Pathophysiology and management of endometriosis.

Marian D. Damewood, M D Damewood
The Journal of family practice · 1993 · vol. 37(1) , pp. 68–75 · PMID:8345342 · W2414718123
article OA: closed CC0 ⤵ 6 in-corpus citations
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This paper reviews the pathophysiology of endometriosis, a common estrogen-dependent disease affecting reproductive-age women, and its management through GnRH analogues to induce a hypoestrogenic state.

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Abstract

Endometriosis is a common disease that affects up to 5 million women in the United States. Specifically the prevalence of endometriosis is 1 in 15 (7%) women of reproductive age, and there is an associated incidence of infertility in as many as 30% to 40% of cases. The precise physiologic mechanism for the development of endometriosis lesions in the pelvis and abdominal cavity has not been elucidated. Substantial evidence exists, however, that endometriosis is dependent on estrogen for continued growth and proliferation. Therefore, suppression of the hypothalamic-pituitary-ovarian axis with analogues of a gonadotropin-releasing hormone is being increasingly undertaken. Since the most effective resolution of endometriosis occurs after oophorectomy or onset of menopause, the hypoestrogenic state induced by GnRH analogues is of major significance for patients with active disease. Medical therapy for endometriosis is often used as primary therapy for symptomatic disease or as an adjunct to surgical management of pelvic pain or infertility.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Pelvic Neoplasms Pelvic Neoplasms Pelvic Neoplasms Pelvic Neoplasms Female Gonadotropin-Releasing Hormone Gonadotropin-Releasing Hormone Humans

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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License: CC0 · commercial use OK