HBeAg阴性高病毒载量谷丙转氨酶≤2倍正常值上限慢性HBV感染者伴明显肝脏组织学改变的独立预测因素

目的探索HBe Ag阴性高病毒载量谷丙转氨酶(alanine transaminase,ALT)≤2倍正常值上限(upper limit of normal,ULN)慢性HBV感染者伴明显肝脏组织学改变(significant liver histopathological changes,SLHC)的独立预测因素。方法回顾性分析113例初治HBe Ag阴性高病毒载量(HBV DNA≥104copies/ml)ALT≤2 ULN(ULN定义为50 IU/L)的慢性HBV感染者。采用T检验、Mann Whitney秩和检验和卡方检验比较各变量的组间差异。单因素和多因素分析筛查SLHC的独立预测因素。结果入组113例患者,其中43例(38.1%)伴SLHC,70例(61.9%)不伴SLHC。多因素分析发现HBV DNA(OR=1.560,P=0.032)和谷氨酰转肽酶(gamma-glutamyl transpeptidase,GGT)(OR=1.089,P=0.022)是HBe Ag阴性高病毒载量ALT≤2 ULN慢性HBV感染者伴SLHC的独立预测因素。4 log10 copies/ml≤HBV DNA≤6 log10 copies/ml组患者SLHC发生率明显低于HBV DNA6 log10 copies/ml组患者(32.3%vs 61.9%,P=0.003);GGT≤50 IU/L组患者SLHC发生率明显低于GGT50 IU/L组患者(33.3%vs 60%,P=0.024)。结论 HBe Ag阴性高病毒载量ALT≤2 ULN慢性HBV感染者中,HBV DNA6 log10 copies/ml或GGT50 IU/L的患者伴SLHC的可能性更大,更加迫切需要肝穿刺组织学评估。     

HCV感染患者436例丙型肝炎病毒载量与抗-HCV及ALT异常的关系

目的 了解丙型肝炎病毒(HCV)载量与HCV抗体(抗-HCV)滴度及丙氨酸氨基转移酶(ALT)水平的关系.方法 采用双抗原夹心酶联免疫吸附测定法(ELISA)检测抗-HCV;用荧光定量逆转录聚合酶链反应(FQ-RT-PCR)检测436例抗-HCV阳性者的HCV RNA定量,同时检测ALT水平.用SAS9.0软件进行分析.结果 HCV RNA阳性率随S/CO值的增大而增高,当S/CO值在11.965时,敏感性为80.83%,特异性为70%;HCV RNA载量与ALT水平呈正相关(r=0.234 10,P<0.05),HCV RNA介于104～105IU/ml时ALT异常率最高,说明异常ALT水平在不同HCV RNA分组中存在统计学差异(P<0.05);随着HCV RNA载量的升高,ALT异常率升高,但以中病毒载量组最明显(χ2=58.4480,P<0.05).结论 抗-HCV滴度越高,HCV RNA阳性率越高;HCV RNA是反映HCV复制的可靠指标,结合ALT结果可帮助了解HCV在体内的复制情况.     

