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。     

氯氮平对精神分裂症患者血脂水平的影响

目的　探讨氯氮平对精神分裂症患者脂质代谢的影响。方法　采用自身对照方法 ,比较 4 5例精神分裂症患者在氯氮平治疗前和治疗后第 8周末的血脂水平变化。结果　氯氮平治疗后患者的TG水平明显升高 (P <0 0 1) ,而HDL则明显降低 (P <0 0 5 ) ;治疗后男性的HDL水平明显降低 (P <0 0 5 ) ;女性的TG水平则明显升高 (P<0 0 1) ;氯氮平剂量与血清TG水平呈正相关 (P <0 0 1) ,与血清HDL水平无明显相关 (P >0 0 5 ) ;治疗后心电图出现异常者的TG水平明显高于无异常组者 (P <0 0 5 )。在治疗第 8周末体重增加与血清高TG和低HDL水平均无明显相关性 ((P >0 0 5 )。结论　氯氮平治疗可引起血脂异常 ,其异常可能与缺血性心脏疾病有关     

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。     

多发性硬化患者脑脊液和血清中髓鞘碱蛋白和白介素-16的相关研究

目的　了解多发性硬化 (MS)患者脑脊液 (CSF)和血清髓鞘碱性蛋白 (MBP)和白介素 16 (IL 16 )的水平 ,探讨两者之间的相关性 ,及其在MS发病过程中的作用。方法　采用ELISA法对 31例MS患者CSF和血清的MBP和IL 16进行测定 ,并与 2 4例炎性脱髓鞘性多发性神经病 (IDP)、2 2例对照者进行比较。结果　MS组CSF和血清中的MBP水平均显著高于IDP组及对照组 (均P <0 .0 1) ;CSF中的IL 16的水平显著高于对照组 (P <0 .0 1) ,而血清中IL 16水平与对照组相比无明显差异 (P >0 .0 5 )。MS组中CSF的MBP水平与IL 16水平显著相关 (r=0 .4 6 8,P <0 .0 1) ,但血清中MBP的水平与IL 16水平无相关性 (r=- 0 .131,P >0 0 5 ) ;CSF中MBP水平和血清中MBP的水平有相关性 (r=0 .5 0 5 ,P <0 .0 1) ,CSF中IL 16和血清中IL 16的水平无相关性 (r=0 .0 2 2 ,P >0 .0 5 )。结论　MBP是诱导MS发病的主要自身抗原之一 ,MBP可能主要在中枢神经系统中刺激IL 16的产生 ;而IL 16主要在中枢神经局部产生并起作用     

复发缓解型多发性硬化患者急性发作期血清尿酸与肌酐的水平变化及意义

目的探讨复发缓解型多发性硬化(multiple sclerosis,MS)患者急性发作期血清尿酸(uric acid,UA)和肌酐(serum creatinine,SCr)水平的变化及意义。方法收集117例复发缓解型MS急性发作期患者,同时收集性别、年龄匹配的125例门诊健康查体者为对照组。于次日06:00抽取空腹肘静脉血,测定血清UA、SCr浓度。结果 MS组血清UA水平明显低于对照组(P0.001);女性患者UA值比较,差异有统计学意义(P=0.000);男性患者UA值比较,差异有统计学意义(P=0.017)。MS组血清SCr水平较对照组明显降低(P0.001);女性患者血清SCr水平比较,差异有统计学意义(P=0.002);男性患者血清SCr水平比较,差异有统计学意义(P=0.000)。MS中女性患者高尿酸血症的患病率低于男性。Pearson相关分析显示,复发缓解型MS患者急性发作期血清UA和SCr水平无相关性。结论血清UA、SCr水平的降低可能与MS患者急性发作期有关,UA、SCr水平是MS的重要生化指标,值得注意的是MS患者中女性较男性不易发生高尿酸血症。     

