肿瘤坏死因子-α及其他细胞因子与吉兰-巴雷综合征
Tumour necrosis factor-alpha and other cytokines in Guillain-Barré syndrome.
作者信息
Exley A R, Smith N, Winer J B
机构信息
Department of Immunology, Medical School, Edgbaston, Birmingham, UK.
出版信息
J Neurol Neurosurg Psychiatry. 1994 Sep;57(9):1118-20. doi: 10.1136/jnnp.57.9.1118.
The efficacy of plasma exchange implicates myelinotoxic humoral factors in the pathogenesis of Guillain-Barré syndrome. Candidate factors include autoantibodies to peripheral nerve myelin, which are not unique to Guillain-Barré syndrome; and cytokines such as tumour necrosis factor-alpha (TNF-alpha) which are T cell/macrophage products. Plasma cytokine concentrations were determined in 26 patients with Guillain-Barré syndrome undergoing plasma exchange, 25 with other acute neurological diseases, and 40 healthy controls. Raised TNF-alpha concentrations (> 25 pg/ml) were found in seven of 26 patients with Guillain-Barré syndrome v none of 23 disease controls (p = 0.001). The peak grade of clinical deficit correlated with TNF-alpha concentrations (r = 0.6, p < 0.01). There was no significant difference between interleukin-1 beta or interferon-gamma concentrations in patients and disease controls. The data suggest that TNF-alpha may be a critical factor in the pathogenesis of Guillain-Barré syndrome.
血浆置换的疗效提示髓鞘毒性体液因子在吉兰-巴雷综合征的发病机制中起作用。候选因子包括外周神经髓鞘自身抗体，这并非吉兰-巴雷综合征所特有；以及细胞因子，如肿瘤坏死因子-α（TNF-α），它是T细胞/巨噬细胞产物。对26例接受血浆置换的吉兰-巴雷综合征患者、25例患有其他急性神经系统疾病的患者以及40名健康对照者测定了血浆细胞因子浓度。26例吉兰-巴雷综合征患者中有7例TNF-α浓度升高（>25 pg/ml），而23例疾病对照者中无一例升高（p = 0.001）。临床缺损的峰值分级与TNF-α浓度相关（r = 0.6，p < 0.01）。患者与疾病对照者之间白细胞介素-1β或干扰素-γ浓度无显著差异。数据表明TNF-α可能是吉兰-巴雷综合征发病机制中的关键因素。
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