抗反转录病毒治疗人类免疫缺陷病毒/丙型肝炎病毒合并感染者终末期肝病的发生率及危险因素

目的 了解抗反转录病毒治疗(ART) HIV/HCV合并感染人群中终末期肝病的发生率及相关的危险因素.方法 回顾性研究HIV/HCV合并感染者的人口学资料和临床资料.单因素和多因素Logistic回归分析各变量[基线时年龄≥40岁、男性、既往有受血史、HCV持续感染时间、合并HBV感染(HBsAg阳性)、随访末时HIV RNA≥1×104拷贝/mL、随访末时HCV RNA≥1×105拷贝/mL、随访末时CD4细胞计数＞200/μL、随访末时ALT≥2×正常值上限(ULN)、包含奈韦拉平的ART、随访时间、ART持续时间＞5年、HCV基因1b型]与终末期肝病发生的相关性;Kaplan-Meier法分析终末期肝病对HIV/HCV合并感染者生存的影响.结果 共纳入427例HIV/HCV合并感染者,平均随访3.7年,55例患者(12.9％)出现终末期肝病,52例患者死亡,病死率为12.2％.多因素Logistic回归分析显示,基线时年龄≥40岁(OR=2.385,P=0.039)、ALT≥2×ULN(OR=16.374,P=0.000)、合并HBV感染(OR=2.507,P=0.042)、ART持续时间＞5年(OR=3.232,P=0.010)及CD4细胞计数≥200/μL(OR=0.364,P=0.011)与终末期肝病的发生显著相关.在有终末期肝病与无终末期肝病的HIV/HCV合并感染者中,病死率分别为50.9％和6.5％,两组比较差异有统计学意义(P=0.000).结论 随着ART的开展,终末期肝病在HIV/HCV合并感染者中仍较常见,合并终末期肝病明显缩短了HIV/HCV合并感染者的生存期.     

艾滋病合并丙型肝炎病毒感染者抗反转录病毒治疗效果和肝脏损伤

目的 评价对AIDS合并HCV感染患者抗反转录病毒治疗(ART)的临床疗效和肝损伤.方法 将患者按有无HCV合并感染分为HIV和HCV合并感染组(HIV/HCV组)65例,HIV感染组(HIV组)52例,应用两个核苷类反转录酶抑制剂(NRTI)联合一个非核苷类反转录酶抑制剂(NNRTI)的ART方案,疗程1年.随访并检测血浆HIV载量、外周血CD4细胞数、ALT.结果 治疗前,HIV/HCV组和HIV组的HIV载量均值分别为5.59和5.89 log10拷贝/mL,治疗1年后,分别降至2.91 log10拷贝/mL(P＜0.05)和2.88 log10拷贝/mL(P＜0.05),两组分别有83.1%和78.9%的患者HIV载量＜500拷贝/mL.HIV/HCV组和HIV组CD4细胞均值由治疗前的73.9和72.4/μL,分别增至215.1/μL和214.8/μL(P值均＜ 0.05).1年内,HIV/HCV组与HIV组肝功能异常率分别为24.6%与7.7%(P＜0.05),但无因发生严重肝损伤而终止ART者.结论 联合应用NRTI、NNRTI治疗AIDS合并HCV感染患者,短期内能有效抑制HIV复制,促进免疫功能重建.HCV感染虽可加重肝损伤,但对ART疗效无明显影响.     

人类免疫缺陷病毒与重叠丙型肝炎病毒感染者免疫指标比较

目的 分析HIV/HCV重叠感染人群与HIV单独感染人群治疗前临床特征及免疫功能的差异,探讨其可能的影响因素.方法 以HIV/HCV重叠感染患者59例、HIV单独感染患者38例为研究对象,取患者治疗前外周血,检测其肝功能、血常规、外周血T细胞亚群(CD4+、CD8+)及HIV、HCV病毒载量,酶联免疫斑点法(ELISPOT)检测HIV特异性细胞毒性T淋巴细胞(CTL)的数量和功能.结果 HIV/HCV重叠感染率达60.8%.重叠感染组ALT、AST均明显高于HIV组(49.8 U/L比23.6 U/L,49.1 U/L比32.3 U/L,P值分别为0.000、0.013);重叠感染组PLT明显低于HIV组[(167.3±59.2)×109/L比(198.0±63.9)×109/L,P=0.040].外周血T细胞亚群检测结果两组间差异无统计学意义.重叠感染组HIV RNA定量为(4.046±0.541)lOglo拷贝/mL,低于HIV组的(4.394±0.507)log10拷贝/mL(P=0.018).重叠感染组对HIV-Gag全序列肽段的阳性孔斑点数(平均秩次30.85)较HIV组(平均秩次44.34)低,阳性孔数(4.60±5.52)低于HIV组(6.24±6.93),但两组比较差异无统计学意义.重叠感染组Alb与HCV病毒载量呈负相关(r=-0.540),CD4+与PLT呈正相关(P=0.000).结论 单采血浆感染HIV患者中,有较高的HIV/HCV重叠感染率和较低的细胞免疫功能.     

