Endometriosis and Infertility: New Concepts

Isabelle P. Ryan, Robert N. Taylor
In: Obstetrical & Gynecological Survey · 1999 · vol. 54(Supplement) , pp. 197–203 · doi:10.1097/00006254-199911001-00030 · W4210674954
article OA: closed CC0 ⤵ 3 in-corpus citations
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This review explores local peritoneal inflammation, angiogenic factors, and endometrial biochemical differences as key concepts in understanding endometriosis pathophysiology and its link to infertility.

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This review examines the cellular and molecular interactions that drive the pathophysiology of endometriosis, focusing on three primary concepts to enhance understanding of the disorder. The authors highlight evidence of a local peritoneal inflammatory process characterized by elevated cytokines and growth factors, alongside the role of angiogenic factors in establishing ectopic implants. Additionally, the paper discusses biochemical differences between eutopic and ectopic endometrium in affected patients, which may contribute to both disease progression and clinical sequelae such as infertility. This paper is centrally about endometriosis — specifically exploring the molecular mechanisms underlying its association with infertility and pelvic pain.

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Abstract

Endometriosis is a common gynecological disorder with varied symptomatology including chronic pelvic pain, dysmenorrhea, and infertility. The association of endometriosis and infertility has been recognized for years, although definite evidence of causality still eludes us. In this review, we will explore three general concepts that enhance our understanding of the cellular and molecular interactions contributing to the pathophysiology of this disorder and that have steered current research in endometriosis. First, we review evidence of a local peritoneal inflammatory process, supported by the findings of elevated cytokine and growth factor concentrations in peritoneal fluid of affected patients. Second, we propose a role for angiogenic factors in the establishment of ectopic implants. Third, we review evidence for biochemical differences of eutopic and ectopic endometrium in endometriosis patients, which may contribute to both the pathogenesis and sequelae of this important disorder. Through information derived from these research efforts, we hope to develop better therapeutic interventions as adjunctive or alternative therapies to our current medical and surgical armamentarium.
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Endometriosis and Infertility: New Concepts - Isabelle P. Ryan - Robert N. Taylor Endometriosis is a common gynecological disorder with varied symptomatology including chronic pelvic pain, dysmenorrhea, and infertility. The association of endometriosis and infertility has been recognized for years, although definite evidence of causality still eludes us. In this review, we will explore three general concepts that enhance our understanding of the cellular and molecular interactions contributing to the pathophysiology of this disorder and that have steered current research in endometriosis. First, we review evidence of a local peritoneal inflammatory process, supported by the findings of elevated cytokine and growth factor concentrations in peritoneal fluid of affected patients. Second, we propose a role for angiogenic factors in the establishment of ectopic implants. Third, we review evidence for biochemical differences of eutopic and ectopic endometrium in endometriosis patients, which may contribute to both the pathogenesis and sequelae of this important disorder. Through information derived from these research efforts, we hope to develop better therapeutic interventions as adjunctive or alternative therapies to our current medical and surgical armamentarium.

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Condition tags

endometriosischronic_pelvic_paindysmenorrheainfertility

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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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