Pathophysiology of polycystic ovary syndrome: the role of hyperandrogenism

The cardinal features of polycystic ovary syndrome (PCOS) are hyperandrogenism and oligoanovulation. The increase in ovarian androgen production is a fundamental characteristic of PCOS and, although enigmatic, it is at the heart of one of the major issues about the pathophysiology of PCOS, i.e. whether it has developmental origins or not. Intraovarian androgens are designated as primarily responsible for the follicle excess. The defective selection of a dominant follicle in anovulatory patients results from both an insufficient secretion of FSH and a local inhibition of FSH action. Anti-müllerian hormone (AMH) seems to be involved in the latter by repressing the FSH-dependent aromatase activity. AMH level is increased in PCOS because of the follicle excess and increased production per follicle. Therefore, in anovulatory patients, serum FSH, although at low to normal plasma concentrations, would not be able to induce a decrease in AMH sufficient to allow the expression of aromatase. In conclusion, the fundamental anomaly of PCOS is still unknown, but it can be hypothesized that any genetic, epigenetic or environmental factor leading to intraovarian hyperandrogenism can result in PCOS.