Gentry W L, Buster J E, Schriock E D, Carson S A
Department of Obstetrics and Gynecology, University of Tennessee, Memphis.
Fertil Steril. 1989 Dec;52(6):949-52. doi: 10.1016/s0015-0282(16)53157-4.
Endometriosis, even in mild cases, decreases monthly fecundity. Immunologic disorders have been suggested as the mechanism. In light of possible increases in serum autoimmune antibodies, increased peritoneal macrophages, and increased sperm phagocytosis associated with this disease, we postulated that peritoneal fluid antisperm antibodies would be increased and might be the cause of increased sperm phagocytosis and its associated infertility. Peritoneal fluid, from 18 patients with endometriosis and 10 infertile controls, was tested with the antisperm antibody immunobead test validated for peritoneal fluid. One of 18 patients with endometriosis and none of 10 controls had antisperm antibodies present. Therefore, increased sperm phagocytosis is unlikely a result of peritoneal antisperm antibodies in endometriosis patients.
子宫内膜异位症,即使是轻度病例,也会降低每月受孕能力。免疫紊乱被认为是其机制。鉴于与该疾病相关的血清自身免疫抗体可能增加、腹腔巨噬细胞增多以及精子吞噬作用增强,我们推测腹腔液抗精子抗体将会增加,并且可能是精子吞噬作用增强及其相关不孕症的原因。采用经过腹腔液验证的抗精子抗体免疫珠试验,对18例子宫内膜异位症患者和10例不孕对照者的腹腔液进行检测。18例子宫内膜异位症患者中有1例出现抗精子抗体,而10例对照者均未出现。因此,精子吞噬作用增强不太可能是子宫内膜异位症患者腹腔抗精子抗体所致。