Anomalies in the inflammatory response in endometriosis and possible consequences: a review.

Minerva endocrinologica · 2012 · vol. 37(1) , pp. 75–92 · PMID:22382616 · W149253570
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This review examines pro-inflammatory cellular and immunological changes observed in endometriosis patients, detailing their impact on angiogenesis, apoptosis, extracellular matrix remodeling, hormonal production, and fertility.

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Abstract

Defined by the presence of endometrial-like cells outside the uterus, endometriosis is one of the most diagnosed gynecological disorders, affecting 5 to 10 % of reproductive age women, but the true incidence is unknown. Endometriosis is a major cause of pelvic pain, dysmenorrhea, dyspareunia, infertility and menstrual irregularities, but there is no clear correlation between the symptoms and the extent of the disease. Despite decades of intensive investigations, little is known about the pathogenesis of endometriosis. The disease is often associated with chronic pelvic inflammation. Abnormal levels of immune cells such macrophages, dendritic and natural killer cells were found in the peritoneal cavity of patients. However these cells seem to be unable to detect and eliminate ectopic endometrial cells. Several studies showed that peritoneal immune cells are dysfunctional and may rather contribute to endometriosis development. A review of relevant clinical and scientific studies was carried out. This review sheds light on cellular and immunological pro-inflammatory changes which were observed in patients with endometriosis, their impact on angiogenesis, apoptosis, extracellular matrix remodeling and hormonal production and consequences on fertility.

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Condition tags

endometriosisdysmenorrheadyspareuniainfertility

MeSH descriptors

Endometriosis Inflammation Apoptosis Autoimmunity Chemokines Chemokines Cytokines Cytokines Cytotoxicity, Immunologic Endometriosis Endometriosis Estrogens Estrogens Extracellular Matrix Proteins Extracellular Matrix Proteins Female Humans Immunity, Cellular Infertility, Female Infertility, Female

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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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