Mechanisms of excessive estrogen formation in endometriosis

Bulun SE, Serdar E Bulun, Bilgin Gürateş, Gurates B, Bilgin Gurates, Zongjuan Fang, Fang Z, Tamura M, Mitsutoshi Tamura, Sebastian S, Siby Sebastian, Jianfeng Zhou, Zhou J, Sanober Amin, Amin S, Yang S, Sijun Yang
Journal of reproductive immunology · 2002 · vol. 55(1-2) , pp. 21–33 · doi:10.1016/s0165-0378(01)00132-2 · PMID:12062819 · W2065466595
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This paper investigates the mechanisms underlying excessive estrogen production in endometriosis, a condition characterized by the abnormal growth of endometrial tissue outside the uterus.

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Abstract

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.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estrogens Aromatase Aromatase Aromatase Aromatase Inhibitors Endometriosis Endometriosis Endometriosis Enzyme Inhibitors Enzyme Inhibitors Estradiol Estradiol Estrogens Female Gene Expression Humans Inflammation Inflammation Inflammation

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Cited by (50)

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