新喋呤在肝病中的变化及临床意义

新喋呤是四氢生物喋呤合成过程中的一个产物 ,主要由激活的Ｔ淋巴细胞释放ＩＦＮ -γ刺激单核/巨噬细胞产生 ,与细胞免疫有关。新喋呤在体内的作用还不清楚 ,但它可以作为巨噬细胞活化的标记物 ,用来监测巨噬细胞的功能。本文就新喋呤在肝炎、肝硬化、原位肝移植中的变化及其意义作一综述。1　急性肝炎急性病毒性肝炎的发生与细胞免疫有关。Ｄａｉｔｏ〔1〕、Ｒｅｒｂｎｅｇｇｅｒ〔2〕 等分别研究急性甲肝、乙肝及非甲非乙型肝炎患者 ,发现其血、尿新喋呤水平均高于正常对照组、ＨＢｓＡｇ健康携带者及非病毒感染引起的肝病患者 ,且甲肝患…     

血清新喋呤与冠心病患者病变程度的关系

目的探讨冠心病(CHD)病患血清新喋呤水平改变的临床评价。方法选择该院2012年1月至2013年6月收治的106例CHD患者,其中急性心肌梗死(AMI)组29例,不稳定型心绞痛(UAP)组40例,稳定型心绞痛(SAP)组37例,另选取同期30例冠状动脉造影显示为正常者作对照组。采用酶联免疫吸附法(ELISA)测定各组血清新喋呤的水平。结果 AMI组和UAP组病患的血清新喋呤水平为(11.85±2.30)nmol/L和(9.94±1.91)nmol/L,显著高于SAP组和对照组的(8.13±2.10)nmol/L、(7.97±1.99)nmol/L(均P<0.05);但AMI组与UAP组的血清新喋呤水平比较无统计学差异(P>0.05);SAP组与对照组之间的血清新喋呤水平比较无统计学差异(P>0.05)。单支病变组、双支病变组和三支病变组病患血清新喋呤水平分别为(9.89±1.28)nmol/L、(10.07±1.81)nmol/L、(9.93±1.91)nmol/L,均显著高于对照组的(7.97±1.99)nmol/L(均P<0.05),但不同冠状动脉病变支数组间比较差异无统计学意义(P>0.05)。Ⅰ型、Ⅱ型、Ⅲ型斑块组血清新喋呤的水平分别为(8.01±1.18)nmol/L、(10.97±2.81)nmol/L、(8.33±2.01)nmol/L,均显著高于对照组的(7.97±1.99)nmol/L(均P<0.05),Ⅱ型斑块组血清新喋呤的水平为(10.97±2.81)nmol/L,显著高于Ⅰ型、Ⅲ型斑块组的(8.01±1.18)nmol/L与(10.97±2.81)nmol/L(均P<0.05),Ⅰ型与Ⅲ型斑块组血清新喋呤的水平比较无统计学差异(P>0.05)。结论 CHD病患血清新喋呤的水平异常升高,病患血清新喋呤的水平与斑块形态有关,与冠状动脉病变支数无关,血清新喋呤的水平可以作为预测不稳定型斑块病变的辅助指标。     

血清新喋呤对射血分数保留的心力衰竭的辅助诊断意义

目的观察射血分数保留的心力衰竭(HFp EF)患者血清新喋呤的水平,探讨血清新喋呤对HFp EF的辅助诊断意义。方法连续入选2016年10月~2017年8月于大连大学附属中山医院心脏中心住院心功能(NYHA分级)Ⅱ~Ⅳ级HFp EF患者共90例(HEp EF组),另选取同期入院基本临床资料相匹配的非心力衰竭患者80例作为对照组(非HFp EF组)。采集入选者临床资料并分析血清新喋呤与N末端脑钠肽前体(NT-pro BNP)、心脏超声有关参数的相关性,采用受试者工作特征曲线(ROC)评估血清新喋呤对HFp EF的辅助诊断意义。结果 HFp EF组中血清新喋呤、NT-pro BNP、肌酐水平均高于非HFp EF组(P0.05),随着NYHA心功能分级的增加,NT-pro BNP与血清新喋呤逐渐升高(P0.05);Spearman相关性分析显示,新喋呤与NT-pro BNP、E/E’、左房内径(LAD)、室间隔厚度(IVSD)呈显著正相关,而与LVEF、LVDD未见明显相关性;血清新喋呤诊断HFp EF的ROC曲线下面积(AUC)为0.720(95%CI:0.600~0.830,P0.05),NT-pro BNP为0.928(95%CI:0.863~0.994,P0.05),二者联合为0.932(95%CI:0.866~0.998,P0.05)。结论 HFp EF患者血清新喋呤明显增高,且与心力衰竭的严重程度相关。     

