CONTEMPORARY VIEW ON ETHIOPATHOGENESIS OF ENDOMETRIOSIS

In: Zdravniški Vestnik, Vol 78, Iss 6/7 (2009) · 2009 · W1891801028
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AI-generated summary by claude@2026-06, 2026-06-08

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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AI-generated deep summary by claude@2026-06, 2026-06-09

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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Abstract

Background Endometriosis is an estrogen dependent disease that affects 5-10% of women in reproductive age. Several theories tend to describe the ethiopathogenesis of the disease. One of them is based on menstrual regurgitation, the second is metaplasia of coelomic epithelium and the third is theory of vascular and lymphatic embolisation. None of these theories manage to explain all types and locations of endometriosis. Nowadays, prevailing opinion about endometriosis is based on presumption, that endometriosis is a result of changed immune system, that is autoimmune theory. Characteristics of autoimmune disease that are also found in endometriosis are female preponderance, multiorgan involvement, family occurence, possible genetic basis, response to hormonal manipulation, tissue damage, polyclonal B lymphocite activation, immunological abnormalities in T lymphocite and B lymphocite function and associated autoimmune disease. Onset of the disease is influenced by different biochemical and cellular composition of peritoneal fluid, local and systemic immune response and characteristics of regurgitated endometrium. After invasion of endometrial cells into peritoneal cavity the cells implant. Modified composition of peritoneal fluid which comprise greater amount of angiogenic substances enables the implantation. Endometriotic cells in peritoneal cavity represent autologic foreign body. The role of immune system is to eliminate the foreign body, what does not occur in women with endometriosis. Humoral immunity is important in modifying acivity of B cells and secretion of autoantibodies is higher. Conclusions Autoimmune theory represents a challenge and at the same time opens the possibility of a new mode of treatement of endometriosis with immunomodulators.

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endometriosis

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