Objectives: Ovulation induction cycles are routinely followed by serum estradiol (E2) and ultrasound changes in follicular growth.Design: We have studied serum androgens in these treated cycles to (1) determine serum levels of testosterone (T) and androstenedione (A) as indicators of ovarian response and (2) monitor serum levels of DHEA, DHEA-S and cortisol as indicators of any effect on adrenal steroidogenesis during this procedure. A recent report suggests that adrenal androgen synthesis during ovulation induction is suppressed.Materials and Methods: Ovulation induction cycles (n = 35) were divided into those who became pregnant (PRG; n = 20) and those who did not (NPRG; n = 15). Serum samples were obtained daily starting on cycle day 2 until hCG administration, which was based on serum E2 and follicle size and number, with less frequent sampling continued into the luteal phase. Serum samples were assayed for E2, P, and T by RIA (Diagnostic Products Inc. Los Angeles, CA) and A, DHEA, DHEA-S and cortisol by RIA (Diagnostic Systems Laboratories, Webster, TX).Results: Serum levels of T and A increased dramatically during the stimulation period generally above the normal range for cycling controls. These androgens declined to normal levels in NPRG subjects, but dropped and elevated again in PRG. There was no significant difference between PRG and NPRG groups in the pattern of max levels of T or A and these androgens correlated with E2 levels. In a group of the same patients (n = 17), serum levels were also assayed for D, DHEAS and cortisol. The pattern of serum DHEA in these subjects was variable but was decreased in almost all subjects but the timing of this decline was variable.Conclusions: In some subjects, DHEA declined during ovulation induction prior to hCG administration, but more frequently the decline occurred several days after hCG administration. The pattern for DHEAS was similar but, probably due to DHEAS longer half life, the decline was not always as evident. Cortisol levels did not usually show the same response as for DHEA or DHEAS, suggesting a difference in regulation for these adrenal steroids.