Seli Emre, Arici Aydin
Division of Reproductive Endocrinology, Department of Obstetrics and Gynecology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8063, USA.
Semin Reprod Med. 2003 May;21(2):135-44. doi: 10.1055/s-2003-41320.
Endometriosis is a common gynecologic disorder characterized by the presence of endometrial tissue outside the uterine cavity. Although no single theory can explain all cases of endometriosis, the most commonly accepted theory is Sampson's theory of retrograde menstruation. Retrograde menstruation occurs in 76 to 90% of women. The much lower prevalence of endometriosis suggests that additional factors determine susceptibility to endometriosis. Endometriosis is associated with changes in both cell-mediated and humoral immunity. Impaired natural killer cell activity resulting in inadequate removal of refluxed menstrual debris may play a role in the development of endometriotic implants. Moreover, although the peritoneal fluid of women with endometriosis contains increased numbers of immune cells, these seem to facilitate rather than inhibit the development of endometriosis. Macrophages that would be expected to clear endometrial cells from the peritoneal cavity appear to enhance their proliferation by secreting growth factors and cytokines. Although it is unclear whether these immunologic alterations induce endometriosis or are a consequence of its presence, they appear to play an important role in allowing endometriosis implants to persist and progress and contribute to the development of associated infertility and pelvic pain. Danazol and gonadotropin-releasing hormone (GnRH) agonists are commonly used for the medical treatment of endometriosis. These medications seem to down-regulate cellular and humoral immune responses concomitant with their effect on endometriotic implants. Immunomodulatory effects of danazol and GnRH agonists are likely to contribute to the observed clinical improvement associated with their use.
子宫内膜异位症是一种常见的妇科疾病，其特征是子宫腔外存在子宫内膜组织。尽管没有单一理论能够解释所有子宫内膜异位症病例，但最被广泛接受的理论是桑普森的经血逆流理论。76%至90%的女性会发生经血逆流。然而，子宫内膜异位症的患病率要低得多，这表明还有其他因素决定了对子宫内膜异位症的易感性。子宫内膜异位症与细胞介导免疫和体液免疫的变化有关。自然杀伤细胞活性受损，导致对逆流月经碎屑清除不足，这可能在内膜异位种植体的形成中起作用。此外，尽管子宫内膜异位症患者的腹腔液中免疫细胞数量增加，但这些细胞似乎促进而非抑制子宫内膜异位症的发展。预期会从腹腔清除子宫内膜细胞的巨噬细胞，似乎通过分泌生长因子和细胞因子来促进其增殖。虽然尚不清楚这些免疫改变是诱发子宫内膜异位症还是其存在的结果，但它们似乎在使子宫内膜异位种植体持续存在和进展，并导致相关不孕症和盆腔疼痛的发展中起重要作用。达那唑和促性腺激素释放激素（GnRH）激动剂常用于子宫内膜异位症的药物治疗。这些药物在对子宫内膜异位种植体产生作用的同时，似乎也下调了细胞免疫和体液免疫反应。达那唑和GnRH激动剂的免疫调节作用可能有助于解释与其使用相关的临床改善。
