Guerrero A L, Martín-Polo J, Laherrán E, Gutiérrez F, Iglesias F, Tejero M A, Rodríguez-Gallego M, Alcázar C
Neurology Unit, Hospital Río Carrión, Palencia, Spain.
Eur J Neurol. 2008 Apr;15(4):394-7. doi: 10.1111/j.1468-1331.2008.02087.x. Epub 2008 Feb 26.
Uric acid (UA), a product of purine metabolism, may be an antioxidant, perhaps acting as a scavenger of peroxynitrite. Patients with gout have a reduced incidence of multiple sclerosis (MS). A number of studies found that patients with MS have low serum levels of UA, although it has not been established whether this represents a primary deficit or a secondary effect. UA has also been proposed as a marker of disease activity and response to immunosuppressive or immunomodulatory treatment. We retrospectively reviewed 83 relapsing-remitting or secondary progressive MS patients (64 females and 19 males) followed in our Neurology Unit. We collected data concerning demographic variables as age and sex, and clinical variables as age of onset, clinical type, disease duration, EDSS score and total number of relapses. We considered UA levels in three different situations: during a relapse, during remission period and during remission period under immunomodulatory treatment [Interferon Beta 1a i.m. (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a s.c. (Rebif; Serono Europe Limited, London, UK), Interferon Beta 1b (Betaferon; Bayer Schering Pharma AG, Berlin, Germany) or Glatiramer Acetate (Copaxone; TEVA Neuroscience LLC, Kansas City, MO, USA)]. A Wilcoxon matched pairs test was carried out to determine differences between groups. A P-value less than 0.05 was considered statistically significant. In 33 patients, we were able to compare at least one UA value obtained during a relapse with at least one when remission without treatment. Mean serum UA levels were significantly lower when measured during a relapse (r: 0.39, P: 0.024). In 27 cases, we compared at least one remission value without treatment with at least one obtained during remission and immunomodulatory treatment. Mean serum UA levels significantly increased when determined during Interferon Beta or Glatiramer Acetate therapy (r: 0.84, P < 0.001). Although we do not know exactly whether and how UA is involved in MS pathogenesis, our data suggest that UA might reflect disease activity or treatment response in MS.
尿酸（UA）是嘌呤代谢的产物，可能是一种抗氧化剂，或许可作为过氧亚硝酸盐的清除剂。痛风患者患多发性硬化症（MS）的几率较低。多项研究发现，MS患者血清UA水平较低，不过尚未确定这是原发性缺陷还是继发性效应。UA也被提议作为疾病活动以及对免疫抑制或免疫调节治疗反应的标志物。我们回顾性分析了在我们神经科接受治疗的83例复发缓解型或继发进展型MS患者（64名女性和19名男性）。我们收集了有关年龄和性别等人口统计学变量，以及发病年龄、临床类型、病程、扩展残疾状态量表（EDSS）评分和复发总数等临床变量的数据。我们考量了三种不同情况下的UA水平：复发期、缓解期以及免疫调节治疗（肌肉注射干扰素β-1a（阿沃尼单抗；美国百健艾迪公司，马萨诸塞州剑桥）、皮下注射干扰素β-1a（利比；欧洲雪兰诺有限公司，英国伦敦）、干扰素β-1b（倍泰龙；德国拜耳先灵医药公司，柏林）或醋酸格拉替雷（考帕松；美国梯瓦神经科学公司，密苏里州堪萨斯城））下的缓解期。采用威尔科克森配对检验来确定组间差异。P值小于0.05被认为具有统计学意义。在33例患者中，我们能够将复发期获得的至少一个UA值与未治疗缓解期的至少一个UA值进行比较。复发期测量时，平均血清UA水平显著更低（r：0.39，P：0.024）。在27例患者中，我们将至少一个未治疗缓解期的值与免疫调节治疗缓解期获得的至少一个值进行了比较。在干扰素β或醋酸格拉替雷治疗期间测定时，平均血清UA水平显著升高（r：0.84，P < 0.001）。尽管我们并不确切知晓UA是否以及如何参与MS发病机制，但我们的数据表明UA可能反映MS的疾病活动或治疗反应。
