多发性硬化患者血清尿酸水平变化的研究

目的　探讨多发性硬化 (MS)患者血清尿酸 (UA)水平的变化及其临床意义。方法　采用酶定量分析法对 4 3例MS患者和 4 5名正常对照者的血清UA水平进行检测。结果　MS组血清UA水平明显低于对照组 (P <0 0 1)。MS组中病程越长 (P <0 0 1)、神经伤残程度越重 (DSS评分越高 ) (P <0 0 5 ) ,血清UA水平越低 ;女性患者UA水平明显低于男性患者 (P <0 0 0 1) ;经过糖皮质激素治疗后血清UA水平明显回升 (P <0 0 0 1) ,但治疗前血清UA水平越低则疗效越差 (P <0 0 1、P <0 0 5 )。结论　MS患者血清UA水平降低 ,且与MS的病程、伤残程度、疗效及性别密切相关。UA水平升高可能为激素治疗MS的一个作用机制     

尿酸与多发性硬化

1　资料和方法1.1　观察组 :54例 (男 2 8例、女 2 6例 )多发性硬化 (ＭＳ)患者均为神经科住院病例 ,年龄 12～ 60岁 ,所有病例均符合Ｐｏｓｅｒ[1] 等提出的ＭＳ诊断标准。1.2　对照组 :( 1)健康对照组 (ＨＣ) ,为体检中心的健康人群共 56例 ,男女各 2 8例 ,年龄 14～ 62岁。     

尿酸与多发性硬化

近年来有关研究发现,多发性硬化病人的血清尿酸水平显著低于对照,且可能与疾病的活动性、病程、神经伤残程度及性别有关。尿酸被成功地用于治疗多发性硬化的动物模型,多发性硬化病人口服尿酸前体肌苷可以使临床症状改善,提示对尿酸与多发性硬化的关系研究,有望为进一步探索多发性硬化发病机理及更合理的治疗方案找到新的突破点。     

血清尿酸水平与多发性硬化的相关性研究

目的研究血清尿酸(UA)水平与多发性硬化(MS)患者病程、病情、EDSS评分的关系,以探讨血清UA水平在MS发病中的作用机制。方法采用酶定量分析法测定MS患者(96例)和对照组(81例)血清UA水平。结果MS患者与对照组血清UA水平差异无统计学意义,各型急性期及女性患者UA水平明显低于对照组(P<0.01)。MS患者UA水平与病程、EDSS呈负相关。结论MS患者低血清UA水平可能与炎症过程UA消耗有关,UA可能会作为MS疾病活动性的标志物之一。     

尿酸与多发性硬化发生和复发的关系

目的 分析多发性硬化(multiple sclerosis,MS)患者血清尿酸水平的变化,探讨尿酸在MS发生和复发中的作用.方法 收集95例确诊的MS患者的临床、影像学、治疗和血生化检查的资料,同时收集性别、年龄匹配的97名健康查体者的血生化检查结果,分析血尿酸水平与MS的关系.结果 (1)MS患者血尿酸水平较对照组明显降低 (195.6±65.0)μmol/L vs.(256.1±48.0)μmol/L,P＜0.01];按性别分层分析,女性患者血尿酸水平较对照组显著降低 (179.8±53.7)μmol/L vs.(253.2±48.3)μmol/L,P＜0.01),男性患者血尿酸水平与对照组比较无统计学变化.(2)女性MS患者活动期[(171.1±52.4)μmol/L]和缓解期[(207.4±49.7)μmol/L]的血尿酸水平均明显低于正常对照组(均P＜0.01),且活动期MS血尿酸水平较缓解期进一步降低(P＜0.05).(3)血尿酸水平与发病年龄、病程和EDSS评分无相关性.结论 血尿酸水平降低可能与MS的发生和复发有关,其机制可能是血尿酸水平的降低削弱了患者对氧化应激的承受能力.     