树突状细胞表面特异性非整联蛋白同源物基因多态性与丙型肝炎病毒感染的相关性

目的 研究丙型肝炎患者树突状细胞表面特异性非整联蛋白同源物(DC-SIGNR)外显子4基因颈区重复序列的遗传多态性分布,探讨DC-SIGNR基因多态性与HCV病毒基因分型及HCV载量的关系. 方法采用PCR结合DNA测序对268例丙型肝炎患者DC-SIGNR重复序列多态性进行基因分型和测序分析,同时检测患者的HCV病毒载量及HCV病毒基因分型.组间两两比较用LSD法.结果 DC-SIGNR基因型或等位基因与HCV基因分型的相关性不显著.HCV载量携带7等位基因的患者为(4.6722±1.9766)log10拷贝/ml,携带9等位基因的患者为(5.3073±1.6795)log10拷贝/ml,P=0.036,两组差异有统计学意义.7/7基因型的患者HCV载量水平为(4.5974±2.0067)log10拷贝/ml,9/7基因型的患者组为(5.2771±1.8587)log10拷贝/ml,P=0.025,两组差异有统计学意义.提示HCV更易与携带较长DC-SINGR等位基因的患者结合.结论 DC-SIGNR遗传多态性可能与HCV在个体内的复制有关,但与HCV基因分型不相关.     

树突状细胞表面特异性非整联蛋白同源物基因多态性与丙型肝炎病毒感染的相关性

目的 研究丙型肝炎患者树突状细胞表面特异性非整联蛋白同源物(DC-SIGNR)外显子4基因颈区重复序列的遗传多态性分布,探讨DC-SIGNR基因多态性与HCV病毒基因分型及HCV载量的关系. 方法采用PCR结合DNA测序对268例丙型肝炎患者DC-SIGNR重复序列多态性进行基因分型和测序分析,同时检测患者的HCV病毒载量及HCV病毒基因分型.组间两两比较用LSD法.结果 DC-SIGNR基因型或等位基因与HCV基因分型的相关性不显著.HCV载量携带7等位基因的患者为(4.6722±1.9766)log10拷贝/ml,携带9等位基因的患者为(5.3073±1.6795)log10拷贝/ml,P=0.036,两组差异有统计学意义.7/7基因型的患者HCV载量水平为(4.5974±2.0067)log10拷贝/ml,9/7基因型的患者组为(5.2771±1.8587)log10拷贝/ml,P=0.025,两组差异有统计学意义.提示HCV更易与携带较长DC-SINGR等位基因的患者结合.结论 DC-SIGNR遗传多态性可能与HCV在个体内的复制有关,但与HCV基因分型不相关.     

丙型肝炎病毒母婴垂直传播的概率及影响因素

目的检测获得母婴配对垂直传播丙型肝炎病毒(HCV)的概率,并分析其与肝功能转氨酶等影响因素之间的关系。方法收集2011年1月至2013年12月在南京市第二医院就诊的门诊及住院的母婴HCV患者共321例,采集空腹静脉血标本,酶联免疫吸附测定法(ELISA)检测HCV抗体(抗-HCV);实时荧光定量聚合酶链反应(FQ-PCR)检测HCV RNA;采用速率法,用电化学发光全自动免疫分析系统Cobas 6000及配套试剂检测ALT、AST,并进行统计学分析。结果纳入的34例孕妇HCV RNA为(5.20±0.88)lgIU/mL,34例产妇中有3例HCV RNA阴性,其余31例HCV RNA均为阳性;婴儿中HCV RNA阳性2例(龙凤胎,病毒载量分别为4.70×103 IU/mL和7.60×104 IU/mL),其余33例均为阴性。孕妇ALT及AST异常率为14.71%(5/34),母婴垂直传播的概率约为2.94%(1/34)。结论本研究母婴垂直传播的风险约为2.94%,垂直传播给婴儿的概率极小;多数产妇的病毒载量为106～107 IU/mL,且肝功能正常者居多,提示孕妇可能发生免疫耐受。     

