82例老年病毒性肝炎患者血清可溶性白细胞介素Ⅱ受体的研究

目的 为了探讨老年病毒性肝炎患者血清可溶性白细胞介素Ⅱ受体(sIL—2R)的变化及其在诊断、病情演变和预后判断中的意义。方法 采用夹心酶联免疫吸附法测定82例老年病毒性肝炎患者血清sIL-2R的水平。结果 sIL-2R的水平在急性病毒性肝炎(AH)、慢性迁延型肝炎(CPH)、慢性活动型肝炎(CAH)、肝炎后肝硬化(HC)和重型肝炎(SH)中分别为643.5±232.6u/ml、452.8±234.3u/ml、632.5±243.3u/ml、693.5±267.3u/ml和901.4±304.8u/ml。病例组 sIL-2R的水平均明显高于对照组(P<0.01)。肝炎活动期均明显(P<0.05),各型肝炎间无明显差异。结论 老年人各型肝炎患者血清中sIL-2R都明显增高,其水平高低在一定程度上反映了机体免疫功能状态,肝细胞损伤及炎症程度。     

慢性肝病患者血清白介素-6及其受体检测的临床意义

目的：观察慢性肝病患者血清白介素-6（IL-6）和可溶性IL-6受体（sIL-6R）的变化。方法：应用酶联免疫吸附试验（EIL-SA）检测慢性肝炎患者86例、肝炎后肝硬化患者18例和20例健康对照组血清中IL-6和sIL-6R水平。结果：慢性肝炎患者血清IL-6和sIL-6R含量均显著高于健康对照组（P〈0．01），其中肝炎后肝硬化组上述2参数高于慢性肝炎组；慢性肝炎组中的上述2参数显示为：重度〉中度〉轻度．各组间差异有显著性（P〈0．05或P〈0．01）：慢性肝病组血清IL-6和sIL-6R水平之间呈正相关（r=0．481，P〈0．05），IL-6和sIL-6R水平与血清总胆红素水平间亦呈正相关（r=-0．417，0．418，P〈0．01），与ALT之间无明显相关性（r=0．173，0．182，P〉0．05）。结论：血清IL-6和sIL-6R与慢性肝病的病情演变有关．对其预后有一定指导意义。     

华支睾吸虫病20例患者血清中可溶性白细胞介素2受体检测的临床意义

目的：探讨华支睾吸虫病患者血清中可溶性白细胞介素2受体（sIL-2R)的作用。方法：选择20例未经治疗的华支睾吸虫病患者（观察组）和20例健康对照组，检测血清中sIL-2R的水平。结果：观察组血清中sIL-2R含量较对照组明显升高。结论：华支睾吸虫病患者细胞免疫功能处于明显抑制状态。     

乙肝患者血清HBV DNA含量与sIL—2R、TNF生活水平关系的研究

目的探讨乙型肝炎(乙肝)病毒数量在乙肝发病中的作用.方法分别用竞争性聚合酶链反应技术、双抗体夹心酶联免疫法(ELISA)和放射免疫分析法(RIA),检测241例各型乙肝患者和20例正常人的血清HBVDNA浓度、血清可溶性白细胞介素2受体(sIL-2R)和肿瘤坏死因子(TNF)水平,进行相关分析.结果急、慢性乙肝患者血清HBVDNA浓度的变化与sIL-2R(r≥0.6979,P＜0.05),TNF(r≥0.7782,P＜0.05)水平呈显著正相关;而重症乙肝、肝炎后肝硬化患者HBVDNA与sIL-2R(r≤0.2963,P＞0.05),TNF(r≤0.3987,P＞0.05)无相关性.结论急、慢性乙肝患者细胞因子sIL-2R、TNF与体内HBV复制程度密切相关,提示抗病毒在急、慢性乙肝治疗中是一个积极有效的措施.     

