was measured serially throughout gestation, beginning before week 12, with a specific RIA using a monoclonal antibody in 54 insulin-dependent diabetic (randomly assigned to strict and customary glycemic control) and 25 nondiabetic pregnancies. hCG was significantly lower in pregnant insulin-dependent diabetic subjects than in nondiabetics subjects until 24 weeks gestation, after which it was higher until delivery. Plasma hCG stabilized in nondiabetics at 32 weeks, whereas it continued to increase in diabetics until delivery, at which time it was 37% greater than that in nondiabetics (mean ± SE, 1441 ± 90 vs. 1052 ± 78 µg/L; P < 0.002). Values in diabetic subjects assigned to strict control were intermediate between those in diabetic subjects assigned to customary control and nondiabetic subjects. hCG was greater in diabetic subjects with pregestational hypertension or micro-vascular disease, but not in those with pregnancy-induced hypertension. These findings were independent of the assigned goals of glycemic control. hCG was not correlated with the duration of diabetes or related to premature delivery, fetal distress, birth asphyxia, or macrosomia. Thus, hCG is increased during the third trimester of the type I diabetic pregnancy and is associated with preexisting hypertension and maternal microangiopathy, but is not a predictor of adverse perinatal outcome. Excessive hCG secretion in diabetes may share patho-physiological mechanisms in common with those underlying diabetic microangiopathy.

^* This work was supported in part by USPHS Grants HD-11725, RR-00068, and DK-38541 (to R.M.C.), a Research and Development Award from the American Diabetes Association (to R.M.C.), and a grant from Eli Lilly, France (to F.C.-B.).

Received December 18, 1989.

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