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     

前列腺液中尿酸引起ⅢB前列腺炎84例报告

目的 :探讨前列腺液 (EPS)中尿酸 (UA)与前列腺素E2 (PGE2 )浓度与慢性盆痛症状之间的相互关系 ,以及UA引发ⅢB前列腺炎的可能机制。方法 :按国际慢性前列腺炎分类诊断标准诊断 ,将 84例慢性前列腺炎患者分为两组 ,即ⅢA组 39例 ;ⅢB组 4 5例 ;正常对照 (对照组 ) 13例。分别进行国际前列腺炎症状评分 (CP SI)和检测EPS中白细胞数、pH值、UA和PGE2 浓度。结果 :①ⅢB组患者慢性盆痛症状评分 (CPSI P)高于ⅢA组 ,EPS中UA浓度高于ⅢA组和正常对照组 ,pH值低于ⅢA和正常对照组 ,均差异有显著性意义 (均 P <0 .0 5 )。②ⅢB组和ⅢA组的PGE2 平均浓度高于正常对照组 ,差异有显著性意义 (P <0 .0 5 ) ,但是ⅢA组和ⅢB组间差异无显著性意义 (P >0 .0 5 )。CPSI P与EPS中的UA ,PGE2 之间存在正相关 (P <0 .0 1)。结论 :ⅢB组患者EPS中高浓度的UA激活环氧化酶 ,使局部的PGE2 升高 ,从而引起慢性盆痛症状 ,其严重程度与EPS中的UA、PGE2 浓度呈正比。同时PGE2 又使UA更容易渗入EPS ,形成UA和PGE2 之间的恶性循环 ,使ⅢB前列腺炎迁延不愈。     

UF-50尿沉渣分析仪常见故障与排除的体会

<正>随着现代科技的发展,实验室自动化分析仪越来越普遍。UF-50尿沉渣分析仪检测仪是对尿液直接做荧光色素染色,利用流式细胞仪和电阻抗的原理,以激光散射强度,散射波幅度和荧光波幅度的技术。识别和计数尿中红细胞、白细胞、上     

肾移植术后早期的高尿酸血症与结石形成（附四例报告）

本文报告了４例肾移植患者术后１－３个月出现高尿酸血症并形成了移植肾、输尿管尿酸盐结石，结合复习文献探讨了环孢素Ａ（ＣｓＡ）引起高尿酸血症的可能机制和促成结石形成的因素。通过回顾４例患者成功治疗的体验，讨论了移植肾、输尿管尿酸结石预防及治疗的选择。     

The influence of uric acid treatments on liver glutathione system prevent oxidative damages in experimental autoimmune encephalomyelitis mice

Recently we reported that antioxidant system in brain and spinal cord in experimental autoimmune encephalomyelitis (EAE) mice is mainly affected at early stages of the disease [M. Zargari, A. Allameh, M.H. Sanati, T. Tiraihi, S.H. Lavasani, O. Emadyan, Relationship between the clinical scoring and demyelination in central nervous system with total antioxidant capacity of plasma during experimental autoimmune encephalomyelitis development in mice, Neurosci. Lett. 412 (2007), 24–28]. The aim of the present study was to investigate the role of uric acid (UA) on antioxidant system in liver and plasma of EAE mice. EAE was induced in C57/BL6 mice (n = 60), followed by i.p. administration of UA (10 mg/kg BW) in 30 mice at three distinct clinical stages (A: prior to onset, B: after onset, C: after development of EAE). Livers were removed and processed for measurement of lipid peroxidation products, reduced glutathione (GSH), and glutathione S-transferase (GST) and total antioxidant capacity of plasma (FRAP). The results showed that lipid peroxidation products in liver of EAE mice was increased significantly (∼85%) as compared to normal. UA administration to EAE mice caused a significant suppression of liver lipid peroxidation products (∼45%) at early stages (A and B). There was an inverse relationship between lipid peroxidation and cellular GSH in liver. GSH was significantly depleted in mice liver during the EAE progression, but it was recovered (∼29%) when UA was injected before the onset of the disease (groups A and B). Plasma total antioxidant capacity was significantly decreased during the development of EAE, however it was subsided in mice treated with UA as compared to the corresponding controls (21%) in groups A and B. Elevated liver GST as a result of EAE induction was reversed in mice treated with UA particularly in groups A and B. These results indicate that hepatic glutathione system, particularly GST plays a major role in modulation of oxidative damages to central nervous system (CNS) during EAE induction. The positive response of antioxidant system to UA administration in EAE mice was corroborated with improvement of clinical manifestation of the animals.     

Renal urate transport during variations in urate synthesis in the rat

Summary In order to determine the effect of intrarenal synthesis of urate upon the urinary urate excretion in the rat, we effected large changes in urate synthesis by increasing it with hypoxanthine and decreasing it with allopurinol. Hypoxanthine infusion increased plasma urate rapidly and also increased the urinary urate excretion and its renal clearance. However, when the plasma urate was maintained constant, hypoxanthine had no effect upon renal urate transport. Conversely, allopurinol infusion rapidly diminished the plasma urate, urinary urate excretion and its renal clearance. Again, the maintenance of a constant plasma urate concentration prevented any change in urate transport during allopurinol. The urinary degradative purine metabolite pattern was altered pre-dictably by hypoxanthine and allopurinol. Assuming that any putative intrarenal component of urate synthesis would be affected predictably and consistently by hypoxanthine and allopurinol, these results suggest that changes in intrarenal urate synthesis are not an important determinant of urate excretion in the rat.Reported in abstract form in Clinical Research23, 508 A (1975)     

