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. Underlyi
ng biochemical abnormalities in PCOS include luteinizing hormone (LH)
hypersecretion, hyperandrogenism, acyclic estrogen production, decreas
ed 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 accompan
ies upper body obesity, occurs independently of obesity alone, and pot
entiates ovarian hyperandrogenism by enhancing LH secretion, potentiat
ing 17-hydroxylase and, to a lesser extent, 17,20-lyase activity, and
suppressing SHBG capacity. All women with suspected hyperandrogenic an
ovulation should undergo an evaluation to rule out other endocrinopath
ies, such as virilizing tumors, adult-onset congenital adrenal hyperpl
asia.