肺癌病人放疗前后血清可溶性白细胞介素-2受体含量变化及临床意义

为探讨肺癌病人放疗前后血清可溶性白细胞介素-2受体(sIL-2R)含量变化与预后的关系,于放疗前后采用双抗体夹心 ELISA 法检测38例肺癌病人血清 sIL-2R 的含量,与健康人作对照。结果显示,放疗前肺癌病人血清 sIL-2R 含量较对照组明显升高,差异有非常显著意义(P&lt;0.01);放疗结束时及3个月、6个月血清 sIL-2R 含量明显下降(P&lt;0.01)。放疗后6个月14例复发或转移的病人血清 sIL-2R 含量再次升高,高于无复发或转移者(P&gt;0.05)。Ⅲa～Ⅳ期者 sIL-2R 含量高于Ⅰb～Ⅱb期者(P&lt;0.05)。结论:血清 sIL-2R含量动态变化,可为肺癌病人免疫功能、病情监测及预后判断提供观察指标。     

雷公藤多甙对重症肌无力患者血清sIL-2R水平的影响

目的 探讨雷公藤多甙(T Ⅱ)对重症肌无力(MG)的免疫调节机制.方法 将52例MG患者随机分为TⅡ治疗组及非T Ⅱ治疗组,观察T Ⅱ治疗组和非T Ⅱ治疗组治疗前后及40例正常对照血清可溶性白细胞介素2受体(sIL-2R)水平.结果 T Ⅱ治疗组及非T Ⅱ治疗组治疗前血清sIL-2R水平较正常对照组明显升高;T Ⅱ治疗组治疗后血清sIL-2R水平较治疗前明显降低,而非T Ⅱ治疗组治疗前后血清sIL-2R水平则无显著性变化.结论 T Ⅱ治疗MG的免疫调节机制可能通过抑制sIL-2R产生而发挥.     

肾移植受者血清可溶性白细胞介素Ⅱ受体检测的意义

本采用ELISA法对39例肾移植病人血清可溶性白细胞介素Ⅱ受体(sIL-2R)进行了检测。结果表明，7例急性排异反应和5例感染病人血清sIL-2R水平明显高于肾功能稳定组和环孢索肾中毒组。7例排异反应病人中5例经抗排异治疗后逆转．血清sIL-2R逐渐降至排异前水平。排异反应时血清sIL-2R升高较血清肌酐升高平均提前1．5天。因此．血清sIL-2R是诊断和预测肾移植排异反应的有用指标．有助于鉴别排异反应和环孢素肾中毒．     

婴幼儿血清可溶性白细胞介素-2受体测定

分析101例健康婴幼儿血清sIL-2R检测结果,资料显示婴幼儿阶段血清中sIL-2R的含量明显高于正常成人。婴幼儿不同阶段sIL-2R均值变化特点同年龄分布有一定相关性,其特点是新生儿明显增高,2岁时达到高峰,之后呈逐年递减趋势。表明新生儿、婴儿阶段机体细胞免疫水平发展迅速,5岁以后逐渐平缓并向正常水平过渡。揭示健康婴幼儿血清sIL-2R水平的变化特点,为了解婴幼儿的免疫功能状态以及推测各种疾病对婴幼儿免疫功能的影响提供了重要的实验方法,并为国人提供了有价值的实验参考数据。     

乙肝患者血清HBV DNA含量与sIL-2R、TNF水平关系的研究

目的探讨乙型肝炎(乙肝)病毒数量在乙肝发病中的作用.方法分别用竞争性聚合酶链反应技术、双抗体夹心酶联免疫法(ELISA)和放射免疫分析法(RIA),检测241例各型乙肝患者和20例正常人的血清HBV DNA浓度、血清可溶性白细胞介素2受体(sIL-2R)和肿瘤坏死因子(TNF)水平,进行相关分析.结果急、慢性乙肝患者血清HBV DNA浓度的变化与sIL-2R(r≥0.6979,P＜0.05),TNF(r≥0.7782,P＜0.05)水平呈显著正相关;而重症乙肝、肝炎后肝硬化患者HBV DNA与sIL-2R(r≤0.2963,P＞0.05),TNF(r≤0.3987,P＞0.05)无相关性.结论急、慢性乙肝患者细胞因子sIL-2R、TNF与体内HBV复制程度密切相关,提示抗病毒在急、慢性乙肝治疗中是一个积极有效的措施.     