病毒性肝炎合并糖尿病预后与病毒因素的研究

目的研究病毒性肝炎合并糖尿病预后与病毒因素临床治疗效果。方法选取2013年4月—2014年1月间该院收治的96例患病毒性肝炎合并糖尿病患者进行回顾性分析,对96例住院患者分析病毒性肝炎合并糖尿病预后与病毒因素研究。结果甲型肝炎病患者均痊愈或好转,无未愈与死亡患者,预后效果较好;重叠型感染患和未定型肝炎者预后效果居中;乙型肝炎预后效果较差。结论重型肝炎组、肝硬化组、乙型肝炎组和重叠感染等病症的预后效果较差,但慢性肝炎合并糖尿病预后总体现象呈现良性发展,临床治愈效果提高。     

重型肝炎患者血清sCR1含量变化与红细胞粘附活性的相关性研究

目的研究重型肝炎患者可溶性补体受体1型(sCR1)浓度及红细胞粘附活性变化的临床意义.方法对76例重型肝炎、22例重型肝炎恢复期、58例肝硬化、58例慢性病毒性肝炎及80例正常人群进行了细胞竞争酶联免疫实验和红细胞天然免疫粘附功能实验.结果重型肝炎及肝硬化患者血清sCR1浓度均高于正常对照组(P＜0.01),重型肝炎患者明显高于肝硬化、慢性病毒性肝炎患者(P＜0.01)并与胆碱酯酶(CHE)、凝血酶原时间(PT)及凝血酶原活动度(PTA)变化明显相关.重型肝炎患者红细胞CR1粘附活性显著下降,与sCR1含量呈负相关.结论重型肝炎患者血清sCR1浓度变化与肝功能损伤程度密切相关,红细胞免疫粘附功能联合检测是评估重型肝炎患者病情严重程度、判断病情发展及预后的重要参考指标.     

乙型肝炎患者外周血单个核细胞中Foxp3 mRNA表达水平

目的探讨乙型肝炎病毒（HBV）感染患者外周血单个核细胞中叉头状螺旋转录因子（Foxp3）mRNA表达及其与HBV感染后转归的关系。方法应用实时RT-PCR方法检测19例急性乙型肝炎、50例慢性乙型肝炎、21例乙型肝炎后肝硬化、15例慢性乙型重型肝炎和15例正常对照组外周血单个核细胞中Foxp3 mRNA表达,应用ELISA法检测其血清中白细胞介素（IL）-10、转化生长因子β（TGF-β）含量,并观察它们与Foxp3 mRNA的相关性。结果急性乙型肝炎、慢性乙型肝炎、肝硬化、慢性重型肝炎患者Foxp3 mRNA水平高于正常对照组（P〈0.05）,重型肝炎Foxp3 mRNA水平高于其他各组（P〈0.05）。HBV感染各组IL-10、TGF-β含量较正常组明显升高（P〈0.05）,急性乙型肝炎组IL-10含量较慢性乙型肝炎组明显升高（P〈0.05）;急性乙型肝炎组TGF-β含量与肝硬化组、重型肝炎组比较差异无统计学意义（P〉0.05）,其他各组两两比较差异有统计学意义（P〈0.05）。IL-10、TGF-β与Foxp3 mRNA表达水平无相关性。结论急性乙型肝炎、慢性乙型肝炎、肝硬化、慢性重型肝炎患者Foxp3 mRNA水平高于正常人,重型肝炎患者Foxp3 mRNA水平高于其他各组HBV感染者,表明Foxp3参与了HBV发病过程,外周血单个核细胞中Foxp3 mRNA表达水平可能与疾病预后密切相关。     

