中国经典型多发性硬化患者β干扰素-1b治疗前后血清尿酸水平

  目的  探讨中国经典型多发性硬化(classical multiple sclerosis, CMS)患者β干扰素-1b治疗前后血清尿酸(uric acid, UA)水平的变化及其与复发率、扩展残疾状态评分(Expanded Disability Status Scale, EDSS)和颅内增强病灶(contrast-enhancing lesions, CELs)数目间的关系。  方法  12例CMS患者(10例女性, 2例男性, 年龄:24~54岁)被纳入至一项为期6个月的疗效观察研究。在疾病缓解期, 给予β干扰素-1b(250 μg, 皮下注射, 隔日1次)治疗。治疗前后评估患者EDSS评分、年复发次数、颅内CELs数目和血清UA水平。  结果  治疗后, 患者年复发次数(0.0比0.9, P=0.011)和颅内CELs数目(0.0比1.5, P=0.007)较治疗前明显减低; EDSS评分有降低趋势(2.0比2.8), 但差异无统计学意义(P=0.064);血清UA水平从222.2 μmol/L升高至234.9 μmol/L, 但差异亦无统计学意义(P=0.213)。进一步研究发现, 血清UA水平升高与颅内CELs数目减低显著相关(r=-0.716, P=0.009)。  结论  血清UA水平有可能成为评估CMS患者对β干扰素-1b治疗反应的一个监测指标。

Serum Uric Acid Levels in Chinese Patients with Classic Multiple Sclerosis:Before and After Treatment with Interferon-beta 1b

Objective To investigate the changes of serum uric acid(UA) level and its relationship with relapse rate,Expanded Disability Status Scale(EDSS) score,and the number of contrast-enhancing lesions(CELs) in Chinese patients with classic multiple sclerosis(CMS) before and after interferon(IFN)-beta 1b treatment.Methods Twelve patients(10 women and 2 men,aged 24 to 54 years) with definite CMS were enrolled into a 6-month open-label observational treatment study.IFN-beta 1b(250 μg,qod) was injected subcutaneously during remission stage.EDSS,relapse rate,number of CELs,and serum UA levels were examined both at baseline and at the end of the study.Results After treatment,the median relapse rate(0.0 vs.0.9,P=0.011) and median number of CELs(0.0 vs.1.5,P=0.007) decreased significantly compared with those before treatment.The median EDSS score also decreased from 2.8 to 2.0,but the difference was not statistically significant(P=0.064).Serum UA level increased from 222.2 μmol/L to 239.4 μmol/L after treatment,although the difference was not statistically significant(P=0.213).However,there was significant correlation between the increase in UA level and the decrease in number of CELs(r=-0.716,P=0.009).Conclusions UA may serve as an easily detectable and economic marker for the blood-brain barrier function in CMS patients and for the responses to IFN-beta 1b treatment.