Polycystic Ovarian Syndrome

Published on 06/06/2015 by admin

Filed under Pediatrics

Last modified 06/06/2015

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84 Polycystic Ovarian Syndrome

Polycystic ovarian syndrome (PCOS), the most common endocrinopathy affecting women, frequently presents during adolescence. PCOS is characterized by anovulatory menstrual dysfunction, hyperandrogenism, obesity, and metabolic disturbances including insulin-resistance and dyslipidemia. Pediatricians who learn to identify and manage PCOS can help address their adolescent patients’ immediate health concerns and reduce the likelihood of later sequelae, including endometrial hyperplasia and cardiovascular disease.

In 1935, Stein and Leventhal first described a syndrome characterized by enlarged ovaries, hirsutism, and chronic anovulation. Since that time, diagnostic guidelines have evolved. In 2009, the Androgen Excess and PCOS (AE-PCOS) Society Task Force published the following diagnostic guidelines for PCOS: (1) hyperandrogenism (clinical, biochemical, or both), (2) ovarian dysfunction (oligoanovulation, polycystic ovaries, or both), and (3) the exclusion of related disorders. Additionally, these new guidelines stress the importance of screening women with PCOS for metabolic syndrome. Metabolic syndrome includes a set of biological risks, including abdominal obesity, elevated serum triglycerides, and insulin resistance, that significantly increase the likelihood that an individual will develop cardiovascular disease.

Etiology and Pathogenesis

PCOS is thought to result from an interaction involving multiple genetic loci and environmental factors that disrupt several metabolic pathways. Resulting androgen excess can present as hyperandrogenism (Figure 84-1). One androgen pathway involved in PCOS is altered luteinizing hormone (LH) function, which can lead to increased androgen production by ovarian theca cells. This finding is especially common in thin or normal weight women with PCOS. Another potential pathway that leads to elevated androgens involves insulin resistance and compensatory hyperinsulinemia. Elevated insulin levels can also stimulate androgen production by ovarian theca cells while simultaneously inhibiting liver synthesis of sex hormone–binding globulin (SHBG), which in turn results in an increased fraction of bioavailable or free testosterone.

Clinical Presentation

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