Polycystic Ovary Syndrome

In 1935, a specific ovarian morphology of cystic and enlarged ovaries was described at laparotomy in seven women with obesity, amenorrhea or menstrual irregularity, hirsutism, and infertility. In several further studies in the 1950s and ‘70s, specific endocrine features of increased luteinizing hormone levels and hyperandrogenemia were described in these women. In the early ‘70s, with the availability of ultrasonography (US), noninvasive assessment of the ovaries was possible and, in 1985, a characteristic US appearance of polycystic ovaries was described. However, debate has remained concerning the correlation between the finding of polycystic ovaries on US and the clinical phenotype—some studies have shown that as many as 33% of apparently normal women will have polycystic ovaries. The etiology of polycystic ovary syndrome (PCOS) is also unknown. In 1935, Stein and Leventhal suggested a primary ovarian defect; however, more recently, a lot of interest has been focused on the role of insulin resistance as a common unifying hypothesis for the varied manifestation of this syndrome. Insulin resistance also has wider health implications such as diabetes, hypertension, and cardiovascular disease, and researchers are trying to quantify the risks of these conditions in PCOS. Therapy has evolved from a philosophy of primarily targeting the presenting clinical problem to ameliorating insulin resistance, which is now thought to be the primary defect. Improving insulin resistance has been shown to improve periods, fertility, and hyperandrogenemia. However, there remains some controversy as to the exact origin of this syndrome and it is still unknown which came first, “the insulin or the egg.”