Storch W B, Eckardt V F, Wienbeck M, Eberl T, Auer P G, Hecker A, Junginger T, Bosseckert H
Institute for Laboratory Medicine, Mönchengladbach, Germany.
Cell Mol Biol (Noisy-le-grand). 1995 Dec;41(8):1033-8.
Achalasia is a motor disorder of the oesopagus characterized by decrease in ganglion cell density in Auerbach's plexus. The cause of the lesion is unknown. This is to repeat on the occurrence of autoimmune phenomena in patients with achalasia, in particular circulating antibodies against Auerbach's plexus and its possible meaning. IgG-antibodies against Auerbach's plexus were determined by standard indirect immunofluorescence. Antibodies to the cytoplasm of Auerbach's plexus were found in 37 of 58 patients with achalasia at variable stages of the disease (I-IV) with a disease duration ranging from 1 to 20 years but only in 4 out of 54 healthy controls (specificity 93%, sensitivity 64%, p < 0.0001), and in none of 12 patients with Hirschsprung's disease as well as 12 patients with cancer of oesophagus and only in one of 11 patients with peptic oesophagitis as well as in one of 13 patients with myasthenia gravis. The present observations suggest that autoimmunity to Auerbach's plexus plays a role in the pathogenesis of achalasia, the mechanism of action is unknown.
贲门失弛缓症是一种食管运动障碍性疾病,其特征为奥尔巴赫神经丛中神经节细胞密度降低。病变原因不明。本文旨在重复探讨贲门失弛缓症患者自身免疫现象的发生情况,尤其是针对奥尔巴赫神经丛的循环抗体及其可能的意义。采用标准间接免疫荧光法测定针对奥尔巴赫神经丛的IgG抗体。在58例处于疾病不同阶段(I-IV期)、病程为1至20年的贲门失弛缓症患者中,有37例检测到针对奥尔巴赫神经丛细胞质的抗体,而在54例健康对照者中仅有4例检测到(特异性93%,敏感性64%,p<0.0001);12例先天性巨结肠患者、12例食管癌患者以及11例消化性食管炎患者中均未检测到,仅13例重症肌无力患者中有1例检测到。目前的观察结果表明,针对奥尔巴赫神经丛的自身免疫在贲门失弛缓症的发病机制中起作用,但其作用机制尚不清楚。