血清可溶性白介素-2受体对小儿结核病的诊断价值

探讨血清可溶性白细胞介素-2受体(sIL-2R)水平对小儿结核病的临床应用价值。报告86例小儿血清sIL-2R的检测结果,其中对照组30例血清sIL-2R水平为(151.67±37.70)mmol/L,结核病活动期组32例血清sIL-2R水平为(289.38±86.62)mmol/L,两者有显著性差异(P<0.01)。经抗痨治疗半年～1年后(即结核病恢复期组),血清sIL-2R水平明显下降至(139.58±49.36)mmol/L,与活动组比较具显著性差异(P<0.01),接近健康对照组水平(P>0.05)。血清sIL-2R水平亦能反映结核病活动期病变的严重程度,重度结核病活动期组sIL-2R水平明显高于轻、中度结核病活动期组(均P<0.01)。sIL-2R检测是结核病诊断的敏感指标之一,可作为判定结核病患儿病情活动的客观指标,并有助判断抗痨治疗的效果。     

充血性心力衰竭患者免疫功能的研究

目的：了解充血性心力衰竭患者的免疫功能状态,是否存在的免疫异常及其与病因,病程和心功能的关系,方法：检测４５例心衰患者外周血Ｔ淋巴细胞亚群,淋巴细胞转化率,可溶性白细胞介素Ⅱ受体ｓＩＬ－２Ｒ及免疫球蛋白和补体Ｃ３的变化。结果：与对照组比较,心衰时ＣＤ＾＋４,ＣＤ＾＋４／ＣＤ＾＋８比值,淋巴细胞转化率明显降低（Ｐ〈０．０５）,ｓＩＬ－２Ｒ水平升高（Ｐ〈０．０５）;重度心衰者ＩｇＧ,ＩｇＭ和补体Ｃ３水     

慢性乙型肝炎患者血清可溶性白细胞介素-2受体水平的变化

目的了解慢性乙型肝炎患者血清可溶性白介素-2受体（SIL-2R）水平的变化及其与肝炎活动的相关性。方法采用酶联免疫法测定40例慢性乙型肝炎患者血清sIL-2R水平。结果慢性乙型肝炎患者血清sIL-2R水平显著增高（P〈0．01）,并与血清丙氨酸转氨酶水平呈正相关（r=0．38,P〈0．05）。结论检测血清SIL-2R对了解免疫功能状态以及判断病情有一定价值。     

76例戊肝病人血清白细胞介素-2受体动态检测及临床意义

目的 为了解血清白细胞介素-2受体(sIL-2R)在戊肝病程中的变化及意义。方法 动态观察了76例戊肝患者急性期及恢复期的sIL-2R水平,并与同期血清ALT及T-Bil水平进行了对比,以健康献血员作对照。结果 戊肝各期sIL-2R水平均高于对照组,戊肝极期sIL-2R水平显著高于恢复期(P<0.01～0.05),戊肝各期sIL-2R水平与ALT及T-Bil呈显著正相关(r=0.58,P<0.ol;r=0.40,P相似文献   

Detection of HCV in bile duct epithelium by laser capture microdissection (LCM)

Chronic hepatitis C affects 0.3 to 1.5% of the general population worldwide. The estimated total number of newly acquired hepatitis C virus (HCV) infections is 28,000 in the USA, with 10,000 deaths each year resulting from HCV-associated chronic liver disease. Histological examination of liver tissue from chronic HCV infection shows lymphoid aggregates or follicles in the portal triads, focal fatty change and lobular inflammation. Hepatitis-associated bile duct lesion (HBL) is seen in 5 - 91% of the cases. While the morphological spectrum of HBL has been well described, its pathogenesis in hepatitis C is not known. To this date, evidence supports both the direct injury and immune-mediated mechanisms, but to what extent these mechanisms are involved in the pathogenesis of HBL in chronic hepatitis C remains unclear. Our study showed the presence of HCV in the bile duct epithelium of patients with chronic hepatitis C infection, using the laser capture microdissection technique. These results will enhance our diagnostic capabilities and treatment of chronic hepatitis C infection.     

