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Initaial hope that ovarian hyperstimulation syndrome (OHSS) would be less likely to occur after pituitary suppression with gonadotropin releasing-hormone agonists (GnRH-a) has not been substantiated. GnRH-alhuman menopausal gonadotropin (hMG) protocols often lead to OHSS with markedly elevated circulating estradiol (E2) levels in susceptible patients. This study was undertaken to determine whether or not intrafollicular E2 secretion is increased in these cases. Fifty-two in vitro fertilization (IVF) and gamete intrafallopian transfer (GIFT) conception cycles treated with GnRH-alhMG were included in the study. GnRH-a, leuprolide, 0.5 mg, was administered subcutaneously from day 20 of the preceding cycle and the ovaries were stimulated with hMG, 75-225 IU bid intramuscularly, followed by human chrionic gonadotropin (hCG), 5000 IU. Twenty cycles (Group I) were associated with moderate or severe OHSS and 32 cycles (Group II) did not result in OHSS. E2 was measured in the serum on the day of hCG (day 0), on the day of oocyte retrieval (day 2), and at midluteal phase (days 6–8), as well as in the follicular fluid (FF) using a solid-phase direct RIA. Mean serum E2 was significantly higher at all three sampling times in Group I (OHSS) than in Group II. Both the number of follicles and the number of oocytes were also significantly higher in Group I. Mean (±SD) FF E2 concentrations in both groups were similar (367±109 and 364±188) in follicles >15 mm in diameter but were increased in follicles =15 mm in diameter in OHSS (479±111) versus non-OHSS (230±32) patients. It appeared that OHSS was a function of an increased number of stimulated follicles as well as a result of altered steroidogenic function at the follicular level.