慢性乙型肝炎患者12周自发性HBV DNA水平变化分析

目的 分析慢性乙型肝炎患者12周内自发性HBV DNA水平下降情况.方法 回顾性分析2003-2005年未接受抗病毒药物治疗的慢性乙型肝炎患者12周内自发性HBV DNA水平下降情况,并根据患者基线ALT、总胆红素(TBil)水平进行分组,分析基线ALT、TBil对自发性HBVDNA水平下降的影响.两组间计量资料比较采用t检验或Wilcoxon符号秩和检验;多组数据均值比较采用方差分析;组间率的比较采用x2检验.结果 共收集213例慢性乙型肝炎患者,男性174例,女性39例,年龄18～65(33.0±10.0)岁.其中慢性乙型肝炎轻～中度124例,慢性乙型肝炎重度89例;12周时失访19例(8.92%).所有患者HBV DNA基线均值为(6.66±1.03)log10拷贝/ml,12周时为(5.98±1.53)log10拷贝/ml(P<0.01).慢性乙型肝炎重度患者基线时HBVDNA水平均值低于慢性乙型肝炎轻～中度患者,分别为(6.45±0.99)log10拷贝/ml与(6.81±1.04)log10拷贝/ml(P<0.05);但两组12周时HBV DNA水平均值及HBV DNA水平下降值的差异均无统计学意义.12周时HBV DNA≤3 log10拷贝/ml患者的基线ALT及TBil值高于HBVDNA>3 log10拷贝/ml组,但差异均无统计学意义.12周时HBV DNA水平下降值≥2 log10拷贝/ml与<2 log10拷贝/ml两组患者的基线ALT、TBil水平相近(P>0.05).基线ALT水平≤5倍正常值上限(ULN)与>5×ULN两组患者12周时HBV DNA水平均值及HBV DNA水平下降值的差异均无统计学意义;两组患者12周时HBV DNA≤3 log10拷贝/ml、HBV DNA水平下降值≥2 log10拷贝/ml的比例,差异也无统计学意义(P>0.05).基线时ALT≤5 × ULN及TBil≤5×ULN组HBV DNA水平均值高于其他3组(P<0.05),但12周时各组HBV DNA水平均值、HBV DNA下降值比较,差异无统计学意义. 结论 慢性乙型肝炎患者12周内存在一定程度的自发性HBV DNA水平下降,但肝脏炎症损伤程度与患者12周内自发性HBV DNA水平下降程度无明显的相关性.     

高效抗逆转录病毒药物联合聚乙二醇化干扰素α-2a治疗艾滋病合并丙型肝炎患者的效果评价

目的探讨高效抗逆转录病毒药物联合聚乙二醇化干扰素α-2a（PEG-IFNα-2a）治疗HIV合并HCV感染者的疗效和不良反应。方法22例HCV/HIV合并感染者,先予高效抗逆转录病毒药物治疗;待所有患者CD4^＋ T淋巴细胞上升至0.20×10^9/L以上,将患者分成CD4^＋T淋巴细胞≥0.35×10^9/L和〈0.35×10^9/L两组,给予PEG-IFNα-2a,180μg,每周肌肉注射1次,检测两组患者的HCV RNA和HIV RNA水平、肝功能和血常规,并做CD4^＋T淋巴细胞计数。结果CD4^＋T淋巴细胞≥0.35×10^9/L组13例,在治疗12、24、48周后,与治疗前比较,HCV RNA平均分别下降2.0650 log10拷贝/ml（t=3.8733,P〈0.01）、2.9146 log10拷贝/ml（t= 7.6741,P〈0.01）、2.4315 log10拷贝/ml（t=5.8202,P〈0.01）。CD4^＋T淋巴细胞〈0.35×10^9/L组9例,分别下降1.1522 log10拷贝/ml（t=2.8937,P〈0.05）、1.4189 log10拷贝/ml（t= 2.4422,P〈0.05）、1.1167 log10拷贝/ml（t=1.1261,P〉0.05）。两组患者HCV RNA早期应答率和治疗结束应答率比较,P值均〉0.05。CD4^＋T淋巴细胞〈0.35×10^9/L组,在治疗24周时白细胞较治疗前下降（t=2.4700,P〈0.05）。CD4^＋T淋巴细胞≥0.35×10^9/L组,治疗24周和48周血小板均较治疗前下降（t=2.3273,P〈0.05;t=3.6149,P〈0.01）。结论PEG-IFNα-2a治疗HIV/HCV患者,能有效降低HCV病毒载量,CD4^＋T淋巴细胞≥0.35×10^9/L组疗效更显著,但两组患者的HCV RNA早期应答率和治疗结束应答率差异无统计学意义。PEG-IFNα-2a可降低外周血白细胞和血小板。     