血尿酸水平在老年帕金森病患者中的检测意义及其影响因素

目的通过对帕金森病(PD)老年患者血尿酸(UA)水平的研究和分析,探讨PD老年患者的UA水平与病程长短、性别以及病情严重程度分级之间的关系。方法分析我院接受治疗的64例PD老年患者(PD组)的临床资料。另外选取68例性别、年龄均与PD组相匹配;非PD患者为本实验的对照组。结果 2组性别、年龄及BMI(体重指数)上的组间差异无统计学意义(P0.05);PD组的UA水平明显比对照组低(P0.01),且PD组男性、女性UA浓度均明显低于对照组(P0.01)。PD组内男、女的UA水平差异有统计学意义(P0.01),对照组内男、女UA水平无统计学差异(P0.05)。PD组各级患者的UA水平比较差异无统计学意义(P0.05),且均明显低于对照组(P0.05)。UA水平与PD的病情分级未存在相关性(r=-0.052,P=0.743);与病程的长短也无相关性(r=0.094,P=0.493)。结论 PD老年患者的UA水平偏低,且可能存在于患者各个病程阶段,低水平UA是PD老年患者发病的潜在的危险因子。     

精神分裂症患者氯氮平治疗前后免疫指标的变化

目的　探讨精神分裂症患者抗精神病药物氯氮平治疗前后总T细胞 (CD3 )、T辅助 /T诱导细胞 (CD4)、T抑制 /T杀伤细胞 (CD8)及血清白细胞介素 6 (IL 6 )水平的变化。方法　对 6 6例精神分裂症患者 (男 32例 ,女 34例 )和 30名健康对照者 (男 16名 ,女性 14名 )的血清CD3 、CD4、CD8、CD4/CD8及IL 6的水平进行检测。用酶联免疫吸附法 (ELISA)及碱性磷酸酶抗碱性磷酸酶法 (APAAP)检测各受试者血清IL 6及T细胞亚群。结果　 (1) 6 6例精神分裂症患者治疗前CD3 、CD4、CD8、CD4/CD8比值均低于对照组 (P <0 0 1～ 0 0 0 1) ,而IL 6 [(1 8± 0 6 )ng/L]则高于对照组 [(1 2± 0 6 )ng/L],P <0 0 0 1;(2 )氯氮平治疗后CD3 、CD4、CD4/CD8高于治疗前 (P <0 0 1) ;(3)阳性、阴性组患者治疗前CD3 、CD4、CD8、CD4/CD8均低于对照组 (P <0 0 1) ,而IL 6水平则高于对照组高 (P <0 0 1) ;(4)治疗后阳性、阴性组患者IL 6水平 [(1 2± 0 3)ng/L、(1 1± 0 5 )ng/L]均较治疗前有所降低 ,与对照组的差异无显著性 (P >0 0 5 ) ;(5 )阳性、阴性组患者治疗后组间比较 ,阳性组CD3 、CD4、CD4/CD8明显高于阴性组 ,CD8低于阴性组 (P <0 0 5 ) ,两组间IL 6水平的差异无显著性 (P >0 0 5 ) ;(6 )多元逐步回归分析显示 ,阳     

糖尿病患者认知功能障碍及其相关因素的分析

目的　探讨 2型糖尿病 (DM)患者的认知功能改变 ,评价 2型DM认知功能障碍的敏感指标及相关危险因素。方法　对 10 0例 2型DM患者和 4 0名健康对照者进行简易智能精神状态检查表 (MMSE)和韦氏记忆量表 (WMS R)评定及事件相关电位 (ERP)测定 ,分析其认知功能、P3 0 0 波的潜伏期 (P3 PL)与病程、治疗状况和糖化血红蛋白 (GhbA1)的关系。结果　 2型DM组MMSE和WMS R评分均低于对照组 (P <0 0 1,P <0 0 5 ) ,N2 PL和P3 PL较对照组均显著延长 (P <0 0 0 1) ,且与MMSE和WMS R呈负相关 (r =- 0 5 13,P <0 0 1;r =- 0 898,P <0 0 0 1)。病程≥ 10年组患者的P3 PL长于病程 5～ 10年组 ,后者又长于病程≤ 5年组 ;未治疗和未进行正规治疗的患者P3 PL长于正规降糖治疗者 (P <0 0 1) ;GhbA1与P3 PL呈正相关 (r=0 718,P <0 0 0 1)。结论　 2型糖尿病患者存在明显的认知功能障碍 ,ERP和其他量表一样能反映认知功能损害的程度 ;2型DM的病程、治疗以及血糖控制状况均与认知功能显著相关。     