肝炎肝硬化及原发性肝癌患者外周血Ｔ淋巴细胞亚群分析

为了探讨慢性肝病合并原发性肝细胞癌患者细胞免疫功能紊乱的发病机理,我们运用流式细胞技术对39例肝炎肝硬化及35例慢性病毒性肝炎合并原发性肝癌患者外周Ｔ血淋巴细胞亚群进行了检测。现将结果分析如下。对象与方法1.对象:74例患者均为1997年1月～1997年6月我院住院病人,分为肝炎肝硬化组(39例)和原发性肝癌组(35例)。肝炎肝硬化的诊断标准符合1995年全国传染病与寄生虫病学术会议修订的《病毒性肝炎防治方案》(北京)标准,男性30例,女性9例,年龄为31～60岁,平均年龄(42.4±11.6)岁。39例肝炎肝硬化患者乙肝病毒标志物均为阳性,其中5例合并…     

血清一氧化氮在病毒性肝炎中的临床意义

目的:探讨NO在病毒性肝炎中的作用及机制。方法:用分光光度比色分析法检测83例病毒性肝炎患者血清NO和内毒素水平。结果:各病毒性肝炎组NO和内毒素水平均高于正常对照组(P<0.01),重型肝炎组NO水平低于急性和慢性组(P<0.01),而内毒素水平高于急性和慢性组(P<0.01)。结论:病毒性肝炎患者NO水平明显升高,且可能对肝脏有保护作用,     

肝动脉热化疗栓塞术后患者血清新喋呤和T淋巴细胞rDNA转录活性的改变

目的 研究原发性肝癌患者肝动脉热化疗栓塞术前后血清新喋呤和外周血T淋巴细胞rDNA转录活性的变化及其临床意义。方法 分别用双抗体夹心酶联免疫法(ELISA)和核仁形成区相关蛋白银染技术测定45例中晚期肝癌行肝动脉热化疗栓塞术治疗前后血清新喋呤和外周血T淋巴细胞rDNA转录活性的改变,并与健康对照组比较分析。结果 肝癌组治疗前新喋呤增高,外周血T淋巴细胞rDNA转录活性降低,与对照组比较有显著性差异(P<0.01);行肝动脉热化疗栓塞术后,患者血清新喋呤降低,外周血T淋巴细胞rDNA转录活性增高,治疗前后有显著性差异(P<0.05);应用免疫调节剂(r-IL-2和r-IFN)组较未用组血清新喋呤下降和外周血T淋巴细胞rDNA转录活性升高更显著。结论 检测原发性肝癌患者血清新喋呤和外周血T淋巴细胞rDNA转录活性的情况,有助于了解病人的免疫状况,肝动脉热化疗栓塞术能改善机体免疫功能,给予合理的过继免疫治疗能增强这种作用。     

病毒性肝炎患者高迁移率族蛋白1的水平及其临床意义

目的研究晚期炎症介质高迁移率族蛋白1（HMGB1）在慢性肝炎及重型肝炎中的临床意义。方法选择慢性乙型病毒性肝炎患者56例、重型乙型病毒性肝炎患者28例、健康对照者20例,应用ELISA法检测血清HMGB1水平;同时检测相关生化指标、肝纤维化指标、凝血酶原时间（PT）。结果重型肝炎组HMGB1水平高于慢性肝炎组及正常对照组（P〈0.01）,且慢性肝炎组高于正常对照组（P〈0.01）;慢性肝炎组HMGB1水平随病情严重程度增加而增高（P〈0.01）。HMGB1水平与谷丙转氨酶、总胆红素、天冬氨酸氨基转移酶线粒体同工酶、透明质酸、层粘连蛋白、Ⅲ型前胶原、PT水平呈正相关,与白蛋白水平呈负相关。结论血清HMGB1含量可作为评价慢性病毒性肝炎病情严重程度的可靠指标。     

Clinical Significance of Serum and Urinary Neopterin Levels in Patients with Various Liver Diseases

Serum and urinary neopterin levels were measured by radioimmunoassay in 120 healthy controls, 16 asymptomatic HBsAg carriers, 12 patients with acute hepatitis, 13 with chronic inactive hepatitis, 35 with chronic active hepatitis, 46 with liver cirrhosis, 18 with hepatocellular carcinoma, and 6 with alcoholic liver disease. Serum and urinary neopterin levels were significantly higher in almost all patients than in normal subjects. Neopterin levels were highest in acute hepatitis and correlated with the results of liver function tests, but did not show this correlation in chronic liver disease. In chronic liver disease, the levels of serum neopterin in non-A non-B viral patients was significantly increased, compared with those in B viral and alcoholic patients. The rate of abnormal urinary neopterin levels in chronic liver disease was higher than the rate of abnormal serum neopterin levels, but no difference was observed between the rates of abnormal serum and urinary levels in acute hepatitis and asymptomatic HBsAg carriers. These results indicate that serum and urinary neopterin levels may be useful markers for cell-mediated immunity in liver disease, and that the immune system response in chronic liver disease may be different for different pathogens.     