尿酸与多发性硬化的关系

目的 探讨多发性硬化患者血清尿酸的水平及其临床意义.方法 采用放射免疫法对24例多发性硬化患者治疗前后进行血清尿酸测定.结果 多发性硬化患者血清尿酸水平均显著降低,与对照组比较有显著性差异,治疗后进入稳定期尿酸水平有所提高,与对照组比较无显著性差异.结论 测定多发性硬化患者血清尿酸水平有助于了解病情,判断病情活动性.尿酸对多发性硬化有保护作用,值得进一步研究.     

多发性硬化患者血清尿酸水平的变化及意义

目的 :探讨多发性硬化 (MS)患者血清尿酸 (UA)水平变化与病情活动性的关系。方法 :比较复发 缓解型MS(relapsing remittingmultiplesclerosis ,RRMS)患者急性期及经大剂量甲泼尼龙 (甲基强的松龙 )冲击治疗后缓解期血清UA值 ,并与其他非炎症性神经系统疾病 (non inflammatoryneurologicaldisease ,NIND)作对照 ,同时对比治疗前后头颅MRI增强检查情况。结果 :RRMS患者急性期血清UA水平显著低于缓解期及NIND组 ,缓解期血清UA值虽低于对照组 ,但差异无显著性。治疗前头颅MRI显示病灶明显强化 ,治疗后强化病灶显著减少 ,同时伴随着UA水平回升 ,临床症状改善。结论 :血清UA水平变化与MS患者病情变化相关 ,UA可作为观察MS病情活动性及激素疗效的指标之一。     

多发性硬化和尿酸水平的病例对照研究

北美和欧洲国家相继有试验报道尿酸可能对多发性硬化 (multiplesclerosis,MS)有预防、治疗作用[1,2 ] ,但尚未见有关亚洲人种的报道。本研究的目的是通过回顾性病例分析研究探讨中国人中MS和尿酸水平的关系 ,试图为MS患者的诊断、预防、治疗找到新的方法和思路。资料和方法 :1997年 10月至 2 0 0 2年 10月间在我院神经内科住院患者 ,其中根据Poser的诊断标准 (临床或实验室证据支持 )确诊的MS患者 6 5例 ,其中男性 2 6例 ,女性 39例 ,平均年龄 (37± 14 )岁。另选择同期其他不影响尿酸水平的神经内科疾病患者 6 9例为病例对照组 ,其中男…     

多发性硬化患者血清尿酸水平变化及与致残状况相关性研究

目的 探讨多发性硬化(MS)患者血清尿酸水平变化及其与致残状况的相关性.方法 收集复发缓解型多发性硬化患者42例,作为MS组,将MS组患者根据不同发作时期再分为MS-复发组和MS-缓解组;收集健康体检者42例作为对照组;比较MS与对照组间以及MS-复发组与MS-缓解组间血清尿酸水平,EDSS量表评价所有MS患者致残状况,对MS患者血清尿酸水平与EDSS评分进行相关性分析.结果 MS组血清尿酸浓度为(205.19±42.99) μmol/L,显著低于正常对照人群的(301.81±87.98) μmol/L,两组间比较差异有统计学意义(t=2.143,P＜0.05);MS组EDSS评分为(3.9±1.1)分,较正常人群表现出显著的功能障碍;MS-复发组血清尿酸浓度为(171.47±38.33)μmol/L,显著低于MS-缓解组的(238.91±47.64) μmol/L,两组间比较差异有统计学意义(t=1.917,P＜0.05);MS患者血清尿酸水平与其EDSS评分呈显著负相关(r=-0.365,P=0.011).结论 机体内尿酸水平的缺失在某种程度上可以影响多发性硬化的发生与进展,还与MS患者功能残障的发生及发展密切相关.     

