Increased Cerebrospinal Fluid Uric Acid Levels in Guillain-Barré Syndrome.
Increased Cerebrospinal Fluid Uric Acid Levels in Guillain-Barré Syndrome.
复制标题
格林-巴利综合征脑脊液尿酸水平升高。
DOI：
10.3389/fneur.2020.589928
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发表时间：
2020
影响因子：
3.4
通讯作者：
Yang L
中科院分区：
文献类型：
--
作者：
Chang SH;Tian XB;Wang J;Liu MQ;Huang CN;Qi Y;Zhang LJ;Gao CL;Zhang DQ;Sun LS;Yang L
尿酸（UA）是过氧亚硝酸盐的天然清除剂，可以反映几种神经系统疾病的抗氧化活性和氧化应激。在多发性硬化症和视神经肌病谱系疾病患者中，血清和脑脊液（CSF）中UA水平的变化已有报道。对格林-巴利综合征（GBS）患者CSF中UA水平的了解相对较少。目前还不清楚UA是否可以发挥抗氧化作用，并反映GBS中的氧化应激。本研究旨在探讨GBS患者脑脊液和血清UA水平及其与临床特征的关系。检测43例GBS患者脑脊液和血清UA水平，其中急性炎性脱髓鞘性多发性神经病（AIDP）14例，急性运动轴索神经病（AMAN）6例，急性运动和感觉轴索神经病（AMSAN）13例，米勒费歇尔综合征（MFS）7例，未分型3例。同时检测30例健康对照者血清UA水平。尿酸水平测定采用尿酸酶为基础的方法与自动生化分析仪。与NIND相比，GBS患者的CSF UA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CSF UA水平较高（p = 0.022），尽管多重检验校正后差异不显著。GBS患者CSF UA水平与血清UA水平（r = 0.455，p = 0.022）和CSF乳酸水平（r = 0.499，p = 0.011）呈正相关。然而，CSF UA水平和GBS残疾评分之间没有显著相关性。GBS、NIND和健康对照组之间血清UA水平无显著差异。这些结果表明，CSF UA可能与GBS患者脱髓鞘的发病机制有关，并可能部分由血清UA和受损的血-神经屏障决定。
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 (p = 0.011), particularly in patients with AIDP (p = 0.004) when compared with NIND. Among patients with GBS, CSF UA levels were higher in those with demyelination (p = 0.022), although the difference was not significant after multiple testing correction. CSF UA levels in GBS were positively correlated with serum UA levels (r = 0.455, p = 0.022) and CSF lactate (r = 0.499, p = 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.
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影响因子：
--
作者：
Ayala A;Muñoz MF;Argüelles S
通讯作者：
Argüelles S
DOI：
10.1073/pnas.78.11.6858
发表时间：
1981-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
AMES, BN;CATHCART, R;HOCHSTEIN, P
通讯作者：
HOCHSTEIN, P
影响因子：
2.2
作者：
Ghabaee, Mojdeh;Jabedari, Behnam;Asadi, Farzad
通讯作者：
Asadi, Farzad
影响因子：
5.1
作者：
Peng, F.;Yang, Y.;Zhong, X.
通讯作者：
Zhong, X.
影响因子：
4.2
作者：
Cutler, Roy G.;Camandola, Simonetta;Mattson, Mark P.
通讯作者：
Mattson, Mark P.