Fibrinogen-like protein 2 fibroleukin expression and its correlation with disease progression in murine hepatitis virus type 3-induced fulminant hepatitis and in patients with severe viral hepatitis B

AIM: To evaluate the expression of fibrinogen-like protein 2 (fgl2) and its correlation with disease progression in both mice and patients with severe viral hepatitis. METHODS: Balb/cJ or A/J mice were infected intraperitoneally (ip) with 100 PFU of murine hepatitis virus type 3 (MHV-3), liver and serum were harvested at 24, 48, and 72 h post infection for further use. Liver tissues were obtained from 23 patients with severe acute chronic (AOC) hepatitis B and 13 patients with mild chronic hepatitis B. Fourteen patients with mild chronic hepatitis B with cirrhosis and 4 liver donors served as normal controls. In addition, peripheral blood mononuclear cells (PBMC) were isolated from 30 patients (unpaired) with severe AOC hepatitis B and 10 healthy volunteers as controls. Procoagulant activity representing functional prothrombinase activity in PBMC and white blood cells was also assayed. A polyclonal antibody against fgl2 was used to detect the expression of both mouse and human fgl2 protein in liver samples as well as in PBMC by immunohistochemistry staining in a separate set of studies. Alanine aminotransferase (ALT) and total bilirubin (TBil) in serum were measured to assess the severity of liver injury. RESULTS: Histological changes were found in liver sections 12-24 h post MHV-3 infection in Balb/cJ mice. In association with changes in liver histology, marked elevations in serum ALT and TBil were observed. Mouse fgl2 (mfgl2) protein was detected in the endothelium of intrahepatic veins and hepatic sinusoids within the liver 24 h after MHV-3 infection. Liver tissues from the patients with severe AOC hepatitis B had classical pathological features of acute necroinflammation. Human fgl2 (hfgl2) was detected in 21 of 23 patients (91.30%) with severe AOC hepatitis B, while only 1 of 13 patients (7.69%) with mild chronic hepatitis B and cirrhosis had hfgl2 mRNA or protein expression. Twenty-eight of thirty patients (93.33%) with severe AOC hepatitis B and 1 of 10 with mild chronic hepatitis B had detectable hfgl2 expression in PBMC. No hfgl2 expression was found either in the liver tissue or in the PBMC from normal donors. There was a positive correlation between hfgl2 expression and the severity of the liver disease as indicated by the levels of TBil. PCA significantly increased in PBMC in patients with severe AOC hepatitis B. CONCLUSION: The molecular and cellular results reported here in both mice and patients with severe viral hepatitis suggest that virus-induced hfgl2 prothrombinase/fibroleukin expression and the coagulation activity associated with the encoded fgl2 protein play a pivotal role in initiating severe hepatitis. The measurement of hfgl2/fibroleukin expression in PBMC may serve as a useful marker to monitor the severity of AOC hepatitis B and a target for therapeutic intervention.     

血清前白蛋白在肝病中的临床意义

了解病毒性肝炎患者血清前白蛋白 (PA)的变化 ,探讨测定血清前白蛋白对病毒性肝炎患者的诊断价值。采用免疫比浊法检测 2 76例病毒性肝炎患者血清前白蛋白 ,比较不同临床类型的血清PA的水平及同一临床类型间PA与A的异常率。血清PA的水平在急性肝炎与轻度慢性肝炎之间、慢性肝炎轻度与中度、中度与重度之间、肝硬化与慢性重型肝炎之间均有显著性差异 (P <0 0 5 ) ;急性肝炎组PA与白蛋白 (A)两者相比有高度显著性差异 (P <0 0 0 1) ;PA值比A值更灵敏地反映肝功能损害。血清PA的水平持续 <10 0mg/L作为重症肝炎早期诊断指标之一。检测血清PA对病毒性肝炎临床诊断、病情判断和预后估计有一定参考价值     

Serum neopterin levels in children with hepatitis-B-related chronic liver disease and its relationship to disease severity