多发性硬化的血清蛋白质组学研究

目的 从多发性硬化患者血清蛋白质表达的差异,探索多发性硬化的致病机制并试图寻找该疾病血清的蛋白质标志物.方法 多发性硬化患者与健康志愿者各8例的血清进行比较蛋白质组学研究.去除高丰度蛋白,双向凝胶电泳,图像分析凝胶图谱,寻找差异性蛋白点,经肽质量指纹质谱技术鉴定蛋白质点.结果 多发性硬化患者与对照组20种蛋白质的表达量...     

Variation of serum uric acid levels in multiple sclerosis during relapses and immunomodulatory treatment

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 im (Avonex; Biogen Idec Inc., Cambridge, MA, USA), Interferon Beta 1a sc (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.     

Serum uric acid, dehydroepiandrosterone sulphate, and apolipoprotein E genotype in benign vs. progressive multiple sclerosis

The majority of patients with multiple sclerosis (MS) experience gradual progression of disability, either as secondary progressive MS (SPMS) or primary progressive MS (PPMS). A subgroup with relapsing-remitting MS shows a benign course with little or no disease progression and minimal disability decades after the first manifestations, so called benign MS (BMS). In our search to identify factors that are associated with progression of MS, we investigated serum levels of uric acid and dehydroepiandrostenedione sulphate (DHEAS), and apolipoprotein (apo)E genotype in 28 patients with BMS, 33 with SPMS, 21 with PPMS, and 29 healthy individuals. We found no significant changes in uric acid levels and apoE genotype between the four groups. Mean DHEAS levels were lower in MS patients compared with healthy controls (P = 0.049), but there were no significant differences between the clinical subgroups of MS. In patients with SPMS and PPMS there was no correlation between progression rate and serum levels of either uric acid or DHEAS. Our results suggest that serum levels of uric acid and DHEAS, and apoE genotype do not differ between patients with a benign and progressive course of MS.     

Linoleate and fatty acid compositions in the serum lipids of Japanese patients with multiple sclerosis

Serum fatty acid compositions were determined in 21 Japanese patients with multiple sclerosis and 14 neurological controls. No statistical difference was found either for linoleic acid or for arachidonic acid between the 2 groups. It may be that neither serum linoleic acid nor arachidonic acid is inevitably associated with the pathogenesis of multiple sclerosis.     

Serum uric acid and multiple sclerosis

Several studies indicate that patients with multiple sclerosis (MS) have low serum levels of the endogenous antioxidant uric acid (UA), although it has not been established whether UA is primarily deficient or secondarily reduced due to its peroxynitrite scavenging activity. We measured serum urate levels in 124 MS patients and 124 age- and sex-matched controls with other neurological diseases. In addition, we compared UA levels when MS patients were stratified according to disease activity (by means of clinical examination and MRI), duration, disability and course. MS patients had significantly lower serum urate levels than controls (p= 0.001). However, UA levels did not significantly correlate with disease activity, duration, disability or course. Our study favors the view that reduced UA in MS is a primary, constitutive loss of protection against oxidative agents, which deserves further pathogenetic elucidation aimed at future therapeutic strategies. Received: 16 January 2002 / Accepted in revised form: 8 July 2002 This work was partially presented at the 4^th EFNS Congress in Lisbon, Portugal, 7–11 September 1999 and has been published in abstract form in the European Journal of Neurology (Eur J Neurol, 1999, pp. 50–51). Correspondence to S. Sotgiu     

Serum uric acid levels in multiple sclerosis patients correlate with activity of disease and blood–brain barrier dysfunction

