Polycystic ovary syndrome

The cardinal clinical features of polycystic ovary syndrome (PCOS) are hirsutism and menstrual irregularity from anovulation. Obesity occurs in one half of these women, some of whom also have diabetes. Underlying biochemical abnormalities in PCOS include luteinizing hormone (LH) hypersecretion, hyperandrogenism, acyclic estrogen production, decreased sex hormone-binding globulin (SHBG) capacity, and hyperinsulinemia from insulin resistance, all of which contribute to increased ovarian androgen production. The hyperinsulinemia found in PCOS women accompanies upper body obesity, occurs independently of obesity alone, and potentiates ovarian hyperandrogenism by enhancing LH secretion, potentiating 17-hydroxylase and, to a lesser extent, 17,20-lyase activity, and suppressing SHBG capacity. All women with suspected hyperandrogenic anovulation should undergo an evaluation to rule out other endocrinopathies, such as virilizing tumors, adult-onset congenital adrenal hyperplasia.