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December 14, 1940


Author Affiliations


From the George F. Baker Clinic of the New England Deaconess Hospital, Elliott P. Joslin, medical director.

JAMA. 1940;115(24):2039-2040. doi:10.1001/jama.1940.02810500007002

Our present conception of the mechanism of the accidents in diabetic pregnancies has been the outcome, first, of our realization that adequate dietary control of diabetes and insulin therapy did not lower the fetal mortality rate and, second, our correlation of the behavior of diabetic pregnancies in relation to the balance of pregnancy hormones—chorionic gonadotropin, estrogen and progesterone.1 We believe (1) that an abnormal rise of chorionic gonadotropin after the twentieth week to a level of 200 rat units per hundred cubic centimeters of blood predicts in the diabetic premature delivery, stillbirth and neonatal deaths, (2) that these accidents are caused by a failure of production or of metabolism of estrogen and progesterone and (3) that they are prevented by continuous substitutional estrogen and progesterone therapy in replacement doses.

These conclusions are based on an analysis of sixty-one completed diabetic pregnancies treated and studied at the George F. Baker

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