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The reproductive phenotype in polycystic ovary syndrome

Nature Clinical Practice Endocrinology & Metabolism volume 3, pages 688–695 (2007)Cite this article

Abstract

The symptoms of women with polycystic ovary syndrome (PCOS) include hirsutism and irregular menstrual bleeding due to ovarian androgen excess and chronic anovulation. Typically, these features emerge late in puberty or shortly thereafter. The proposed mechanism(s) responsible for increased ovarian androgen production include heightened theca cell responsiveness to gonadotropin stimulation, increased pituitary secretion of luteinizing hormone, and hyperinsulinemia. The cause of ovulatory dysfunction is not well understood, but is linked to abnormal follicle growth and development within the ovary. As a result, infertility is common among women with PCOS and, in many instances, is the initial presenting complaint. Insulin resistance and obesity are frequently associated with PCOS and probably contribute to the severity of symptoms. The polycystic ovary that accompanies the syndrome has recently been defined as having 12 or more follicles per ovary or an ovarian volume greater than 10 ml as determined by ultrasonography. In addition, there is an increased number of growing follicles in the polycystic ovary. Despite this distinctive appearance, the cause and development of the polycystic ovary are completely unknown.

Key Points

  • Diagnostic criteria for polycystic ovary syndrome (PCOS) include hirsutism, irregular menstrual bleeding and evidence of polycystic ovaries

  • In women with PCOS, the primary source of excess androgen production is the ovary

  • The mechanism for irregular menstrual bleeding is endometrial responses to persistent and variable unopposed estrogen secretion

  • Women with PCOS at increased risk for endometrial adenocarcinoma

  • The presence of obesity and insulin resistance increases the severity of clinical presentation in women with PCOS

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Figure 1: Pathophysiology of polycystic ovary syndrome (PCOS).

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Article 18 October 2019

Selma Feldman Witchel, Helena J. Teede & Alexia S. Peña

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Acknowledgements

This work was supported in part by the National Institute of Child Health and Human Development (NICHD) and NIH through cooperative agreement U54 HD 12303-20 as part of the Specialized Cooperative Centers Program in Reproduction and Infertility Research and in part by NIH grant MO1 RR00827. Désirée Lie, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape-accredited continuing medical education activity associated with this article.

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  1. Division of Reproductive Endocrinology, Department of Reproductive Medicine, University of California, San Diego School of Medicine-0633, La Jolla, CA 92093-0633, USA rjchang@ucsd.edu

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  1. RJ Chang is Professor and Director in the Division of Reproductive Endocrinology, Department of Reproductive Medicine, University of California, San Diego School of Medicine, La Jolla, CA, USA.,

    R Jeffrey Chang

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Chang, R. The reproductive phenotype in polycystic ovary syndrome. Nat Rev Endocrinol 3, 688–695 (2007). https://doi.org/10.1038/ncpendmet0637

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