Progestins for the Treatment of Endometriosis: An Update

Lucia Lazzeri, Stefano Luisi, Felice Petraglia
In: Journal of Endometriosis · 2010 · vol. 2(4) , pp. 169–181 · doi:10.1177/228402651000200401 · W4246119652
article OA: closed CC0 ⤵ 4 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

This review examines the rationale and mechanisms of progestin therapy for endometriosis, evaluating established agents and highlighting the recent progestin dienogest.

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Abstract

Endometriosis is a gynecological condition that affects approximately 10% of women of reproductive age, including 25–40% of infertile women. Dysmenorrhea, dyspareunia and chronic pelvic pain are the most common symptoms. Currently available medical therapies for endometriosis do not cure the disease, but are directed at symptom relief, typically utilizing the hormone responsiveness of endometriotic tissue to induce lesion atrophy. Unfortunately, pain relapse after treatment suspension is a common event. Treatment with pharmacological therapies for endometriosis should be conceived in terms of years, thus agents that must be withdrawn after a few months due to poor tolerability or severe metabolic side effects do not greatly benefit women with symptomatic endometriosis. The characteristics of progestins render this class an ideal pharmacological choice for administration over extended periods. The present paper will review the rationale for using progestins and their mechanism of action in endometriosis. Thereafter, the results obtained by various progestins in the treatment of endometriosis will be evaluated (danazol, gestrinone, norethisterone acetate, desogestrel, cyproterone acetate, megestrol acetate, medroxyprogesterone acetate, and levonorgestrel). A progestin called dienogest, recently introduced for the treatment of endometriosis, will be given special focus, describing its mechanism of action and clinical results.

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Condition tags

endometriosischronic_pelvic_paindysmenorrheadyspareunia

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.

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