摘要
目的探讨Guillain-Barré综合征(GBS)患者CNS内源性免疫反应与CSF蛋白的关系及临床意义。方法收集69例GBS患者的临床资料,采用免疫散射比浊法测定CSF和血清免疫球蛋白G(Ig G)、白蛋白水平,计算CSF白蛋白/血清白蛋白(QALB)、Ig G指数、24 h鞘内Ig G合成率。结果 CSF蛋白正常与偏高患者性别、年龄、残疾量表评分、上呼吸道感染、胃肠感染、肺部感染、近期疫苗接种比率差异无统计学意义。CSF蛋白正常患者CSF蛋白、QALB、Ig G、24 h鞘内Ig G合成率均显著低于CSF蛋白异常患者(均P<0.01),Ig G指数差异无统计学意义。24 h鞘内Ig G合成率正常患者CSF蛋白[0.49(10.84)]g/L显著低于偏高患者[0.98(12.97)]g/L(U=205.50,P<0.01)。24 h鞘内Ig G合成率与CSF蛋白呈正相关(r=0.599,P<0.01)。结论 GBS患者CSF蛋白水平随CNS内源性免疫反应增强而增加,24 h鞘内Ig G合成率有助于GBS的病情监测及预后评估。
Objective To explore the correlation between the endogenous immune response in the CNS and CSF protein in patients with Guillain-Barre syndrome ( GBS ). Methods Clinical data of 69 patients with GBS were retrospectively analyzed. IgG and album level in CSF and serum were detected by the way of immune nephelometry. CSF albumin/serum albumin (QALB) , IgG index, and 24 h intrathecal IgG synthesis rate were calculated. Results There was no significant difference in rate variance of gender, age, disability scale score, upper respiratory tract infection, gastrointestinal infection, pulmonary infection, and recent vaccination between the normal and high level CSF protein patients. CSF protein, QALB, IgG and 24 h intrathecal IgG synthesis rate of normal level CSF protein patients were significantly lower than that of high level CSF protein patients ( all P 〈 0. 01 ). There was no significant difference in IgG index between the two groups. CSF protein of normal 24 h intratheeal IgG synthesis rate patients [ 0.49 ( 10.84 ) ] g/L was significantly lower than that of high 24 h intrathecal IgG synthesis rate patients [ 0.98 ( 12. 97 ) ] g/L ( U = 205.50 ,P 〈 0. 01 ). The 24 h intrathecal IgG synthesis rate was positively correlated with CSF protein ( r =0. 599, P 〈 0. 01 ). Conclusion The CSF protein increased accompany with the endogenous immune response, and the 24 h intrathecal IgG synthesis rate may be helpful in monitoring and prognosis of GBS.
出处
《临床神经病学杂志》
CAS
北大核心
2017年第1期13-15,共3页
Journal of Clinical Neurology
基金
中国博士后基金面上项目资助课题(2014M560297)
医学院科技重点项目资助课题(CDFY-KJ1504)