Endometriozis Gelişiminde İmmun Sistemin Rolü
Synopsis
Östrojene bağlı enflamatuar bir hastalık olan endometriozis genel popülasyonun neredeyse %5-10'unda saptanmaktadır. Endometriozis üreme çağındaki kadın nüfusu incelendiğinde pelvik ağrısı ve infertilitesi olan hasta grubunun yaklaşık %20-90'’nını oluşturur. Birçok immünolojik faktörün endometriozis gelişiminde büyük ölçüde neden olduğu bilinmektedir. Endometrioziste hem kronik lokal enflamasyon hem de otoantikorların otoimmün hastalıklarla birçok benzerlik gösterdiği bilinmektedir. Bununla birlikte, endometriozisdeki otoimmün etiyoloji tartışmalı olmaya devam etmektedir ve otoimmün temele ilişkin kanıtları sınırlı olabilir. Endometriozis incelendiğinde karşımıza farklı fenotipler çıkmaktadır. Semptomatik olgularda mekanizmlar incelendiğinde progesterona dirençte görülmekle birlikte çalışmalar daha çok düzensiz sitokin üretiminin araştırılması olarak karşımıza çıkar bu durum hem ektopik hem ötopik endometriyumda saptanır. İmmünolojik faktörler de endometriotik odak hücrelerin oluşmasında neden olabilir. İmmünolojik değişimler arasında peritoneal makrofaj sayı ve aktivitesindeki artış, antikorların artan dolaşımı, azalan T-hücre sayısı, natürel killer hücre sitotoksisitesi azalma ve sitokin salınımındaki diğer faktörler sayılabilir. Kitabımızın bu bölümündeki amacı, endometriozis gelişiminde immün sistemin rolü ve tüm bu bilgiler değerlendirildiğinde endometriozis etyopatogenezinde inflamasyonun oynadığı potansiyel role ışık tutmaktır.
Endometriosis, an oestrogen-dependent inflammatory disease, is found in almost 5-10% of the general population. In the female population of reproductive age, this disease accounts for approximately 20-90% of patients with pelvic pain and infertility. It is known that many immunological factors are largely responsible for the development of endometriosis. It is known that both chronic local inflammation and autoantibodies in endometriosis show many similarities with autoimmune diseases. However, the autoimmune aetiology in endometriosis remains controversial and evidence for an autoimmune basis may be limited. When endometriosis is analysed, different phenotypes appear. In symptomatic cases, resistance to progesterone and dysregulated cytokine production are found in both ectopic and eutopic endometrium. Immunological factors may also cause the formation of endometriotic focal cells. Immunological changes include increased peritoneal macrophage number and activity, increased circulation of antibodies, decreased T-cell count, decreased natural killer cell cytotoxicity and other factors in cytokine release. The aim of this chapter is to shed light on the role of the immune system in the development of endometriosis and the potential role of inflammation in the etiopathogenesis of endometriosis.
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