丙型肝炎患者白细胞介素-2受体和肝功能损伤的相关研究

目的 探讨血清可溶性白细胞介素－2受体（SIL－2R）、T淋巴细胞亚群群等在丙型肝炎病毒感染中的作用。方法 应用双抗体夹心ELISA法和单克隆抗体测定法对58例丙型肝炎患进行了血清SIL－2R和T淋巴细胞亚群等进行相关研究，并以正常人35名作对照。结果 丙型肝炎患血清SIL－2R水平显地高于正常人组（P＜0．001），尤以肝硬变组明显。SIL－2R水平与T细胞亚群中CD8细胞比例，与ALT密切相关。结论 检测丙型肝炎患血清中SIL－2R、T淋巴细胞亚群等水平可做为丙肝患病情变化、预后判断及临床用药的监测指标。     

HCVRNA载量在慢性丙肝、肝硬化、肝癌患者中的变化及基因分型

目的了解丙型肝炎病毒RNA（HCVRNA）载量在慢性丙型肝炎、丙型肝炎肝硬化、丙肝相关的肝癌（HCV—HCC）患者中的变化及基因分型对疾病进展的影响。方法回顾性分析2010年2月至2013年8月门诊及住院的1386例HCVRNA阳性且未进行抗病毒治疗的丙型肝炎患者的临床病例资料,把患者按诊断分为丙型肝炎组、丙肝肝硬化组、丙肝相关的肝癌组,采用qRT—PCR检测患者血清的HCVRNA载量与基因分型,多组比较采用方差分析或卡方检验,两组间比较采用t检验。结果丙型肝炎组、丙肝肝硬化组及丙肝相关的肝癌组患者HCVRNA载量分别为（6．47±1．03）lgIU／mL,（6．18±1．09）lgIU／mL和（6．07±1．13）lgIU／mL,三组患者HCVRNA载量不同,丙型肝炎组HCVRNA明显高于其他二种,且差别有统计学意义（F=12．80,P〈0．05）,但丙肝肝硬化组与HCV—HCC组患者HCVRNA载量差别无统计学意义（t=0．65,P〉0．05）。1386例患者中816例进行了HCV基因型检测,1型基因型529例（64．83％）,2型基因型287例（35．17％）,丙型肝炎组患者1型基因型者为400例,2型基因型者为226例,1b型基因型为主（63．10％）,丙肝肝硬化组1型基因型117例,2型基因型为57例,1b型基因型为主（65．52％）,HCV—HCC组1型基因型为12例,2型基因型为4例,1b型基因型为主（68．75％）,三组患者基因型比例无明显差别（x^2=1．02,P=0．31）。结论HCVRNA载量在慢性丙型肝炎发展为肝硬化、肝癌的过程中减低,河南地区丙肝患者以1型基因型为主,且1型、2型基因型对疾病的进展没有影响。     

The metabolism and disposition of a potent inhibitor of hepatitis C virus NS3/4A protease

Compound A ((1aR,5S,8S,10R,22aR)-5-tert-butyl-N-{(1R,2S)-1-[(cyclopropylsulfonyl)carbamoyl]-2-ethenylcyclopropyl}-14-methoxy-3,6-dioxo-1,1a,3,4,5,6,9,10,18,19,20,21,22,22a-tetradecahydro-8H-7,10-methanocyclopropa[18,19][1,10,3,6]dioxadiazacyclononadecino[12,11-b]quinoline-8-carboxamide) is a prototype of a series of subnanomolar inhibitors of genotypes 1, 2, and 3 hepatitis C virus (HCV) NS3/4A proteases. HCV NS3/4A protease inhibitors have demonstrated high antiviral effects in patients with chronic HCV infection and are likely to form a key component of future HCV therapy. Compound A showed excellent liver exposure in rats, which is essential for compounds intended to treat HCV. The compound was mainly eliminated intact in bile and showed greater than dose proportional systemic exposure in rats. Compound A demonstrated time- and temperature-dependent uptake into rat and human hepatocytes and proved to be a substrate for rat hepatic uptake transporter Oatp1b2 and for human hepatic uptake transporters OATP1B1 and OATP1B3. The liver selectivity observed for this compound is likely to be due to transporter-mediated hepatic uptake together with moderate passive permeability. Metabolism was mainly CYP3A-mediated and generated a reactive epoxide on the vinylcyclopropyl sulfonamide moiety that could be quenched by glutathione. Similar metabolic profiles of Compound A were obtained in liver microsomes of rats and humans. The oral bioavailability at 5?mg/kg was low due to extensive hepatic first-pass effect but clearly the intestinal absorption was enough to deliver a high amount of the compound to the liver. The metabolism and disposition properties of Compound A are particularly attractive to support its evaluation as a drug candidate for the treatment of hepatitis C.     

