Endometriosis: The Ultimate Hormonal Disease

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AI-generated summary by claude@2026-06, 2026-06-07

Endometriosis exhibits progesterone resistance and altered expression of aromatase, 17beta-HSD type 2, and PR-B/PR-A ratio, contributing to its hormonal pathology.

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AI-generated deep summary by claude@2026-06, 2026-06-07

This review discusses estrogen and progesterone regulation in endometrium versus endometriosis, focusing on steroidogenic and metabolic pathways involving aromatase, 17β-hydroxysteroid dehydrogenase type 2, and progesterone receptor isoforms. It reports that progesterone normally inhibits estrogen-driven proliferation and induces 17β-HSD type 2 to inactivate estradiol in endometrium, whereas these progesterone-dependent inhibitory/differentiative effects are less pronounced in endometriosis tissue. The review highlights observed abnormalities in endometriosis tissue expression of aromatase, 17β-HSD type 2, and the PR-B/PR-A ratio, and considers their functional consequences, while noting the paper is a narrative review synthesizing prior findings rather than presenting new experimental data. This paper is centrally about endometriosis — it frames endometriosis as a progesterone-resistant hormonal disorder driven by altered estrogen synthesis and metabolism.

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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 17beta-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, 17beta-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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Condition tags

endometriosis

MeSH descriptors

Endometriosis Hormones 17-Hydroxysteroid Dehydrogenases 17-Hydroxysteroid Dehydrogenases Animals Aromatase Aromatase Aromatase Inhibitors Drug Resistance Endometriosis Endometriosis Enzyme Inhibitors Enzyme Inhibitors Estradiol Estradiol Estrogens Estrogens Female Hormones Humans

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Cited by (50)

Source provenance

europepmc
last seen: 2026-06-13T06:22:48.782012+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:12:50.257867+00:00
License: CC0 · commercial use OK