首页> 中文期刊> 《中国神经精神疾病杂志》 >精神分裂症伴发迟发性运动障碍的血清S100B蛋白浓度研究

精神分裂症伴发迟发性运动障碍的血清S100B蛋白浓度研究

         

摘要

目的 比较伴发和未伴发迟发性运动障碍(tardive dyskinesia,TD)的慢性精神分裂症患者血清S100B蛋白的浓度,探索S100B蛋白在TD发生中的作用.方法 采用酶联免疫吸附法检测95例伴发TD(TD组,n = 40)与未伴发TD(非TD组,n = 55)的慢性精神分裂症患者和40名正常对照的血清S100B蛋白浓度,比较3组间的差异;采用阳性和阴性症状量表(positive and negative syndrome scale,PANSS)评定精神病理症状,采用异常不自主运动量表(abnormal involuntary movement scale,AIMS)评定TD严重程度,分析血清S100B蛋白浓度与精神病理症状、TD严重程度的关系.结果 TD组、非TD组和对照组的血清S100B蛋白浓度分别为(0.17 ± 0.04)μg/L、(0.15 ± 0.02)μg/L和(0.10 ± 0.03)μg/L,3组的差异有统计学意义(F = 53.07,P < 0.01),前两者均明显高于对照组(P < 0.01),且TD组高于非TD组(P < 0.01).TD组血清S100B蛋白浓度与AIMS总分正相关(r = 0.52,P < 0.01).结论 TD患者血清S100B蛋白浓度较非TD患者还高,而且与TD严重程度正相关,提示胶质细胞功能异常可能在TD发生、发展过程中可能起一定作用.%Objective To investigate the role of S100B protein in the pathophysiology of tardive dyskinesia (TD) by analyzing the serum levels of S100B in schizophrenic patients with and without TD. Methods The serum S100B levels were examined by using enzyme-linked immuno- sorbent assay (ELSLA)in 95 schizophrenic patients with (TD group, n = 40)and without (non-TD group, n = 55) TD and 40 healthy volunteers (control group). The serum S100B levels were compared among the three groups. Psychopathological symptoms were assessed by using the positive and negative syndrome scale (PANSS) and the severity of TD was evaluated using ahnormal involuntary movement scale (AIMS). Results There were significant differences in the serum S100B levels among TD [ (0.17 ± 0.04)μg/L] , non-TD [ (0.15 ± 0.02) μg/L] and control [ (0.10 ± 0.03 ) μg/L] groups(F = 53.07 , ρ< 0.01). The S100B levels in patients with TD or without TD were significantly higher compared with controls (ρ<0.01). Moreover, the serum SIOOB levels in TD group were signif'icantly higher than those in non-TD group (ρ<0.01). The serum S100B levels markedly correlated with the total score of AIMS (γ = 0.52,ρ<0.01) in the TD group. Conclusion The serum levels of S100B in patients with TD are significantly increased. which is positively correlated with the total score of AIMS . indicating dysfunction of glia cell might play key roles in pathophysiological mechanisms of TD.

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