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Effect of Androgen on Adrenal Steroidogenesis in Normal Women^*

Department of Obstetrics and Gynecology, University of Southern California School of Medicine, and Los Angeles County/University of Southern California Medical Center, Women's Hospital Los Angeles, California 90033

Address requests for reprints to: Rogerio A. Lobo, M.D., Women's Hospital, Room 1M2,1240 North Mission Road, Los Angeles, California 90033.

Ovarian hyperandrogenism may induce adrenal enzymatic defects that mimic true inherited disorders of adrenal hormone biosynthesis. To assess the effect of hyperandrogenism on adrenal steroidogenesis, seven normal ovulatory women were studied on 2 days during the early follicular phase of their cycles. Plasma 17-hydroxyprogesterone (17-Prog), 17-hydroxypregnenolone, dehydroepiandrosterone (DHEA), DHEA sulfate, androstenedione (Adione), testosterone (T), 11-deoxycortisol, and cortisol concentrations were measured every 15 min for 3 h after iv injection of 0.25 mg ACTH (day 1) and pretreatment with dexamethasone on each day. On the second study day, T (80 µg/h) was infused iv for 5 h, and ACTH was given after 2 h of T infusion. The T infusion raised mean serum T levels from 1.2 ± 0.3 (±SE) to 8.6 ± 0.6 nmol/L. The maximum incremental ( max) plasma Adione response to ACTH was significantly higher (2.6 ± 0.3 to 3.2 ± 0.4 nmol/L; P < 0.009) during the T infusion, while the max responses of the other steroids did not change. There was an increase in the max 17-Prog to cortisol ratio (4.9 ± 0.7 to 7.0 ± 1.0; P < 0.05), but no change in the max 17-Prog to Adione or 17-hydroxypregnenolone to DHEA ratios and no changes in the max ⁵- to ⁴-steroid ratios. These data suggest that acute T elevations result in subtle inhibition of 21- and/or 11β-hydroxylase activities, but not in 17-20-desmolase or 3β-ol activities.

^* This work was supported in part by NIH Grant HD-17519 and General Clinical Research Center Grant RR-43.

Received June 12, 1987.

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