CONTEMPORARY VIEW ON ETHIOPATHOGENESIS OF ENDOMETRIOSIS
This paper reviews the ethiopathogenesis of endometriosis, highlighting the prevailing autoimmune theory which posits that immune system dysfunction prevents the elimination of implanted endometrial cells.
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This 2009 review article discusses the ethiopathogenesis of endometriosis, contrasting major theories such as menstrual regurgitation, coelomic metaplasia, and vascular/lymphatic embolization, noting that none explain all types and locations. It presents a prevailing autoimmune framework in which altered immune responses contribute to implantation and survival of endometrial cells, describing links to female preponderance, family occurrence and possible genetics, hormonal responsiveness, tissue damage, and immunologic abnormalities in T and B lymphocyte function including polyclonal B-cell activation and higher autoantibody secretion, with onset influenced by peritoneal fluid biochemical/cellular composition and local/systemic immune responses. A key mechanistic emphasis is that modified peritoneal fluid with greater angiogenic substances supports implantation, and that immune failure to clear an “autologic foreign body” is central. The paper does not explicitly discuss adenomyosis, and is centrally about endometriosis — it focuses on current theories of its immune/autoimmune pathogenesis.
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