AIM： To evaluate serum neopterin levels and their correlations with liver function tests and histological grade in children with hepatitis-B-related chronic liver disease. METHODS： The study population comprised 48 patients with chronic active hepatitis B, 32 patients with hepatitis-B-related active liver cirrhosis and 40 normal controls. Serum neopterin was measured using an enzyme-linked immunosorbent assay. RESULTS： The mean ＋ SD serum neopterin levels were 14.2 ± 5.6 nmol/L in patients with chronic hepatitis, 20.3 ± 7.9 nmol/L in patients with liver cirrhosis and 5.2 ± 1.4 nmol/L in control group. Serum neopterin levels were significantly higher in patients with chronic hepatitis （P = 0.005） and cirrhosis patients （P = 0.008）, than in control subjects. Cirrhotic patients had significantly higher serum neopterin levels than patients with chronic hepatitis （P = 0.004）. There was a positive correlation between serum neopterin levels and alanine aminotransferase levels in patients with chronic hepatitis （r = 0.41, P = 0.004） and cirrhotic patients （r = 0.39, P = 0.005）. Positive correlations were detected between serum neopterin levels and inflammatory score in patients with chronic hepatitis （r = 0.51, P = 0.003） and cirrhotic patients （r = 0.49, P = 0.001）. CONCLUSION： Our results suggest that serum neopterin levels can be considered as a marker of inflammatory activity and severity of disease in children with hepatitis-B-related chronic liver disease.     

血清氨基酸指标在病毒性肝炎及肝炎肝硬化诊断中的意义

通过临床研究，探讨急慢性病毒性肝炎、肝炎肝硬化患者氨基酸分析指标中可作为对诊断有独立项报作用的指标，并对其意义进行分析。123例患者分为急性病毒性肝炎组22例，慢性病毒性肝炎组59例，肝炎肝硬化组42例，用比色法测定各自血清氨基酸分析指标，行对数校正后的逐步判别分析。经逐步判别分析确定血清牛磺酸、亮氨酸、酪氨酸、尿素、甘氨酸是三组间的独立判别因素，另外急肝与慢肝之间天冬氨酸、慢肝与肝硬化之间苏氨酸也有重要意义。氨基酸分析指标中，牛磺酸、亮氨酸、酪氨酸、尿素、甘氨酸等在嗜肝病毒感染引起的肝病中对诊断及明确肝功储备情况有重要的临床意义。     

慢性肝病患者电解质异常的临床研究

研究慢性肝炎、肝硬化患者电解质异常情况。分别采用ELISA法、自动生化分析仪检测慢性肝炎轻度、慢性肝炎重度及肝硬化患者的肝功能、血生化。慢性重度肝炎与轻度比较血清Glu、Ca下降,肝硬化与重度比较BUN、Glu升高,Na、Ca、P、Mg均下降。随肝脏疾病的逐渐进展,病人低血Na、低血Ca的比例逐渐提高。BUN与血清白蛋白、胆碱脂酶呈负相关,Cr与胆碱脂酶呈负相关。Ca、Na、P均与血清白蛋白、胆碱脂酶呈正相关。随着慢性肝病进展,血电解质紊乱逐渐加重,血清Ca、Na、P水平可较好地反应肝脏的储备功能。     

Transfusion-transmitted virus in association with hepatitis A-E viral infections in various forms of liver diseases in India

AIM: To describe the prevalence of transfusion-transmitted virus (TTV) infection in association with hepatitis A-E viral infections in different forms of liver diseases in North India. METHODS: Sera from a total number of 137 patients, including 37 patients with acute viral hepatitis (AVH), 37 patients with chronic viral hepatitis (CVH), 31 patients with cirrhosis of liver and 32 patients with fulminant hepatic failure (FHF), were analyzed both for TTV-DNA and hepatitis A-E viral markers. Presence of hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis E virus (HEV) infections was detected in different proportions in different groups. Moreover, TTV-DNA was simultaneously tested in 100 healthy blood donors also. RESULTS: None of the patients had hepatitis A virus (HAV) and hepatitis D virus (HDV) infections. Overall prevalence of TTV-DNA was detected in 27.1% cases with AVH, 18.9% cases with CVH, 48.4% cases with cirrhosis and 9.4% cases with FHF. TTV-DNA simultaneously tested in 100 healthy blood donors showed 27% positivity. On establishing a relation between TTV infection with other hepatitis viral infections, TTV demonstrated co-infection with HBV, HCV and HEV in these disease groups. Correlation of TTV with ALT level in sera did not demonstrate high ALT level in TTV-infected patients, suggesting that TTV does not cause severe liver damage. CONCLUSION: TTV infection is prevalent both in patients and healthy individuals in India. However, it does not have any significant correlation with other hepatitis viral infections, nor does it produce an evidence of severe liver damage in patients with liver diseases.     