人类精液中一氧化氮和尿酸含量检测的关系

目的探讨人精液中一氧化氮(N0)与尿酸含量的关系,对精了质量的影响。方法参照WHO标准方法,进行精液常规分析,按精子密度、活动率不同分为(正常、<20、20~40、>40)4个组。采用镀铜镉还原荧光法检测NO代谢产物硝酸盐(NO3-)。采用尿酸酶一过氧化物酶偶联法检测精液尿酸含量。结果70例不育组精液中尿酸含量和NO含量为(236.4±47.8)μmol/L、(78.7±1.6)μmol/L与正常生育组(398.6±52.3)μmol/L、(41.84±1.6)μmol/L呈显著性差异(P<0.01)。将尿酸含量与NO含量进行相关性分析,两者呈显著性负相关(r=-0.96,P<0.05)。不育各精子密度和活动率组精液尿酸含量随精子密度及活动率增加而上升,N0含量随之下降(P<0.01),结论精液尿酸含量测定可作为评价精子受活性氧损害的重要指标,证明尿酸对活性氧尤其在医学领域极为重视的NO损害精子具有保护性作用。     

原发性高尿酸血症发病机制的研究进展

高尿酸血症和痛风的患病率逐年升高，而且与代谢综合症密切相关，因此对高尿酸血症发病机制的研究日益增多。高尿酸血症是由于尿酸合成增加及/或尿酸排泄减少所引起。长期的高尿酸血症易诱发痛风，还可伴发高血压、肥胖、糖尿病、肾脏疾病及心脑血管疾病等。近年来，尿酸合成增加的机制已基本明确，而导致尿酸排泄减少的分子机制尚不清楚。本文从尿酸合成增加和排泄减少两方面对原发性高尿酸血症的发病机制研究进展进行综述。     

3-硝基酪氨酸在细菌内毒素诱导大鼠血管低反应性中的介导作用

目的：观察3-硝基酪氨酸（3-NT）对感染性休克大鼠血管低反应性的介导作用及抗氧化剂对此的治疗效果。 方法： 40只雄性SD大鼠随机分成空白对照组(n=10); LPS休克组（LPS 15 mg·kg-1 iv, n=10）; 尿酸(UA)治疗组（注射LPS 1 h后200 mg·kg-1 ip, n=10）; N-乙酰-5-甲氧基色胺（melatonin）治疗组（注射LPS 1 h后10 mg·kg-1 ip, n=10）。空白对照组及注射LPS 6 h后各组动物，静注去氧肾上腺素（PE, 0.5-2.5 μg·kg-1）,记录注药后MAP的增加百分比。所有in vivo实验结束后取大鼠胸主动脉环作张力实验,，建立PE的剂量-反应曲线并计算相应的Emax、EC50值。注射LPS 6 h后检测各组动物血浆丙二醛（MDA）、硝酸盐/亚硝酸盐（nitrate/nitrite）与3-NT的含量。 结果： 静脉注射PE后，休克组动物MAP的平均增长率与对照组相比显著降低至54.60%（P<0.01）；而UA组、melatonin组MAP对PE反应的增长率较之休克组分别增高了37.70%、40.03%(P<0.05)。休克组大鼠胸主动脉环对PE的反应［(Emax，35.30%±9.80%； EC50， (15.70±4.50)nmol/L］与对照组相比有显著差异［（Emax，100%； EC50， (4.71±2.04) nmol/L, P<0.05］，经UA、melatonin治疗后血管反应性有显著改善(P<0.05)。尿酸、N-乙酰-5-甲氧基色胺治疗组的血浆MDA、硝酸盐/亚硝酸盐和3-NT的浓度也明显低于休克组(P<0.05)。 结论： 3-NT是感染性休克血管低反应的重要介导因子，抗氧化剂通过清除氧自由基，减少脂质过氧化物的形成、抑制体内NO的过量合成及有效清除3-NT，从而改善α-肾上腺素能受体介导的血管低反应性，对临床感染性休克病人的治疗可能有积极作用。     

枸橼酸氢钾钠在大负荷肾尿酸结石治疗中的应用(附6例报告并文献复习)

目的探讨枸橼酸氢钾钠在大负荷肾尿酸结石治疗中的效果。方法回顾性分析2018年1月至2020年7月天津医科大学第二医院以枸橼酸氢钾钠治疗的6例大负荷肾尿酸结石(长径>4cm)患者的临床资料。患者均为男性,平均年龄51.3(42~66)岁,平均结石长径6.0(4.1~7.6)cm,腹部X线片(KUB)阴性,平均CT值475(418~535)HU,治疗前尿pH均≤5.5。6例血尿酸平均453.3(258.7~570.0)μmol/L,其中3例高于正常值,3例有痛风病史;2例有肾结石手术病史,结石成分回报为无水尿酸,其余4例根据病史及影像学检查诊断为尿酸结石。所有患者均无泌尿系感染病史及泌尿系梗阻。6例均予口服枸橼酸氢钾钠颗粒治疗,以10g/d为起始剂量,按早餐后2.5g、午餐后2.5 g、晚餐后5.0 g分次服用,根据尿液pH值调整剂量,保持尿pH值6.5~7.0。治疗期间每2~3个月复查CT平扫以评价治疗效果。结果6例治疗2.5~8.0个月,无明显胃肠道不适等不良反应。结石负荷均有不同程度降低,平均长径缩短3.2(1.4~5.9)cm,其中2例结石基本消失。枸橼酸氢钾钠治疗后复查CT示,结石边缘由光滑变粗糙,结石表面及内部出现虫蚀样缺损及空洞,表现出明显的溶石现象。结论枸橼酸氢钾钠对大负荷肾尿酸结石具有较好的治疗效果。对于临床考虑尿酸结石的非感染患者可尝试应用枸橼酸氢钾钠治疗。