Polycystic Ovarian Syndrome

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POLYCYSTIC OVARIAN SYNDROME
(1) Etiology
Women with polycystic ovarian syndrome (PCOS) have abnormalities in the metabolism of androgens and estrogen and in the control of androgen production. High serum concentrations of androgenic hormones, such as testosterone, androstenedione, and dehydroepiandrosterone sulfate (DHEA-S), may be encountered in these patients. However, individual variation is considerable, and a particular patient might have normal androgen levels. PCOS is also associated with peripheral insulin resistance and hyperinsulinemia, and obesity amplifies the degree of both abnormalities. Insulin resistance in PCOS can be secondary to a postbinding defect in insulin receptor signaling pathways, and elevated insulin levels may have gonadotropin-augmenting effects on ovarian function. In addition, insulin resistance in PCOS has been associated with adiponectin, a hormone secreted by adipocytes that regulates lipid metabolism and glucose levels; lean and obese women with PCOS have lower adiponectin levels than do women without PCOS.[5] A proposed mechanism for anovulation and elevated androgen levels suggests that, under the increased stimulatory effect of luteinizing hormone (LH) secreted by the anterior pituitary, stimulation of the ovarian theca cells is increased. These cells, in turn, increase the production of androgens (eg, testosterone, androstenedione). Because of a decreased level of follicle-stimulating hormone (FSH) relative to LH, the ovarian granulosa cells cannot aromatize the androgens to estrogens, which leads to decreased estrogen levels and consequent anovulation. Growth hormone (GH) and insulin-like growth factor–1 (IGF-1) may also augment the effect on ovarian function.[6] Hyperinsulinemia is also responsible for dyslipidemia and for elevated levels of plasminogen activator inhibitor-1 (PAI-1) in patients with PCOS. Elevated PAI-1 levels are a risk factor for intravascular thrombosis. Polycystic ovaries are enlarged bilaterally and have a smooth, thickened capsule that is avascular. On cut sections, subcapsular follicles in various stages of atresia are seen in the peripheral part of the ovary. The most striking ovarian feature of PCOS is hyperplasia of the theca stromal cells surrounding arrested follicles. On microscopic examination, luteinized theca cells are seen. Causes of PCOS

The cause of PCOS is unknown, although some evidence suggests that patients have a functional abnormality of cytochrome P450c17, the 17-hydroxylase, which is the rate-limiting enzyme in androgen biosynthesis.[5] Cytochrome P450c17 is active in the adrenals and ovaries, and excess activity of this enzyme could explain the increased androgen production from both sources in PCOS. PCOS is, in some cases, a familial disorder, but the genetic basis of the syndrome remains unclear.[6] Studies of family members with PCOS indicate that an autosomal dominant mode of inheritance, with premature male pattern baldness as the male phenotype, may occur. Full expression of the syndrome may require an insulin abnormality and a defect in androgen biosynthesis, but no gene (or genes) has been identified. Risk Factors

* Hyperinsulinemia secondary to insulin resistance; associated with type 2 diabetes mellitus * Obesity, especially upper body obesity, which is probably related to insulin resistance and hyperinsulinemia * Family history of PCOS among first-degree relatives

(2) Epidemiology
In the United States, polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders of women in the reproductive age group, with a prevalence of 4-12%.[7, 8] In various European studies, the prevalence of PCOS was 6.5-8%.[9, 10] A great deal of ethnic variability in hirsutism is observed. For instance, Asian women have less hirsutism given the same serum androgen values as white women. On the other hand, southern Mediterranean women more often are hirsute. PCOS affects premenopausal women, and the age of...
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