ROLE OF THE OVARY IN THE ADRENAL ANDROGEN EXCESS OF HYPERANDROGENIC WOMEN

Objective: To test the hypothesis that ovarian hormones in women with hyperandrogenism alter adrenocortical steroidogenesis. Design: Combina tion of two prospective studies. Setting: Academic medical centers. Pa tient(s): Eighteen hyperandrogenic patients demonstrating hirsutism wi th either hyperandrogenemia, oligomenorrhea, or both. Eighteen healthy nonhirsute eumenorrheic untreated women served as controls. Intervent ions: Blood sampling basally and after acute adrenal stimulation with ACTH, before and after 30-24 weeks of leuprolide administration. Nine patients also received 0.625 mg/d of oral conjugated esterified estrog ens and 10 mg of medroxyprogesterone acetate days 1-12 of the month (i .e., estrogen replacement therapy [ERT]), whereas the remaining nine d id not. Main Outcome Measure(s): Before and after the administration o f the GnRH agonist (GnRH-a), the basal concentrations of DHEAS; and th e levels of androstenedione (A4), DHEA, androstenediol, 11 beta-hydrox yandrostenedione (11-OHA4), and cortisol before and 60 minutes after a cute adrenal stimulation, were measured.Result(s): Levels of DHEAS, an drostenediol, and 11-OHA4 decreased by 15%-30%, regardless of whether patients initially had or did not have DHEAS excess. However, only hyp erandrogenic patients with elevated levels of DHEAS showed a significa nt decrease in basal DHEA levels. No statistically significant differe nce in the response of either androgen to ACTH (1-24) stimulation was noted with ovarian suppression, regardless of initial DHEAS level or u se of ERT. Conclusion(s): We found no evidence that ovarian hormone se cretion affected adrenal steroidogenesis, and those women with the hig hest adrenal androgen levels had the least response to GnRH-a suppress ion. These findings further support the concept of an intrinsic, and p ossibly primary, abnormality of adrenocortical steroidogenesis in a su bset of hyperandrogenic women that is independent of ovarian abnormali ties. (C) 1998 by American Society for Reproductive Medicine.