&NA;In order to assess the ovarian and adrenal contribution to peripheral steroid levels in 2 hirsute women, 1 with regular menstrual cycles (H‐E) and the other with oligomenorrhea (HOA), daily blood samples were collected during two consecutive menstrual cycles. The first cycle served as control, and dexamethasone (Dex), 0.5 mg four times a day, was administered during the second cycle. The serum levels of the following steroids were measured: pregnenolone (&Dgr;5‐P), 17‐hydroxy‐pregnenolone (17‐&Dgr;5‐P), progesterone (P), 17‐hydroxy‐progesterone (17‐P), cortisol (F), dehydroepiandrosterone (DHEA), its sulfate (DHEA‐S), androstenedione (A), testosterone (T), 5&agr;‐dihydrotestosterone (DHT), estrone (E1), and estradiol‐17&bgr; (E2). Peripheral levels of P were suggestive of ovulatory cycles in all four cycles studied. Peripheral levels of 17‐P were elevated during the follicular phase of both control cycles and did not suppress to normal levels during the treated cycle, suggesting the ovary as the main source of excess 17‐P secretion in both subjects. The H‐E subject showed elevated F levels during the control cycle. In both subjects, F suppressed maximally within 5 days of treatment and remained low during Dex administration. Assuming that Dex treatment had no significant effect on ovarian steroidogenesis and suppressed completely the zona fasciculata and reticularis of the adrenal cortex, the following conclusions can be made: 1) the steroid 17‐&Dgr;5‐P is almost exclusively of adrenal origin in both subjects; 2) there is an increased secretion of &Dgr;5‐P during the luteal phase which was masked by the adrenal contribution to peripheral &Dgr;5‐P; 3) in both subjects there is evidence for mixed adrenal and ovarian causes of excess androgens; 4) the elevated DHEA and DHEAS levels observed in both subjects were of adrenal origin; 5) the elevated T and DHT were of ovarian origin in the H‐OA subject and of mixed adrenal‐ovarian origin in the H‐E subjects; and 6) the data suggest a different mechanism of control for DHEA‐S and F secretion by the adrenal cortex.