Oide Takashi, Tokuda Takahiko, Yazaki Masahide, Watarai Megumi, Mitsuhashi Shigeaki, Kaneko Kazuma, Hashimoto Takao, Ohara Shinji, Ikeda Shu-ichi
Third Department of Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
J Neurol Sci. 2004 Jan 15;217(1):7-12. doi: 10.1016/j.jns.2003.08.005.
Hashimoto's encephalopathy (HE) is thought to be caused by disorders of immune mechanisms. Although immunologically mediated central nervous system vasculitis or unidentified anti-neuronal autoantibodies have been suspected of causing HE, its pathogenesis is still unclear. For the study presented here, two patients with typical clinical and laboratory/electrophysiological findings of HE were analyzed to clarify the role of anti-neuronal autoantibodies in the pathogenesis of HE. The autopsied brain of one of the patients was histopathologically examined. For Western blotting analysis and immunohistochemistry, serum and purified immunoglobulin G obtained from the other patient were used. Autopsy revealed no evidence of central nervous system vasculitis or other abnormal findings in the brain. The patient's serum contained an anti-neuronal autoantibody that immunohistochemically labeled neurons of mouse and human cerebral cortices and reacted with the 36-kDa antigenic protein present in a soluble fraction obtained from human cerebral cortex. Our results indicate that anti-neuronal autoantibodies may be associated with the pathogenesis of HE.
桥本脑病（HE）被认为是由免疫机制紊乱引起的。尽管免疫介导的中枢神经系统血管炎或不明的抗神经元自身抗体被怀疑是导致HE的原因，但其发病机制仍不清楚。在此项研究中，对两名具有典型HE临床及实验室/电生理表现的患者进行了分析，以阐明抗神经元自身抗体在HE发病机制中的作用。对其中一名患者的尸检大脑进行了组织病理学检查。在蛋白质印迹分析和免疫组织化学中，使用了从另一名患者获得的血清和纯化的免疫球蛋白G。尸检未发现中枢神经系统血管炎或大脑中的其他异常表现。该患者的血清含有一种抗神经元自身抗体，该抗体通过免疫组织化学标记小鼠和人类大脑皮质的神经元，并与从人类大脑皮质获得的可溶性部分中存在的36 kDa抗原蛋白发生反应。我们的结果表明，抗神经元自身抗体可能与HE的发病机制有关。
