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University Hospital Clinical Laboratories and the Department of Obstetrics and Gynecology, University of Wisconsin, Madison, Wisconsin 53792
Address requests for reprints to: Dr. Ray V. Haning, Jr., Department of Obstetrics and Gynecology, University of Wisconsin, 600 Highland Avenue, Madison, Wisconsin 53792.
In normal pregnancy, maternal serum hCG reaches a maximum concentration about 8–10 weeks after the last menstrual period and then decreases. To investigate the possibility that this decrease in hCG is produced by an inhibitory effect of steroids originating in the feto-placental unit, hCG, progesterone, 17β-estradiol, and estriol were determined by specific RIAs in 341 serum specimens obtained from 229 different pregnancies. Expressions for predicted hCG as a function of estimated trophoblastic mass and percent predicted hCG were determined to correct for the increase in hCG with increasing trophoblastic mass. The relationships between hCG and progesterone, 17β-estradiol, estriol, or estimated trophoblastic mass were not linear. Expression of the hCG data as percent predicted hCG produced linear relationships between hCG and each of the above steroids. Both hCG itself and percent predicted hCG were shown to have a negative regression on estriol (P < 0.001) and a positive regression on progesterone (P < 0.001), but not on 17β-estradiol (P > 0.05), in a multiple linear regression on all three steroids. These data suggest that hCG production is inhibited by a steroid originating in the fetal adrenal. This inhibitory effect plateaus in late pregnancy, allowing a minor late increase in hCG due to increasing trophoblastic mass. (J Clin Endocrinol Metab 56:1188,1983)
* This work was supported by Bassil O'Connor Starter Research Grant 5-232 from the March of Dimes Birth Defects Foundation.
Received January 18, 1982.
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