Biochemical and virologic parameters in patients co-infected with hepatitis C and HIV versus patients with hepatitis C mono-infection

BACKGROUND: Previous studies of patients with hepatitis C virus (HCV) infection looking at the effect of human immunodeficiency virus (HIV) co-infection on biochemical parameters and HCV RNA level have shown conflicting results. Accurate characterization of the effect of HIV is important for evaluation and treatment of HCV in co-infected persons. METHODS: We studied 315 HCV mono-infected and 75 HCV-HIV co-infected subjects to determine the effect of HIV on biochemical parameters and HCV RNA and to determine the predictors of elevated serum alanine aminotransferase (ALT) levels and HCV RNA levels. RESULTS: The co-infected subjects were more likely to be African-American (55% vs 26%, P < 0.0005), have used injection drugs (68% vs 60%, P = 0.02), have detectable HCV RNA (84% vs 70.5%, P = 0.018), have HCV RNA levels >6 log10 IU/mL (60% vs 38%, P = 0.001), and have lower mean serum ALT levels (50.4 IU/mL vs 73.7 IU/mL, P = 0.006). In multivariable analyses, the following factors predicted an ALT level >50 IU/mL: log10 HCV RNA (OR, 1.15; 95% CI, 1.00 to 1.32); HIV co-infection (OR, 0.48; 95% CI, 0.25 to 0.89); and having ever been treated for HCV (OR, 1.92; 95% CI, 1.16 to 3.18). The only significant predictor of HCV RNA level >6 log10 IU/mL was HIV co-infection (OR, 2.75; 95% CI, 1.46 to 5.15). Significant predictors of having a detectable HCV RNA level were female sex (OR, 3.81; 95% CI, 1.18 to 12.25); HIV co-infection (2.45; 95% CI, 1.14 to 5.26); and ever being treated for HCV (OR, 1.96; 95% CI, 1.10 to 3.48). CONCLUSIONS: HCV-HIV co-infected persons have higher HCV RNA levels but lower serum ALT levels than HCV mono-infected patients. Criteria for performing liver biopsy and treating HCV infection in co-infected patients may need to be revisited.     

Long-term interleukin 10 therapy in chronic hepatitis C patients has a proviral and anti-inflammatory effect

