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The Polycystic Ovary Syndrome: Pathogenesis and Treatment

Randall Barnes; and Robert L. Rosenfield, MD
[+] Article and Author Information

Grant Support: Supported in part by USPHS grants RR-00035 and HD-06308.

Requests for Reprints: Randall Barnes, MD, Department of Obstetrics/Gynecology, Box 446, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637.

Current Author Addresses: Dr. Barnes: Department of Obstetrics/Gynecology, Box 446, University of Chicago, 5841 S. Maryland Avenue, Chicago, IL 60637.

Dr. Rosenfield: Wyler Children's Hospital, University of Chicago, 5841 S. Maryland Avenue (Box 118), Chicago, IL 60637.


© 1989 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1989;110(5):386-399. doi:10.7326/0003-4819-110-5-386
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Purpose: To propose a theory for the pathogenesis of the polycystic ovary syndrome that explains the endocrinologic abnormalities of the syndrome and provides a rational approach to therapy.

Data Identification: An English-language literature search using MEDLINE (1975 to 1988) and extensive bibliographic reviews of identified articles.

Study Selection: We reviewed the literature and selected 169 articles considered most relevant for the definition of the endocrinologic abnormalities, elucidation of pathogenic mechanisms, or delineation of therapeutic interventions.

Data Extraction: The authors independently assessed study quality and data concerning endocrinologic abnormalities, pathogenic mechanisms, and therapy of the polycystic ovary syndrome.

Results of Data Synthesis: The polycystic ovary syndrome may be best defined as functional, gonadotropin-dependent ovarian hyperandrogenism. The polycystic ovary syndrome results when a primary defect increases one of three variables: the ratio of the serum concentrations of luteinizing hormone to follicle stimulating hormone, the ratio of the intraovarian concentrations of androgen to estrogen, or follicular atresia. An increase in one of these variables can then induce successive abnormalities in one or more of the remaining two variables in a to-and-fro manner.

Conclusions: Evidence suggests that several causes exist, each of which can produce the clinical syndrome by a to-and-fro interaction among pathogenic mechanisms. Treatment objectives for the syndrome include amelioration of hirsutism, induction of ovulation, and weight reduction.

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