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Endometriosis: the ultimate hormonal disease
Bilgin Gurates1, Serdar E Bulun
1Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Illinois at Chicago, 820 S. Wood Street, M/C 808, Chicago, IL 60612, USA.
Seminars in Reproductive Medicine
|August 15, 2003
Summary
Endometriosis tissue is resistant to progesterone, unlike normal endometrium. This resistance is linked to abnormal expression of aromatase, 17beta-HSD type 2, and progesterone receptors (PR-B/PR-A ratio).
Area of Science:
- Reproductive Endocrinology
- Gynecologic Pathology
Background:
- Estrogen promotes endometrial and endometriosis proliferation.
- Progesterone inhibits estrogen's mitogenic effects and promotes differentiation.
- Endometriosis exhibits reduced sensitivity to progesterone compared to normal endometrium.
Purpose of the Study:
- To review the molecular mechanisms underlying progesterone resistance in endometriosis.
- To investigate the role of aromatase, 17beta-hydroxysteroid dehydrogenase (HSD) type 2, and progesterone receptor (PR) expression in endometriosis.
Main Methods:
- Review of existing literature on gene and protein expression in endometriosis and endometrium.
- Analysis of the functional consequences of altered gene expression.
Main Results:
- Endometriosis tissue shows abnormal expression of aromatase, which synthesizes estrogen.
- 17beta-hydroxysteroid dehydrogenase (HSD) type 2, an enzyme that inactivates estrogen, is abnormally expressed.
- The ratio of progesterone receptor subtypes (PR-B/PR-A) is altered in endometriosis.
Conclusions:
- Abnormalities in aromatase, 17beta-HSD type 2, and PR-B/PR-A ratio contribute to progesterone resistance in endometriosis.
- These molecular alterations have significant functional implications for endometriosis development and progression.