吉兰 - 巴雷综合征患者脑脊液蛋白水平与周围神经髓鞘损伤的 相关性分析
Association between cerebrospinal fluid protein level and peripheral nerve demyelination in patients with Guillain-Barré syndrome#br#

目的 · 探讨吉兰–巴雷综合征（Guillain-Barré snydrome，GBS）患者脑脊液蛋白水平与周围神经髓鞘损伤的关系及其临床意义。 方法 · 回顾性分析 86 例 GBS 患者临床与生化资料，根据周围神经肌电图检测结果将患者分为周围神经髓鞘损伤组与轴索变性组，并 比较 2 组患者间的临床、生化特征；分析脑脊液蛋白水平与周围神经髓鞘损伤的相关性。结果 · 髓鞘损伤组与轴索变性组之间患者性 别、年龄、Hughes 残疾量表评分、上呼吸道感染、胃肠感染、皮肤过敏、神经节苷脂钠注射液及免疫球蛋白 G（IgG）指数比较，差 异无统计学意义（P>0.05）；周围神经髓鞘损伤组脑脊液蛋白、脑脊液白蛋白 / 血清白蛋白、IgG 与 24 h 鞘内 IgG 合成率等指标水平 均显著高于周围神经轴索变性组（P<0.01）；脑脊液蛋白水平与周围神经髓鞘损伤呈正相关（r=0.345，P=0.001）。 结论 · GBS 患者脑脊 液蛋白水平越高，周围神经髓鞘损伤发生的可能性越大。脑脊液蛋白水平的分析有助于 GBS 患者周围神经髓鞘损伤免疫机制的探讨。
：Objective · To explore the association between cerebrospinal fluid (CSF) protein level and peripheral nerve demyelination in patients with Guillain-Barré syndrome (GBS). Methods · Clinical and biochemical data of 86 patients with GBS were retrospectively analyzed. According to electromyograms examination of peripheral nerve, GBS patients were divided into group with demyelination and group with axonal degeneration, and their clinical and biochemical characteristics were compared between the two groups. The correlation between CSF protein level and peripheral nerve demyelination was assessed by Spearman’s correlation analysis. Results · Between the group with demyelination and group with axonal degeneration, there was no significant difference in gender, age, Hughes score, respiratory infection, gastrointestinal infection, erythra, ganglioside sodium injection and immunoglobulin G (IgG) index (P>0.05). Significant higher level of CSF protein, CSF albumin/serum albumin, IgG, and 24 h IgG intrathecal synthesis rate were detected in group with demyelination than that of in group with axonal degeneration (P<0.01). CSF protein level was positively correlated with peripheral nerve demyelination (r=0.345, P=0.001). Conclusion · The incidence of peripheral nerve demyelination increased accompanied with CSF protein level, and analysis of CSF protein level may be helpful in investigating the immunologic mechanism of peripheral nerve demyelination in GBS patients