慢性肝病的血栓前状态评价

目的　探讨慢性肝病是否存在血栓前状态。方法　检测 5 1例慢性乙型肝炎及 2 9例肝硬化患者血浆血管性假性血友病因子 (vWF)含量、D 二聚体含量及血清纤维蛋白原降解产物 (FDP)水平 ,并对肝组织进行vWF的免疫过氧化物酶染色观察。结果　慢性乙型肝炎患者血浆vWF含量、D 二聚体含量及血清FDP水平均较正常对照升高 ,但差异无显著性。而肝硬化患者血浆vWF含量、D 二聚体含量及血清FDP水平与正常对照相比差异均有显著性。肝硬化患者的血浆D 二聚体含量及血清FDP水平与慢性乙型肝炎患者相比差异有显著性。 5 1例慢性乙型肝炎肝组织中 3 3例沿肝窦壁有vWF的阳性表达 ,阳性率为 64 .71%,随病变加重 ,阳性率增加。结论　慢性乙型肝炎患者的凝血、纤溶系统已发生紊乱。当患者病情进展到肝硬化阶段 ,凝血、纤溶系统即已出现显著紊乱 ,存在一定程度的弥漫性血管内凝血     

Role of viral factors in the natural course and therapy of chronic hepatitis B

Hepatitis B virus (HBV) infection is a global health problem that causes a wide spectrum of liver disease, including acute or fulminant hepatitis, inactive carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The pathogenesis of hepatocyte damage associated with HBV is mainly through immune-mediated mechanisms. On the basis of the virus and host interactions, the natural history of HBV carriers who are infected in early life can be divided into four dynamic phases. The frequency, extent, and severity of hepatitis flares or acute exacerbation in the second immune clearance and/or fourth reactivation phase predict liver disease progression in HBV carriers. In the past decade, hepatitis B viral factors including serum HBV DNA level, genotype, and naturally occurring mutants predictive of clinical outcomes have been identified. The higher the serum HBV DNA level after the immune clearance phase, the higher the incidence of adverse outcomes over time. In addition, high viral load, genotype C, basal core promoter mutation, and pre-S deletion correlate with increased risk of cirrhosis and HCC development. As to the treatment of chronic hepatitis B, patients with high HBV DNA level and genotype C or D infection are shown to have a worse response to interferon therapy. In conclusion, serum HBV DNA level, genotype, and naturally occurring mutants are identified to influence liver disease progression and therapy of chronic hepatitis B. More investigations are needed to clarify the molecular mechanisms of the viral factors involved in the pathogenesis of each stage of liver disease and the response to antiviral treatments.     

Adenosine deaminase isoenzymes and neopterin in liver cirrhosis

The aim of this study was to define the pattern of neopterin and ADA isoenzymes in liver cirrhosis. A total of 117 patients with liver cirrhosis were included. Serum levels of ADA were assayed in the presence and absence of a specific inhibitor for ADA1. Serum neopterin was measured using a competitive enzyme-linked immunosorbent assay. The grade of liver insufficiency was assessed according to the Child-Pugh classification and the monoethylglycinexylidide test. Serum ADA, ADA1, ADA2 and neopterin were higher in cirrhotic patients than in control subjects. A stepwise increase in serum ADA level was observed with increasing severity of liver cirrhosis. The probability of ADA2 being greater than the mean was approximately 2.5 times higher (2.48, CI 95%: 1.36-4.52) in patients with liver cirrhosis due to hepatitis C virus (HCV) infection than in those patients with cirrhosis of a different etiology. No correlation was found between ADA2 and neopterin. Our data show that liver insufficiency and HCV infection increase the serum levels of ADA and its major isoenzyme ADA2. Furthermore, ADA isoenzyme determination adds no value to total ADA value. The absence of a correlation between ADA2 and neopterin suggests that different physiologic processes are involved in their increase.