Neural autoantibody profile of primary achalasia.

Neural autoantibody profile of primary achalasia.
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DOI:
10.1007/s10620-009-0838-9
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发表时间:
2010-02
影响因子:
3.1
通讯作者:
Lennon, Vanda A.
Lennon, Vanda A.
中科院分区:
医学3区
文献类型:
--
作者:
Kraichely, Robert E.;Farrugia, Gianrico;Pittock, Sean J.;Castell, Donald O.;Lennon, Vanda A.

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原发性贲门失弛缓症的病因和发病机制尚不清楚。假定的机制包括自身免疫、病毒免疫和中枢神经变性。本研究的目的是调查原发性贲门失弛缓症患者血清中神经自身抗体的分布。编码的70例原发性贲门失弛缓症患者和161名健康对照受试者的血清,匹配的性别,年龄和吸烟习惯,筛选针对神经元,神经胶质和肌肉自身抗原的抗体。未发现特异性肌间神经元抗体。然而,原发性贲门失弛缓症患者神经自身抗体的总体患病率显著高于健康对照组(25.7% vs 4.4%,p < 0.0001)。最值得注意的是,在不存在糖尿病或预测1型糖尿病的伴随抗体的情况下,贲门失弛缓症患者中谷氨酸脱羧酶-65(GAD 65)抗体的频率为21.4%(对照受试者为2.5%)。这种自身抗体谱提示原发性贲门失弛缓症亚群的自身免疫基础。
The etiology and pathogenesis of primary achalasia are unknown. Postulated mechanisms include autoimmune, viral-immune, and central neurodegenerative. The aim of this study was 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 (GAD65) 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.
DOI: 10.1002/ana.20269
发表时间: 2004-11-01
影响因子: 11.2
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