Objective: To explore the abnormalities of serum inhibin isoform concentrations in a large group of patients with polycystic ovary syndrome (PCOS) and to evaluate the influence of body mass index (BMI), age, LH, and androgens on serum inhibin levels.
Design: Prospective study.
Setting: Reproductive endocrinology unit of an academic medical center.
Patient(s): Forty-one women with PCOS were compared with 24 healthy women.
Intervention(s): Blood sampling was performed in the early follicular phase in patients and in control women.
Main outcome measure(s): Serum levels of inhibin A, inhibin B, alpha-inhibin, pro-alphaC (alpha-inhibin precursor proteins), LH, FSH, E(2), T, and androstenedione (A) were assessed in all subjects.
Result(s): Serum alpha-inhibin levels together with LH, T, and A levels were significantly increased in women with PCOS. Serum inhibin A levels were lower in patients with PCOS than controls (median +/- SD: 7.35 +/- 2.9 vs. 9.4 +/- 4.7 pg/mL), pro-alphaC levels were higher (264 +/- 136.7 vs. 127 +/- 81.5 pg/mL), and inhibin B levels did not differ between the groups (110.5 +/- 51.5 vs. 108 +/- 47.5 pg/mL). Simple regression analysis showed that inhibin A and B levels were negatively correlated with BMI in patients with PCOS (r = -0.43 and r27 kg/m(2)) displayed significantly lower inhibin A and inhibin B levels and a higher pro-alphaC-inhibin A ratio than nonobese patients with PCOS (BMI </=27 kg/m(2)). In this last subgroup, the mean inhibin B level was significantly higher than in controls (median +/- SD: 144 +/- 53.5 vs. 108 +/- 47.5 pg/mL). Partial regression analysis, after controlling for age and BMI, demonstrated that in patients with PCOS, pro-alphaC levels were positively and independently correlated with LH and A levels.
Conclusion(s): Among women with PCOS, the trend toward an excess serum inhibin B level is observed exclusively in nonobese patients. The higher pro-alphaC levels and the lower inhibin A levels might reflect a defect in the processing of inhibins specific to polycystic ovaries. In addition, our data suggest that pro-alphaC originates from the theca-interstitial cells and could participate in control of the androgen production by these cells.