Mechanisms of excessive estrogen formation in endometriosis.

Published

Journal Article (Review)

Estrogen is produced in a number of human tissues including the ovary, placenta and extraglandular sites such as adipose tissue, skin and the brain. Aromatase is the key enzyme that regulates estrogen formation in these tissues. Aromatase activity is not detectable in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by PGE(2). This results in local production of estrogen, which induces PGE(2) formation and establishes a positive feedback cycle. Another abnormality in endometriosis, i.e. deficient 17beta-hydroxysteroid dehydrogenase (17beta-HSD) type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE(2) in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis using an aromatase inhibitor.

Full Text

Duke Authors

Cited Authors

  • Bulun, SE; Gurates, B; Fang, Z; Tamura, M; Sebastian, S; Zhou, J; Amin, S; Yang, S

Published Date

  • May 2002

Published In

Volume / Issue

  • 55 / 1-2

Start / End Page

  • 21 - 33

PubMed ID

  • 12062819

Pubmed Central ID

  • 12062819

International Standard Serial Number (ISSN)

  • 0165-0378

Language

  • eng

Conference Location

  • Ireland