肺癌患者血清可溶性白细胞介素-6受体和一氧化氮检测的临床意义

目的：评价可溶性白细胞介素－6受体（sIL-6R)与一氧化氮（NO）水平对肺癌诊断和病情评估的临床价值。方法：用双抗体夹心酶联免疫吸附 试验（ELISA）检测了20例正常对照和60例肺癌患者发病不同阶段，及化疗前、后血清中sIL-6R水平，及光度法检测NO水平。结果：肺癌患者血清中sIL-6R水平高于正常对照组，IV期肺癌组血清中sIL-6R水平又高于I期肺癌组。化疗后，肺癌患者血清中的sIL-6R水平明显下降，不但低于化疗前水平，更低于对照组水平。肺癌患者血清中NO水平也低于正常对照组。结论：肺癌患者NO水平下降，提示肺癌局部抗肿瘤功能可能存在缺陷。肺癌患者体内存在sIL-6R的高表达，随着肺癌病情进展sIL-6R表达增多，sIL-6R的测定有助于临床肺癌发病的辅助诊断，并且对肺癌分期和预后判断有一定的临床意义。经直线相关性分析未发现血清sIL-6R水平与NO间有明显相关性。     

Hepatotoxicity of antiretrovirals: incidence, mechanisms and management.

Hepatotoxicity is a relevant adverse effect derived from the use of antiretrovirals that may increase the morbidity and mortality among treated HIV-infected patients and challenges the treatment of HIV infection. Although several antiretrovirals have been reported to cause fatal acute hepatitis, they most often cause an asymptomatic elevation of transaminase levels. In addition to ruling out a variety of processes not related to the use of antiretrovirals or to the HIV infection, for appropriate management of the complication it is necessary to deduce the possible pathogenic mechanisms of the hepatotoxicity. Among these mechanisms, direct drug toxicity, immune reconstitution in the presence of hepatitis C virus (HCV) and/or hepatitis B virus (HBV) co-infections, hypersensitivity reactions with liver involvement and mitochondrial toxicity play a major role, although several other pathogenic pathways may be involved. Liver toxicity is more frequent among subjects with chronic HCV and/or HCB co-infections and alcohol users. Complex immune changes that alter the response against hepatitis virus antigens might be involved in the elevation of transaminase levels after suppression of the HIV replication by highly active antiretroviral therapy (HAART) in patients co-infected with HCV/HBV. The contribution of each particular drug to the development of hepatotoxicity in a HAART regimen is difficult to determine. The incidence of liver toxicity is not well known for most of the antiretrovirals. Although it is most often mild, fatal cases of acute hepatitis linked to the use of HAART have been reported across all families of antiretrovirals. Acute hepatitis is related to hypersensitivity reactions in the case of non-nucleosides and to mitochondrial toxicity in the case of nucleoside analogues. Alcohol intake and use of other drugs are other co-factors that increase the incidence of transaminase level elevation among HIV-infected patients. The management of liver toxicity is based mainly on its clinical impact, severity and pathogenic mechanism. Although low-grade HAART-related hepatotoxicity most often spontaneously resolves, severe grades may require discontinuation of the antiretrovirals, for example when there is liver decompensation, hypersensitivity reaction or lactic acidosis.