脑卒中患者血清甲状腺激素变化及临床意义

目的　探讨脑卒中患者血清甲状腺激素的变化与病灶范围、预后的关系及临床意义。方法　应用放射免疫分析法 (RIA)测定 5 3例脑卒中患者入院后 4 8小时内及入院 4周后 ,血清甲状腺激素水平和T3 /rT3 值 ,并与 4 5例对照组比较。结果　 (1)脑卒中组与对照组比较T3 、FT3 显著降低 (P <0 .0 1) ,T4、FT4、rT3 、TSH显著升高 (P <0 .0 1) ,T3 、FT3 出血组较梗死组变化显著 (P <0 .0 5 ) ,治疗 4周后 ,T3 、FT3 明显升高 (P <0 .0 1) ,T4、FT4、rT3 、TSH明显降低 (P <0 .0 5 ) ;(2 )甲状腺激素变化和病灶范围关系密切 ,当出血量>30ml、梗死面积 >2 0cm2 时和T3 、FT3 、T3 /rT3 值呈负相关 ;与rT3 值呈正相关 ,上述变化与病灶部位无明显关系 ;(3)T3 /rT3 比值与病情严重程度成反比 ,其比值越低 ,病情越严重 ,病死率越高。结论　动态检测脑卒中患者血清甲状腺激素水平对判断患者病情及估计预后及疗效有重要的临床价值。     

精神分裂症患者冠心病风险的因素分析

目的:探讨精神分裂症患者冠心病风险的因素。方法:收集180例精神分裂症患者(病例组)的人口学及临床资料,并进行弗雷明汉10年冠心病风险评分,检测其血清甲状腺激素(TSH)、血清白蛋白(Alb)、总胆红素(TBIL)、三酰甘油(TG)、肌酐(Cr)、尿酸(UA)、尿素氮(BUN)水平;结果与性别和年龄相匹配的279名健康对照者(对照组)比较,分析精神分裂症患者冠心病风险的因素。结果:病例组冠心病风险(4. 3%)明显高于对照组(2. 3%),吸烟、合并高血压和糖尿病比率及收缩压、舒张压水平明显高于对照组(P 0. 05或P 0. 001)。与对照组相比,病例组血清Alb、TBIL、TC、HDL明显降低,TG和UA水平明显升高(P均0. 01);相关性分析显示病例组冠心病风险与其精神分裂症病程、治疗时长、发作次数及血清TG、BUN、UA水平呈正相关,与TSH水平呈负相关;线性回归分析显示,精神分裂症病程及血清TG、TSH水平与冠心病风险相关。结论:精神分裂症患者的冠心病风险升高;其病程及血清TG、TSH水平是其冠心病风险的影响因素。     

血清尿酸与多发性硬化关系的研究

目的 探讨多发性硬化（MS）患者血清尿酸水平的改变与临床的关系。方法 检测88例MS患者（MS组）血清尿酸水平,分析其与临床分期、病程、病情的关系;并与其他神经系统炎症性疾病患者（OIND组）和健康体检人员（正常对照绀）比较。结果 MS组血清尿酸水平明显低于OIND组及正常对照组（均P〈0．05）,处于MS急性复发期患肯的血清尿酸水平低于缓解期患者（P〈0．05）。血清尿酸水平与MS的临床分期独口相关（P〈0．05）,与病橼和扩展后的功能障碍状况量表评分不相关（均P〉0．05）。结论 血清尿酸水平的变化可作为MS诊断及判断MS患者不同临床分期的辅助指标。     