An imbalance in Th1 and Th2 cytokine production is implicated in disease progression of HCV. Our aim was to determine the effect of IL-10 administration in patients with HCV-related liver disease. Thirty patients with advanced fibrosis who had failed antiviral therapy were enrolled in a 12-month treatment regimen with SQ IL-10 given daily or thrice weekly. Liver biopsies were performed before and after therapy. Serum and PBMC were collected for HCV RNA, ALT, and functional T-cell analysis. IL-10 led to significant improvement in serum ALT (mean ALT: day 0 = 142 +/- 17 vs. month 12 = 75 +/- 10; P <.05). Hepatic inflammation score decreased by at least 2 in 13 of 28 patients (mean decrease from 4.6 +/- 0.3 to 3.7 +/- 0.3, P <.05) and 11 of 28 showed a reduction in fibrosis score (mean change from 5.0 +/- 0.2 to 4.5 +/- 0.3, P <.05). Serum HCV RNA levels increased by 0.5 log during therapy (mean HCV RNA day 0: 12.3 +/- 3.0 Meq/mL; 12 months: 38 Meq/mL; P <.05) and returned to baseline at the end of follow-up (11.0 +/- 2.4 Meq/mL). Five patients developed viral loads of greater than 120 Meq/mL and two of these developed an acute flare in serum ALT. IL-10 caused a decrease in the number of HCV-specific CD4+ and CD8+ IFN-gamma secreting T cells and alterations in PBMC cytokine production towards a Th2 dominant profile. These changes parallel the improvement in ALT and rise in HCV RNA. In conclusion, long-term rIL-10 therapy appears to decrease disease activity, but also leads to increased HCV viral burden via alterations in immunologic viral surveillance.     

Quantitation of HCV RNA in liver of patients with chronic hepatitis C

BACKGROUND/AIMS: Liver HCV RNA has been quantitated in few studies and the feasibility and the role of this parameter in the evaluation of patients with chronic HCV hepatitis still warrant study. Our aim was to determine the concentrations of HCV RNA in the liver of chronic HCV patients and to correlate the results with serum viral load. We also studied the relation of levels of HCV RNA in the liver with serum aminotransferases levels and with the presence of cirrhosis. METHODS: Twenty patients (14 males, aged 28 to 61 years) were studied. Twelve were infected by HCV type 1, six by type 3 and one by type 5. Percutaneous liver biopsy samples were obtained from 14 patients, and the remainder from liver explant in patients undergoing OLT. Twelve had chronic hepatitis and eight cirrhosis. HCV RNA levels were determined by bDNA. RESULTS: HCV RNA levels below the detection limit were found in one liver and in five serum samples. HCV RNA (mean +/- SD) was 2.1 x 10(8) +/- 2.2 x 10(8) Eq/gm in the liver and 94 x 10(5) +/- 93 x 10(5) Eq/mL in serum, with a significant correlation between these values (r = 0.89; P < 0.0001). Serum HCV RNA levels were significantly lower (P = 0.001) in cirrhotic than in chronic hepatitis patients, while the groups did not differ in liver HCV RNA levels. No correlation was observed between liver or serum HCV RNA and serum ALT or AST. CONCLUSIONS: Quantitation of HCV RNA is possible even in small liver samples. Although average levels are more than one log higher than those observed in serum, hepatic concentrations correlate with those observed in serum. The application of this technology to monitoring antiviral therapy and understanding the pathogenesis of the disease remains to be determined.     

Serum HCV RNA titer does not predict the severity of liver damage in HCV carriers with normal aminotransferase levels

AIMS/BACKGROUND: Many HCV RNA positive subjects with normal aminotransferase levels have significant liver damage despite normal liver biochemistry. In these patients it is not possible to discriminate between "healthy" carriers and subjects with chronic liver damage, unless liver biopsy is performed. The aim of this study was to evaluate the usefulness of HCV RNA quantitation as a non invasive tool to predict the severity of liver injury in a group of HCV carriers with normal amino-transferase levels. METHODS: 59 HCV RNA positive subjects (20 males) with persistently normal ALT levels were studied. All patients underwent HCV RNA quantitation and percutaneous liver biopsy. RESULTS: No correlation was found between serum HCV RNA titers and grading, while viraemia did correlate with staging. Patients were categorized into four subgroups, according to arbitrary serum HCV RNA cut-offs. Grading was not different between the four groups. Staging was significantly higher among subjects with viraemia > 1000 x 10(3) copies/mL than in patients with HCV RNA titers < 1000 x 10(3) copies/mL. CONCLUSIONS: In HCV carriers with normal aminotransferase levels viraemia does not predict the grade of HCV-related chronic liver disease (CLD), although subjects with higher HCV RNA levels seem to have more severe fibrosis. Although these data suggest that patients with higher viraemia might have more intense architectural changes and more severe progression of liver disease than those with lower levels of HCV replication, the weak and imprecise correlation leads us to conclude that HCV RNA quantitation is not a useful indicator in clinical practice in the selection of patients for liver biopsy.     

