Selective Estrogen-Receptor Modulators and Aromatase Inhibitors: Promising New Medical Therapies for Endometriosis?

Simsa P, Peter Simsa, Péter Simsa, Attila Mihalyi, Mihalyi A, Cleophas Kyama, Cleophas M Kyama, Mwenda JM, Jason M. Mwenda, Fülöp V, Vilmos Fülöp, D'Hooghe TM, Thomas D'Hooghe, Thomas D’Hooghe, Thomas M D'Hooghe
Women's health (London, England) · 2007 · vol. 3(5) , pp. 617–628 · doi:10.2217/17455057.3.5.617 · PMID:19804039 · W2157072388
article OA: gold CC0 ⤵ 17 in-corpus citations
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Aromatase inhibitors, COX-2 inhibitors, and selective estrogen-receptor modulators are under investigation for endometriosis treatment due to their estrogen-targeting mechanisms, but their clinical value remains uncertain.

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Abstract

Endometriosis is an estrogen-dependent disease and estrogen-related pathways are imbalanced in women with endometriosis. One of the key enzymes in estrogen synthesis is aromatase. Inhibiting this pathway at several points is a promising idea for the treatment of endometriosis. The third generation of aromatase inhibitors is becoming more potent in efficacy, with fewer side effects than previous generations, but cotreatment with other hormones is needed to inhibit ovarian stimulation. Other components that promote estrogen synthesis such as COX-2 can also be potentially targeted. Selective estrogen-receptor modulators could also be interesting in view of their tissue-specific effect. However, all these new drugs are still in an early phase of development. At present, it is too early to conclude that aromatase inhibitors, COX-2 inhibitors or selective estrogen-receptor modulators really present any added value compared with the existing drugs that can be used to achieve hormonal suppression in the medical treatment of endometriosis.

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endometriosis

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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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