Sex Steroids and Endometriosis

Jo Kitawaki
In: Endometriosis · 2014 · pp. 147–154 · doi:10.1007/978-4-431-54421-0_10 · W1041122072
book-chapter OA: closed CC0
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-06 ⓘ

Endometriosis growth is estrogen dependent, with altered expression of steroid receptors and metabolic enzymes potentially increasing local estrogenic activity, and gene polymorphisms investigated for susceptibility.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-06 ⓘ

This chapter reviews why sex steroid biology is thought to contribute to endometriosis, focusing on estrogen-dependent lesion growth, differences in estrogen metabolism between women with normal endometrium and those with estrogen-dependent uterine diseases (including endometriosis and adenomyosis), and altered expression of estrogen and progesterone receptors plus 17β-hydroxysteroid dehydrogenase enzymes and aromatase in endometriotic tissue. It summarizes evidence that dysregulated receptor expression and steroidogenic enzyme activity may increase local estrogenic activity, and it surveys studies examining genetic polymorphisms in ESR1, ESR2, PR, HSD17B1, CYP17A1, and CYP19 for associations with endometriosis susceptibility. A major caveat is that, as a review/chapter, it compiles findings across heterogeneous studies rather than presenting new experimental data or a unified effect estimate. This paper is centrally about endometriosis — it synthesizes evidence on sex steroid receptors, steroidogenic enzymes, and related genetic polymorphisms in endometriosis.

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endometriosis

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last seen: 2026-06-10T17:14:06.276822+00:00
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