A study of primary- and re-infection with hepatitis C virus in blood transfusion recipients

A nested polymerase chain reaction was used to assess viraemia in blood transfusion recipients with no serological evidence of hepatitis C virus (HCV) infection (naive recipients) and in recipients with prior or existing HCV infection (infected recipients), who were transfused with HCV-positive blood. In 10 hepatitis cases in naive recipients, defined as primary infection, nine showed clinical hepatitis, and one was sub-clinical; the time between transfusion and elevation of alanine aminotransferase (ALT) levels was 15–60 days (37.9 ± 13.9). All 10 naive recipients showed abnormal ALT, and 10/10 and 7/10 were persistently positive for anti-HCV and HCV-RNA, respectively, for more than 1 year. Similarly, in five cases in previously infected recipients, defined as re-infection, 4/5 showed clinical hepatitis, the time to elevation of ALT was 30–46 days (34.8 ± 6.4), and 5/5 and 3/5 were persistently positive for anti-HCV and HCV-RNA, respectively, for more than 1 year. All five infected recipients showed abnormal ALT. In conclusion, there was no significant difference (P= 0.05) in the frequency of the markers of infection resulting from primary or re-infection with HCV, suggesting that primary infection fails to induce a protective immune response.     

Hepatitis C virus load and survival among injection drug users in the United States

Persons chronically infected with hepatitis C virus (HCV), some of whom may be coinfected with HIV and human T-lymphotropic virus type II (HTLV-II), are at high risk for end-stage liver disease (ESLD). We evaluated whether ESLD death was associated with premorbid HCV RNA level or specific HCV protein antibodies among persons with or without HIV/HTLV-II coinfection in a cohort of 6,570 injection drug users who enrolled in 9 US cities between 1987 and 1991. We compared 84 ESLD descendents and 305 randomly selected cohort participants with detectable HCV RNA, stratified by sex, race, HIV, and HTLV-II strata. Relative hazard (RH) of ESLD death was derived from the proportional hazard model. Risk of ESLD death was unrelated to the intensity of antibodies against the HCV c-22(p), c-33(p), c-100(p), and NS5 proteins, individually or combined, but it increased with HCV RNA level (RH(adj) = 2.26 per log(10) IU/mL, 95% CI: 1.45-5.92). The association between HCV RNA level and ESLD death remained significant after adjustment for alcohol consumption (RH(adj) = 2.57 per log(10) IU/mL, 95% CI: 1.50-8.10). Deaths from AIDS (n = 45) and other causes (n = 43) were unrelated to HCV RNA (RH(adj)= 1.14 and 1.29 per log(10) IU/mL, respectively). HIV infection was not associated with ESLD risk in multivariate analyses adjusted for HCV RNA. Men had an increased risk of ESLD death in unadjusted analyses (RH = 1.92, 95% CI: 1.15-3.56) but not in multivariate analysis (RH(adj) = 0.98, 95% CI: 0.48-2.88). Non-black patients were at increased risk for ESLD death (RH(adj)= 2.76, 95% CI: 1.49-10.09). In conclusion, HCV RNA level is a predictor of ESLD death among persons with chronic HCV infection.     

