Correlation of Human Follicular Fluid Inhibin Activity with Spontaneous and Induced Follicle Maturation*

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Abstract
We sought to correlate the inhibin activity of individual ovarian follicles (>16 mm in diameter) from untreated (7 patients; 7 follicles), clomiphene-stimulated (150 mg/day; menstrual cycle days 5–9; 9 patients, 14 follicles), and human menopausal gonadotropin(hMG)-stimulated (150 IU/day; menstrual cycle days 3–11; 8 patients; 23 follicles) ovarian cycles and to correlate these results with the follicular fluid (FF) steroid concentration.Follicular aspirates were obtained via laparoscopy from 24 regularly menstruating patients when the diameter of the largest follicle reached 20 mm, as determined by serial ultrasonography. FF concentrations of estradiol, progesterone, testosterone, 17 - hydroxyprogesterone, and androstenedionewere determined by RIA. Inhibin activity was determined using the inhibition of basal 24-h FSH secretion by dispersed rat anterior pituitary cells. Inhibin values were highest among the follicles aspirated from those patients who received hMG [277 ± 31 (±SE) U/ml] compared to untreated subjects (51 ± 13 U/ml) or those who received clomiphene (96 ± 14 U/ml). Estradiol was highest in FF from untreated patients (2295 ± 1155 ng/ml) compared to levels in patients who received hMG (368 ± 1.76 μg/ml) or clomiphene (1049 ± 174 ng/ml). FF progesterone values were highest in untreated patients (9.4 ± 2.59 μg/ml) compared to those in hMG-treated (5.04 ± 1.76 μg/ml) and clomiphene-treated patients (7.82 ± 1.24 ng/ml). FF 17-hydroxyprogesterone values were similarly higher in the untreated (1.55 ± 0.21 μg/ml) and clomiphene-treated (2.54 ± 0.27 μg/ml) patients than in the hMG-treated group (0.73 ± 0.09 μg/ml). FF androstenedione (untreated, 50.7 ± 30 ng/ml; clomiphene-treated, 73.4 ±23.4 ng/ml; hMG-treated, 60.2 ± 19.8 ng/ml) and testosterone (6.66 ± 2.45, 5.98 ± 1.46, and 6.39 ± 2.16 ng/ml, respectively) concentrations in all three patient groups were similar. In untreated patients, there was a highly significant positive correlation between intrafollicular inhibin activity and FF estradiol, testosterone, and androstenedione concentrations and a statistically significant negative correlation between intrafollicular inhibin activity and FF progesterone concentrations. Patients receiving clomiphene therapy demonstrated at least two different response patterns, one with a positive and one a negative correlationbetween intrafollicular inhibin activity and FF steroid concentrations. The patients receiving hMGtherapy had no statistically significant correlation between intrafollicular inhibin activity and FF estradiol, progesterone, testosterone, and andos-tenedione levels. In conclusion, correlation of FF inhibin activity with FF steroid levels in normally cycling patients as opposed to those stimulated with clomiphene or hMG suggests that inhibin, in conjunctionwith gonadotropins, plays a central role in the regulation of folliculogenesis.