Polycystic ovary syndrome (PCOS) is a syndrome of chronic androgen excess that may have its origins in childhood or even in utero. The anovulation of PCOS usually seems to be attributable to intraovarian androgen excess, which in turn arises from functional ovarian hyperandrogenism. PCOS typically appears to arise as a complex genetic disorder in which an intrinsic genetic trait interacts with other congenital or extrinsic environmental factors to cause dysregulation of steroidogenesis. Insulin-resistant hyperinsulinism related to type 2 diabetes mellitus is often an important factor in the development of PCOS. PCOS should be suspected in an adolescent female with hirsutism, acne, seborrhea, diffuse alopecia, hyperhidrosis, menstrual irregularity, or obesity. Any one of these may be the sole feature. The natural history of PCOS is not known with certainty; yet, intrauterine growth retardation, premature pubarche and other forms of sexual precocity, and obesity seem to be risk factors and/or antecedents of PCOS. The diagnosis is based on clinical and biochemical criteria and exclusion of other causes of hyperandrogenism. Oral contraceptive therapy is usually first-line treatment. Adolescents with PCOS are at risk for diabetes mellitus and cardiovascular disease, as are their family members.
*Instructor of Pediatrics and †Professor of Pediatrics and Medicine, Departments of Pediatrics and Medicine, The University of Chicago Pritzker School of Medicine, Chicago, Illinois.
CHIEF EDITOR’S NOTE: This article is the 23rd of 36 that will be published in 2002 for which a total of up to 36 Category 1 CME credits can be earned. Instructions for how credits can be earned appear after the Table of Contents.
Acknowledgments: HD-39627 and RR-00055.
Address correspondence to: Elizabeth E. Baumann, M.D., University of Chicago Children’s Hospital, 5841 S. Maryland Avenue (MC 5053), Chicago, IL 60637-1470. Phone: 773-702-6432; Fax: 773-702-0443; E-mail: email@example.com OR firstname.lastname@example.org
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