由一个献血员所致83例丙型肝炎病毒感染者10年的自然转归

目的 了解输血后丙型肝炎病毒感染者的临床特征及其自然病史.方法 采用横断面调查与回顾性调查相结合的方法,对1998年1月-2002年7月输受同一供血者血液的83侈HCV感染患者进行临床资料调查,同时进行抗-HCV,HCV RNA,肝功能生物化学指标,腹部B型超声检查.计量资料用7检验,计数资料用x2检验,等级资料用秩和检验.结果 抗-HCV阳性83例,HCV RNA阳性56例,丙型肝炎慢性化率为67.4%,其中男性76.3%(29/38),女性60.00%(27/45),两者差异无统计学意义(x2=2.99,P=0.11).HCV RNA阳性组的平均年龄为(36.54±14.37)岁,HCV RNA阴性组平均年龄为(27.43±12.51)岁,差异有统计学意义(T=-2.41,P=0.018).供血者感染HCV基因为1b型.HCV RNA阳性患者中有10例表现为轻度乏力、纳差、腹胀,9例ALT轻度升高,12例B型超声检查提示有慢性肝炎改变,1例为肝硬化失代偿期.结论 输血后感染HCV者临床表现隐匿,慢性化与受感染时的年龄有一定关系.

Abstract：

Objective To find out clinical characteristics and natural history of post transfusion HCV infection. Methods 83 subjects who have received the blood from a same blood donor from January 1998 to July 2002 were investigated by the method combining cross-sectional study with retrospective study. HC V-antibody, HCV RNA, liver function, abdomen B-ultrasound and Fibroscan were detected. Results The HCV-antibody were all positive. The HCV RNA of 56 out of the 83 cases were positive. The chronicity rates of hepatis C were 76.3% (29/38) in male patients and 60.00% (27/45) in female patients respectively, without significant difference (x2 = 2.99, P = 0.11). The average age of the HCV RNA positive patients was (36.54 ± 14.37) years old. The average age of the HCV RNA negative patients was (27.43 ± 12.51) years old. A significant difference (T = -2.41, P = 0.018) existed between. The HCV genotype was typelb. Among the HCV RNA positive patients, 10 cases were with mild asthenia, anorexia and abdominal distention, 9 cases with increased serum ALT, 12 cases.with chronic hepatitis and 1 case was diagnosed with decompensated liver cirrhosis. Conclusion The clinical manifestations of HCV infection are occult and chronic. The chronicity rate is related to gender and the age when infection was caught.     

慢性丙型肝炎患者肝组织学改变及其影响因素分析

目的探讨慢性丙型肝炎患者肝组织学改变及其影响因素。方法选择经皮肝组织活检的慢性丙型肝炎患者102例,记录患者年龄、性别、体质指数(BMI)、感染途径等,检测ALT水平、AST水平、HCV基因分型、病毒载量和肝脏组织学改变。统计学处理采用t检验和Logistic回归分析。结果肝脏炎症活动指数( HAI)≥4的慢性丙型肝炎患者的ALT、AST水平较高,PLT较低,与HAI＜4的患者相比差异有统计学意义(t=2.209、2.298、2.565,均P＜0.05)。纤维化分期评分(F)≥3的患者平均年龄、ALT水平、AST水平以及感染时间均高于F＜3的患者（t=2.340、3.497、2.758、2.570,均P＜0.05）,而PLT则较低(t=2.761,P=0.007)。女性、ALT＞1×正常值上限(ULN)、AST水平、F≥3、HCV RNA≥6 lgIU/mL和PLT计数是HAI≥4的单因素预测因子;经多因素分析后,Ishak纤维化分期评分是HAI≥4的唯一独立预测因子(OR 3.098,95％ Cl1.884～5.092,P＜0.01)。单因素分析F≥3的预测因子为年龄、BMI≥24 kg/m2、ALT＞1×ULN、AST水平、HAI≥4、PLT计数以及感染年限≥15年;多因素回归分析显示,年龄(OR 1.074,95％CI1.006～1.146,P=0.033)、ALT水平(OR 1.035,95％CI 1.015～1.055,P＜0.01)、AST水平(OR0.969,95％CI 0.948～0.990,P=0.005)、感染年限≥15年(OR 37.215,95％CI 5.816～238.127,P＜0.01)和HAI≥4(OR 1.939,95％CI 1.426～2.636,P＜0.01)是F≥3的独立危险因素。结论年龄、ALT水平、AST水平、感染年限≥15年和HAI≥4是肝组织学显著纤维化的独立预测因子。