Ulukus M, Arici A
Department of Obstetrics and Gynecology, Ege University School of Medicine, Bornova, Izmir, Turkey.
Minerva Ginecol. 2005 Jun;57(3):237-48.
Endometriosis is classically described as the presence of both endometrial glandular and stromal cells outside the uterine cavity, mainly in the pelvis. The pathogenesis of this enigmatic disorder still remains controversial despite extensive research. Although multiple theories have been put forth to explain the pathophysiology and pathogenesis of endometriosis, the retrograde menstruation theory of Sampson is the most widely accepted. However, since retrograde menstruation occurs in most of the reproductive age women, it is clear that there must be other factors which may contribute to the implantation of endometrial cells and their subsequent development into endometriotic disease. There is substantial evidence to support that the alterations in both cell-mediated and humoral immunity contribute to the pathogenesis of endometriosis. Increased number and activation of peritoneal macrophages, decreased T cell and natural killer (NK) cell cytotoxicities are the alterations in cellular immunity and result in inadequate removal of ectopic endometrial cells from the peritoneal cavity. Moreover, increased levels of several cytokines and growth factors which are secreted by either immune and endometrial cells seem to promote implantation and growth of ectopic endometrium by inducing proliferation and angiogenesis. In addition to the impaired capacity of the immune cells to mediate endometrial cell removal, inherent resistance of the ectopic endometrial cells against immune cells is another interesting concept in the pathogenesis of endometriosis. Endometriosis has also been considered to be an autoimmune disease, since it is often associated with the presence of autoantibodies, other autoimmune diseases, and possibly with recurrent immune-mediated abortion.
子宫内膜异位症的经典描述是子宫腔外存在子宫内膜腺细胞和间质细胞，主要位于盆腔。尽管进行了广泛研究，但这种神秘疾病的发病机制仍存在争议。虽然已经提出了多种理论来解释子宫内膜异位症的病理生理学和发病机制，但桑普森的经血逆流理论是最被广泛接受的。然而，由于大多数育龄妇女都会发生经血逆流，显然一定还有其他因素可能导致子宫内膜细胞的植入及其随后发展为子宫内膜异位症。有大量证据支持细胞免疫和体液免疫的改变都有助于子宫内膜异位症的发病机制。腹膜巨噬细胞数量增加和激活、T细胞和自然杀伤（NK）细胞细胞毒性降低是细胞免疫的改变，导致从腹腔中清除异位子宫内膜细胞不足。此外，免疫细胞和子宫内膜细胞分泌的几种细胞因子和生长因子水平升高，似乎通过诱导增殖和血管生成来促进异位子宫内膜的植入和生长。除了免疫细胞介导清除子宫内膜细胞的能力受损外，异位子宫内膜细胞对免疫细胞的固有抗性是子宫内膜异位症发病机制中的另一个有趣概念。子宫内膜异位症也被认为是一种自身免疫性疾病，因为它通常与自身抗体的存在、其他自身免疫性疾病以及可能与复发性免疫介导的流产有关。
