Polycystic Ovary Syndrome (PCOS)

Polycystic ovary syndrome results from interacting androgen excess, insulin resistance, and altered follicle development. Insulin resistance plays a central role—elevated insulin levels stimulate the ovaries to produce excess male hormones (androgens). Higher insulin also reduces sex hormone–binding globulin, increasing the amount of biologically active androgen. The follicles then stop developing before one becomes dominant and releases an ovum. This chronic anovulation produces infrequent or unpredictable menstrual bleeding, acne, hirsutism, and sometimes scalp hair thinning. The many small follicles seen on ultrasound are arrested follicles, not dangerous ovarian cysts; ovarian morphology is only one possible diagnostic feature. Without regular ovulation, progesterone is not produced cyclically. The endometrium may therefore remain exposed to estrogen without adequate progestational opposition, increasing the risk of endometrial hyperplasia and, over time, endometrial cancer. PCOS can occur at any body size, although excess adiposity may worsen insulin resistance and metabolic risk. Acanthosis nigricans—dark, thickened, velvety skin in the neck or skin folds—supports insulin resistance but does not establish the diagnosis.