Chang Sheng-Hui, Tian Xiao-Bing, Wang Jing, Liu Ming-Qi, Huang Chen-Na, Qi Yuan, Zhang Lin-Jie, Gao Chun-Li, Zhang Da-Qi, Sun Li-Sha, Yang Li
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Department of Neurology, The First Affiliated Hospital of Hainan Medical University, Haikou, China.
Front Neurol. 2020 Nov 12;11:589928. doi: 10.3389/fneur.2020.589928. eCollection 2020.
Uric acid (UA) is a natural scavenger for peroxynitrite and can reflect antioxidant activity and oxidative stress in several neurological disorders. Changes in serum and cerebrospinal fluid (CSF) levels of UA have been reported in patients with multiple sclerosis and neuromyelitis optica spectrum disorders. The levels of UA in CSF are relatively poorly understood in patients with Guillain-Barré syndrome (GBS). It remains unclear whether UA can play an antioxidant role and reflect oxidative stress in GBS. The purpose of this study is to investigate CSF and serum UA levels in patients with GBS and their relationship with clinical characteristics. The CSF and serum UA levels were detected in 43 patients with GBS, including 14 acute inflammatory demyelinating polyneuropathy (AIDP), 6 acute motor axonal neuropathy (AMAN), 13 with acute motor and sensory axonal neuropathy (AMSAN), 7 Miller Fisher syndrome (MFS), and 3 unclassified, and 25 patients with non-inflammatory neurological disorders (NIND) as controls. Moreover, serum UA levels were also detected in 30 healthy controls. The levels of UA were measured using uricase-based methods with an automatic biochemical analyzer. CSF UA levels were significantly increased in patients with GBS ( = 0.011), particularly in patients with AIDP ( = 0.004) when compared with NIND. Among patients with GBS, CSF UA levels were higher in those with demyelination ( = 0.022), although the difference was not significant after multiple testing correction. CSF UA levels in GBS were positively correlated with serum UA levels ( = 0.455, = 0.022) and CSF lactate ( = 0.499, = 0.011). However, no significant correlations were found between CSF UA levels and GBS disability scores. There were no significant differences in serum UA levels among GBS, NIND, and healthy controls. These results suggest that CSF UA may be related to the pathogenesis of demyelination in patients with GBS and may be partially determined by serum UA and the impaired blood-nerve barrier.
尿酸（UA）是过氧亚硝酸盐的天然清除剂，可反映多种神经系统疾病中的抗氧化活性和氧化应激。多发性硬化症和视神经脊髓炎谱系疾病患者的血清和脑脊液（CSF）尿酸水平变化已有报道。格林-巴利综合征（GBS）患者脑脊液中尿酸水平的相关情况相对了解较少。目前尚不清楚尿酸是否能在GBS中发挥抗氧化作用并反映氧化应激。本研究的目的是调查GBS患者的脑脊液和血清尿酸水平及其与临床特征的关系。对43例GBS患者进行了脑脊液和血清尿酸水平检测，其中包括14例急性炎症性脱髓鞘性多发性神经病（AIDP）、6例急性运动轴索性神经病（AMAN）、13例急性运动和感觉轴索性神经病（AMSAN）、7例米勒-费希尔综合征（MFS）和3例未分类患者，同时选取25例非炎性神经系统疾病（NIND）患者作为对照。此外，还对30例健康对照者进行了血清尿酸水平检测。采用基于尿酸酶的方法，使用自动生化分析仪测量尿酸水平。与NIND相比，GBS患者的脑脊液尿酸水平显著升高（P = 0.011），尤其是AIDP患者（P = 0.004）。在GBS患者中，脱髓鞘患者的脑脊液尿酸水平较高（P = 0.022），尽管在多重检验校正后差异不显著。GBS患者脑脊液尿酸水平与血清尿酸水平呈正相关（r = 0.455，P = 0.022），与脑脊液乳酸水平也呈正相关（r = 0.499，P = 0.011）。然而，脑脊液尿酸水平与GBS残疾评分之间未发现显著相关性。GBS患者、NIND患者和健康对照者的血清尿酸水平无显著差异。这些结果表明，脑脊液尿酸可能与GBS患者的脱髓鞘发病机制有关，可能部分由血清尿酸和血-神经屏障受损所决定。
