Semin Reprod Med 2003; 21(2): 125-134
DOI: 10.1055/s-2003-41319
Copyright © 2003 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

Endometriosis: The Ultimate Hormonal Disease

Bilgin Gurates, Serdar E. Bulun
  • Division of Reproductive Endocrinology Infertility, Departments of Obstetrics Gynecology and Molecular Genetics University of Illinois at Chicago Chicago, Illinois
Further Information

Publication History

Publication Date:
14 August 2003 (online)

ABSTRACT

Estrogen is an extremely potent mitogen for endometrium and endometriosis. Progesterone, on the other hand, inhibits the mitogenic action of estrogen on endometrium and enhances differentiation. These antiproliferative and differentiative effects of progesterone are less pronounced on endometriosis tissue compared with endometrium. Thus, endometriosis is, at least in part, resistant to progesterone action. The product of a single gene named aromatase synthesizes estrogen. The potent estrogen estradiol is metabolized and thus inactivated by an enzyme termed 17β-hydroxysteroid dehydrogenase (HSD) type 2 that is normally induced by progesterone in endometrium. Progesterone action is mediated by its receptor subtypes progesterone receptor (PR)-A and PR-B. We found a number of abnormalities in the expression of aromatase, 17β-HSD type 2, and the PR-B/PR-A ratio in endometriosis tissue. These abnormalities and their functional consequences are discussed in this review article.

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