Uric acid levels in sera from patients with multiple sclerosis

The levels of uric acid (UA), a natural peroxynitrite scavenger, were measured in sera from 240 patients with multiple sclerosis (MS) and 104 sex- and age-matched control patients with other neurological diseases (OND). The mean serum UA concentration was lower in the MS than in the OND group, but the difference did not reach the level of statistical significance (P=0.068). However, the mean serum UA level from patients with active MS (202.6+67.1 μmol/l) was significantly lower than that in inactive MS patients (226.5+78.6 μmol/l; P=0.046) and OND controls (P=0.007). We found a significant inverse correlation of serum UA concentration with female gender (P=0.0001), disease activity (P=0.012) and duration (P=0.017), and a trend towards an inverse correlation with disability as assessed by EDSS score, which did not reach statistical significance (P=0.067). Finally, multivariate linear regression analyses showed that UA concentration was independently correlated with gender (P=0.0001), disease activity (P=0.014) and duration of the disease (P=0.043) in MS patients. These findings suggest that serum UA might serve as a possible marker of disease activity in MS. They also provide support to the potential beneficial therapeutic effect of radical-scavenging substances in MS. Received: 8 March 2000 / Received in revised form: 20 July 2000 / Accepted: 13 August 2000     

糖皮质激素对多发性硬化患者血清MMP-9、TIMP-1水平的调控作用

目的观察糖皮质激素(GC)治疗多发性硬化(MS)患者过程中血清MMP-9和TIMP-1水平的动态变化,探讨GC治疗MS的作用机制。方法收集80例MS患者不同时间点外周血;急性初期进行EDSS评分,根据EDSS评分将MS患者分为2组,其中GC治疗组(EDSS≧5分)急性期50例、追踪至缓解期46例,空白对照组(EDSS<5分)急性期30例、缓解期26例;健康对照组50例。采用酶联免疫吸附试验法检测血清MMP-9与TIMP-1水平。结果 (1)急性期MS血清MMP-9水平高于缓解期和健康对照组,而TIMP-1水平降低(P<0.05),缓解期和健康对照组间差异无统计学意义(P>0.05)。(2)MMP-9在MS血清中呈先升后降的趋势;GC治疗组不同时间点间差异有统计学意义(F=16.35,P<0.01),治疗1w时MMP-9水平达高峰,治疗4w时较治疗前降低(P<0.05);而空白对照组发病2w时MMP-9水平达高峰,且高于GC治疗组高峰(P<0.05)。(3)GC治疗组TIMP-1水平呈缓慢增高趋势,不同时间点间差异有统计学意义(F=4.27,P<0.05),与治疗前相比,治疗4w时TIMP-1水平升高(P<0.05);而空白对照组TIMP-1水平随病情波动变化不大。结论 MMP-9在MS急性期血清中表达增强,TIMP-1表达降低,MMP-9、MMP-9/TIMP-1水平反应了MS疾病活动性,监测其水平具有一定的诊断价值;MMP-9在MS血清中呈先升后降趋势,GC治疗可降低MMP-9上升的幅度,缩短MMP-9升高的时间,降低MMP-9的表达,并诱导TIMP-1的表达,这可能是GC治疗MS、加速MS病情缓解、缩短其病程的机制之一。     

Serum uric acid and multiple sclerosis

Peroxynitrite (PN) has been implicated in multiple sclerosis (MS) and its animal model experimental allergic encephalomyelitis. Uric acid (UA) serum levels of MS patients, a natural scavenger of PN, were found lowered in some recent studies. OBJECTIVE/PURPOSE: The objective of our study was to correlate UA serum levels and several clinical parameters of MS. We also tried to investigate serum UA changes during treatment with immunomodulating or immunosuppressing drugs in the last 6 months. PATIENTS AND METHODS: We measured UA serum levels in 190 patients with MS and 58 age and gender matched patients with inflammatory (IND) and non-inflammatory diseases (NIND) studied as control groups. UA levels were correlated with clinical parameters as type of the disease, duration, disability, magnetic resonance imaging (MRI) activity and female gender. RESULTS: In the overall MS group, patients were found to have significantly lower mean serum uric acid levels compared with the IND (p = 0.0029) and the NIND group (p < 0.0001). UA serum concentrations were not inversely correlated with duration of the disease (p = 0.87), with disability as assessed by Expanded Disability Status Scale (EDSS) score (p = 0.67) and MRI activity (p = 0.36). Treatment with immunomodulating or immunosuppressing drugs had no influence in UA levels (p = 0.85). Patients with Clinically Isolated Syndromes (CIS) were found to have significantly lower UA concentrations compared with IND and NIND patients (p = 0.009 and <0.001, respectively). CONCLUSIONS: Our findings suggest that lower serum UA levels in MS patients may represent a primary, constitutive loss of protection against nitric oxide and the development of CNS inflammation and tissue damage may not have a direct effect to UA serum levels. They also provide support that the earlier increase of UA serum levels might be beneficial in the future treatment of MS.     