Several findings suggest lower levels of serum uric acid in multiple sclerosis (MS) patients. The aim of this study is to investigate relationships of uric acid serum levels in relapse-remitting (RR) MS patients with clinical activity of disease and blood-brain barrier (BBB) condition. Sixty-three definite RRMS patients and 40 controls divided into two groups: 20 healthy donors and 20 patients with other inflammatory neurological diseases (OINDs) were analysed. By using a quantitative enzymatic assay according to the manufacture's protocol and a commercial uric acid standard solution, serum uric acid levels were measured and the results were standardized. To investigate BBB function, magnetic resonance imaging after administration of gadolinium was used. MS patients were found to have significantly lower serum uric acid levels (193.89 +/- 49.05 micromol/l; mean value +/-SD) in comparison with healthy donors (292.7 +/- 58.65 micromol/l; P=0.000) and OIND patients (242.7 +/- 46.66 micromol/l; P=0.001). We found that MS patients with relapse had significantly lower serum uric acid levels (161.49 +/- 23.61 micromol/l) than MS patients with remission (234.39 +/- 41.96 micromol/l; P=0.000) and more over, MS patients with BBB disruption had significantly lower serum uric acid levels (163.95 +/- 26.07 micromol/l) than those with normal BBB (252.48 +/- 25.94 micromol/l; P=0.000). Further, we also found that serum uric acid level independently correlated with disease activity, BBB disruption, and gender. These results indicate that lower uric acid levels in MS patients are associated with relapse and suggest that uric acid might be beneficial in the treatment of MS.     

迟发性运动障碍与血清尿酸的关系

目的：观察伴迟发性运动障碍（TD）的精神分裂症患者血清尿酸变化,探索尿酸与TD的关系。方法：采用尿酸酶法测定23例TD患者、相匹配的23例非TD患者及24例正常对照的血清尿酸水平,使用异常不自主运动量表（AIMS）评定TD的严重程度。结果：TD组血清尿酸水平显著低于非TD组及对照组（P均〈0．01）,而非TD组与对照组之间血清尿酸水平无差异。TD组中AIMS评分与血清尿酸水平呈负相关（r=-0．435,P〈0．05）。结论：TD患者存在低血清尿酸水平并与TD的严重程度有关,尿酸可能参与了TD的病理生理过程。     

血管周围间隙与多发性硬化的相关性研究

目的研究血管周围间隙与多发性硬化的相关性。方法对38例多发性硬化患者(多发性硬化组)及50名健康体检者(对照组)进行头颅MRI检查,计数其血管周围间隙并测量其直径。对结果进行组间比较。结果多发性硬化组患者血管周围间隙检出率(42.1%,16/38)明显高于对照组(16.0%,8/50)(P0.01)。多发性硬化组患者血管周围间隙的数目[(5.4±2.4)个/例]明显多于对照组[(2.7±2.0)个/例](P0.01)。多发性硬化组患者血管周围间隙的直径[(3.0±1.0)mm]明显大于对照组[(2.2±0.7)mm](P0.05)。线性回归分析显示,对照组中血管周围间隙的数目、直径均与年龄呈正相关(r1=0.857,r2=0.956,均P0.01)。结论血管周围间隙与多发性硬化有一定的相关性。     

Association between serum uric acid levels and cerebral white matter lesions in Chinese individuals

Purpose/aim of the study: We aimed to evaluate the association between serum uric acid (SUA) levels and cerebral white matter lesions (WMLs) in Chinese individuals. Material and methods: We prospectively identified patients aged 50 years and older in neurology department from July 2014 to March 2015. Both periventricular WMLs (P-WMLs) and deep WMLs (D-WMLs) were identified on magnetic resonance imanging (MRI) scans and the severity was graded using the Fazekas method. Multivariate logistic regression analyses were performed to examine the association between SUA and WMLs. Results: A total of 480 eligible participants were enrolled in this study. SUA level in severe group was much higher than that in mild group (for P-WMLs: 320.21 ± 79.97 vs. 286.29 ± 70.18, p = 0.000; for D-WMLs: 314.71 ± 74.74 vs. 290.07 ± 74.04, p = 0.031). Subgroup analyses showed that higher SUA level was associated with higher severity of P-WMLs in women, but not in male patients. Multivariate logistic regression analyses showed that SUA was still associated with increased risk of higher severity of P-WMLs (OR = 1.003, 95% = 1.000–1.006), but not D-WMLs. Conclusion: Elevated SUA level was independently associated with greater odds of higher severity of P-WMLs, particularly in women.