Polycystic ovary <br />one of the first descriptions of a complex phenotype today known as the polycystic ovary syndrome.1 Insight into the pathogenesis and treatment of the polycystic ovary syndrome has increased substantially in the decade since this topic was last addressed in the Journal . 2 The condition is now well recognized as having a major effect throughout life on the reproductive, metabolic, and cardiovascular health of affected women. This review addresses current knowledge regarding the diagnosis, cause, and treatment of the polycystic ovary syndrome. <br />Several factors contribute to difficulties in the diagnosis of the polycystic ovary syndrome. Presenting signs and symptoms are heterogeneous and vary over time; in addition, a precise and uniform definition of the syndrome has been lacking. An international consensus group3 recently proposed that the syndrome can be diagnosed after the exclusion of other medical conditions that cause irregular menstrual cycles and androgen excess. <br />the determination that at least two of the following are present: oligoovulation or anovulation (usually manifested as oligomenorrhea or amenorrhea), elevated levels of circulating androgens (hyperandrogenemia) or clinical manifestations of androgen excess (hyperandrogenism), and polycystic ovaries as defined by ultrasonography. These criteria acknowledge the condition as functional: polycystic ovaries need not be present to make a diagnosis of the polycystic ovary syndrome, and conversely, their presence alone does not establish the diagnosis.<br /> Women with the polycystic ovary syndrome almost always have some aberration in gonadotropin secretion as compared with women who have normal menstrual cycles.8 However, since gonadotropin concentrations vary over the menstrual cycle and are released in a pulsatile fashion into the circulation, a single measurement of luteinizing hormone and follicle-stimulating hormone provides little diagnostic sensitivity. Thus, in routine clinical practice, abnormal gonadotropin levels (an elevated level of luteinizing hormone or an elevated ratio of luteinizing hormone to follicle-stimulating hormone) need not be documented to diagnose the polycystic ovary syndrome. <br />Insulin plays both direct and indirect roles in the pathogenesis of hyperandrogenemia in the polycystic ovary syndrome. Insulin acts synergistically with luteinizing hormone to enhance the androgen production of theca cells. Insulin also inhibits hepatic synthesis of sex hormone–binding globulin, the key circulating protein that binds to testosterone, and thus increases the proportion of testosterone that circulates in the unbound, biologically available, or free, state. Because women with the polycystic ovary syndrome typically have hyperinsulinemia, the concentration of free testosterone is often elevated when the total testosterone concentration is at the upper range of normal or only modestly elevated . <br />The polycystic ovary syndrome might thus be viewed as a sex-specific form of the metabolic syndrome, and the term “syndrome XX” has been suggested as an apt term to underscore this association :<br />OBESITY -1 2 - IMPAIRED GLUCOSE TOLERANCE AND TYPE 2 DIABETES <br />3 -HYPERTENSION AND VASCULAR DYSFUNCTION -Coronary and other vascular disease 4<br />OBSTRUCTIVE SLEEP APNEA -5<br />ASSOCIATION WITH CANCER -6<br /> References :- Stein IF, Leventhal ML. Amenorrhea associated with bilateral polycystic ovaries. Am J Obstet Gynecol 1935;29:181-191. .<br />-Franks S. Polycystic ovary syndrome. N Engl J Med 1995;333:853-861[Erratum, N Engl J Med 1995;333:1435. <br />