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     

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 levels and freezing of gait in Parkinson’s disease

Uric acid (UA) is a natural antioxidant and iron scavenger in the human body, which has been hypothesized to exert an anti-oxidative effect in Parkinson’s disease (PD). This study aimed to investigate the relationship between serum UA levels and freezing of gait (FOG) in PD. A total of 321 Chinese PD patients with fasting serum UA evaluated were included in the cross-sectional study. Demographics, clinical features, and therapeutic regimen were collected. The Unified PD Rating Scale (UPDRS) III and Hoehn and Yahr (H and Y) stage were used to evaluate the severity of disease, and the Frontal Assessment Battery (FAB) and Montreal Cognitive Assessment (MoCA) scales were used to assess the cognitive function. Patients with FOG showed lower proportion of male, longer disease duration, lower body mass index, lower concentrations of serum UA, higher total levodopa equivalent daily dosage, higher UPDRS III score, greater median H and Y stage, lower scores of FAB and MoCA, and higher frequencies of motor fluctuation, dyskinesia, falls, and festination compared to patients without FOG (P < 0.05). The binary logistic regression model indicated that high UPDRS III score (OR = 1.049, P < 0.001), fluctuation (OR = 2.677, P = 0.035), dyskinesia (OR = 6.294, P = 0.003), festination (OR = 3.948, P < 0.001), falls (OR = 7.528, P < 0.001), and low serum UA levels (OR = 0.990, P < 0.001) were associated with FOG. Our study suggests that low serum UA concentration is associated with the occurrence of FOG in PD.     

血清和脑脊液CXCL13水平与临床孤立综合征、多发性硬化和视神经脊髓炎的关系

目的探讨临床孤立综合征(CIS)、复发缓解型多发性硬化(RRMS)、视神经脊髓炎(NMO)患者血清和脑脊液内B淋巴细胞趋化因子-1(BLC-1/CXCL13)的水平与疾病进展、扩展残障状态量表(EDSS)评分及MRI表现的关系。方法选择CIS患者18例、RRMS患者22例、NMO患者21例,以及神经系统非炎性疾病(neurological non-inflammatory disease,NND)患者(作为对照组)17例,采用酶联免疫吸附试验法检测4组患者血清和脑脊液CXCL13水平并进行比较;对4组患者进行发病期EDSS评分及MRI检查,比较EDSS评分≥3.5分和EDSS评分<3.5分患者血清和脑脊液CXCL13水平,分析CXCL13水平与EDSS评分的相关性,比较头颅和脊髓增强扫描阳性与阴性患者血清及脑脊液CXCL13水平;随访18例CIS患者2年,比较脑脊液CXCL13水平>10pg/mL患者与脑脊液CXCL13水平<10pg/mL的患者转化为MS的病例数。结果 CIS组、RRMS组及NMO组与NND组患者相比,血清和脑脊液中CXCL13的水平高(均P<0.01),其中RRMS组患者脑脊液中CXCL13的水平较CIS组和NMO组高(均P<0.01);EDSS评分≥3.5分患者血清和脑脊液CXCL13水平比EDSS评分<3.5分患者高(均P<0.01),4组患者血清和脑脊液中CXCL13水平与患者EDSS评分值呈正相关(r=0.881,P<0.01;r=0.753,P<0.01);行头颅和脊髓MRI增强扫描的48例患者中,有增强病灶者脑脊液中CXCL13水平比无增强病灶者高(P<0.01);脑脊液CXCL13水平>15pg/mL的患者转化为MS的比例(37.5%)与脑脊液CXCL13水平<10pg/mL的患者(10.0%)比较无统计学差异(P>0.05)。结论脑脊液CXCL13水平高的CIS患者可能较早地转化为MS,CXCL13可能是预测CIS转化的标记物。