Uterine Adenomyosis: From Disease Pathogenesis to a New Medical Approach Using GnRH Antagonists

Jacques Donnez, Christina Anna Stratopoulou, Marie-Madeleine Dolmans, Marie‐Madeleine Dolmans
International journal of environmental research and public health · 2021 · vol. 18(19) , pp. 9941 · doi:10.3390/ijerph18199941 · PMID:34639243 · W3198978806
review OA: gold CC0 ⤵ 32 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review explores adenomyosis pathogenesis and hyperestrogenism mechanisms, discussing the potential of GnRH antagonists for treating the disease and alleviating symptoms.

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Abstract

Uterine adenomyosis is a common chronic disorder frequently encountered in reproductive-age women, causing heavy menstrual bleeding, intense pelvic pain, and infertility. Despite its high prevalence, its etiopathogenesis is not yet fully understood, so there are currently no specific drugs to treat the disease. A number of dysregulated mechanisms are believed to contribute to adenomyosis development and symptoms, including sex steroid signaling, endometrial proliferation and invasiveness, and aberrant immune response. Abnormal sex steroid signaling, particularly hyperestrogenism and subsequent progesterone resistance, are known to play a pivotal role in its pathogenesis, which is why various antiestrogenic agents have been used to manage adenomyosis-related symptoms. Among them, gonadotropin-releasing hormone (GnRH) antagonists are swiftly gaining ground, with recent studies reporting efficient lesion regression and symptom alleviation. The aim of the present review is to compile available information on the pathogenesis of adenomyosis, explore the etiology and mechanisms of hyperestrogenism, and discuss the potential of antiestrogenic therapies for treating the disease and improving patient quality of life.

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Condition tags

adenomyosisinfertility

MeSH descriptors

Adenomyosis Adenomyosis Uterine Diseases Endometrium Female Gonadotropin-Releasing Hormone Humans Quality of Life

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (93)

Cited by (32)

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