Estrogen Production and Metabolism in Endometriosis

Serdar E Bulun, Sijun Yang, Zhojuan Fang, Bilgin Gürateş, Bilgin Gurates, Mitsutoshi Tamura, Siby Sebastian
Annals of the New York Academy of Sciences · 2002 · vol. 955(1) , pp. 75–85 · doi:10.1111/j.1749-6632.2002.tb02767.x · PMID:11949967 · W1975163471
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Endometriosis tissue aberrantly expresses aromatase, stimulated by PGE2, leading to local estrogen production and a positive feedback cycle, while deficient 17beta-HSD type 2 impairs estrogen inactivation.

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Abstract

Aromatase activity is absent in normal endometrium. In contrast, aromatase is expressed aberrantly in endometriosis, which gives rise to strikingly high levels of aromatase activity in this tissue. Both aromatase expression and activity are stimulated by PGE2. This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis, that is, deficient 17beta-HSD type 2 expression, impairs the inactivation of estradiol to estrone. These molecular aberrations collectively favor accumulation of increasing quantities of estradiol and PGE2 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.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Estrogens Aromatase Aromatase Aromatase Inhibitors Dinoprostone Dinoprostone Endometriosis Endometriosis Endometriosis Endometrium Endometrium Enzyme Inhibitors Enzyme Inhibitors Enzyme Inhibitors Estrogens Estrogens Female Humans

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