Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
Dig Dis Sci. 2010 Feb;55(2):307-11. doi: 10.1007/s10620-009-0838-9. Epub 2009 Jun 5.
The etiology and pathogenesis of primary achalasia are both unknown. Postulated mechanisms include autoimmune, viral-immune, and central neurodegenerative. The aim of this study is to investigate the serum profile of neural autoantibodies in patients with primary achalasia. Coded sera from 70 patients with primary achalasia and 161 healthy control subjects, matched in sex, age, and smoking habits, were screened for antibodies targeting neuronal, glial, and muscle autoantigens. No specific myenteric neuronal antibody was identified. However, the overall prevalence of neural autoantibodies in patients with primary achalasia was significantly higher than in healthy control subjects (25.7 vs. 4.4%, P < 0.0001). Most noteworthy was the 21.4% frequency of glutamic acid decarboxylase-65 antibody in patients with achalasia (versus 2.5% in control subjects), in the absence of diabetes or companion antibodies predictive of type 1 diabetes. This profile of autoantibodies suggests an autoimmune basis for a subset of primary achalasia.
原发性贲门失弛缓症的病因和发病机制均不清楚。推测的机制包括自身免疫、病毒免疫和中枢神经退行性变。本研究旨在探讨原发性贲门失弛缓症患者血清中神经自身抗体的谱。对 70 例原发性贲门失弛缓症患者和 161 例健康对照者的编码血清进行了检测，这些对照者在性别、年龄和吸烟习惯方面与患者相匹配，以检测针对神经元、神经胶质和肌肉自身抗原的抗体。未发现特定的肌间神经元抗体。然而，原发性贲门失弛缓症患者的神经自身抗体总体患病率明显高于健康对照组（25.7% vs. 4.4%，P<0.0001）。最值得注意的是，贲门失弛缓症患者谷氨酸脱羧酶-65 抗体的频率为 21.4%（对照组为 2.5%），而这些患者没有糖尿病或预测 1 型糖尿病的伴随抗体。这种自身抗体谱提示原发性贲门失弛缓症的一部分患者存在自身免疫基础。
