酒精性肝病与乙型、丙型肝炎病毒感染

本文通过对38例酒精性肝病(ALD)患者血清HBV标志物和抗HCV的检测，探讨HBV、HCV感染与ALD的关系。     

慢性肝病与乙型,丙型肝炎病毒感染关系的探讨

采用ELISA法对25例慢性肝炎,105例肝硬化,64例肝癌以及8例急性黄疸型肝炎进行了HBV标志物及抗-HCV的检测.结果:HBV感染率为80.6%,抗-HCV检测阳性率为46%,二者均阳性的双重感染率为32%.其中肝癌组双重感染明显高于肝硬化组P<0.001.单纯抗-HCV检出率为10.8%,说明HBV是引起肝炎、肝硬化、肝癌的主要病因,而HCV感染也是致病因素.对有输血史的慢性肝炎、肝硬化、肝癌100例进行抗-HCV检测,其阳性率59%,而102例无输血史的肝病患者抗-HCV检出率为25%,输血组抗HCV检出率明显高于无输血组P<0.001.其中慢性肝炎、肝硬化、肝癌病人输血组抗-HCV检出率亦明显高于无输血组,各组P<0.001.故提示:HCV感染与输血有密切关系.50例HBV标志物阴性的健康献血员抗-HCV阳性率为6%.     

丙型肝炎病毒感染与各类肝病关系的探讨

为了解肝病患者丙型肝炎病毒（ＨＣＶ）的感染状况，用ＲＴＰＣＲ及ＥＬＩＳＡ法测定肝炎病毒标志。有受血史者，急性丙肝（６０５３％）高于急性乙肝（１０５３％，Ｐ＜００１）。无受血史者，急性肝炎以甲、乙型肝炎为主（４１６７％、３０５６％），高于丙肝（４１７％，Ｐ＜００１）。有受血史者的急、慢性丙肝及无症状ＨＣＶ感染者（６０５３％、２０３４％，２９１７％），高于无受血史者的４２％、８７４％，３３３％（Ｐ＜００１～００５）。慢性及重型肝炎、肝硬化、肝癌及无症状感染者乙肝病毒（ＨＢＶ）感染均高于ＨＣＶ感染（Ｐ＜００１）。提示ＨＣＶ感染多与血制品有关；慢性及重型肝炎、肝硬化及肝癌主要由ＨＢＶ所致。     

乙型及丙型肝炎病毒感染与原发性肝癌的临床研究

目的研究HBV DNA、HBsAg、HBeAg、HBeAb、HBcAb及抗-HCV与原发性肝癌发生的相关性。方法采用回顾性调查分析方法,对58例原发性肝癌患者（病例组）,同期收治的58例其他恶性肿瘤患者（对照组）HBV和HCV感染情况进行统计,并分析HBV血清标志物及HBV DNA与原发性肝癌发生发展的规律。结果两组资料的HBV感染率分别为82.76%和44.83%,病例组与对照组比较有显著性差异（P〈0.05）,单纯HCV感染及HBV/HCV混合感染率两组无明显差异（P〉0.05）;血清HBV DNA阳性率在病例组和对照组分别为72.92%、23.08%（P〈0.05）;HBsAg、HBeAb和HBcAb检出率病例组高于对照组（P〈0.05）;而HBeAg阳性率两组比较无显著性差异（P〉0.05）。结论在慢性HBV感染的肝癌高发人群中,HBV DNA、HBsAg、HBeAg、HBeAb及HBcAb所反映的HBV感染状态及不同临床演变过程与肝癌的发生发展密切相关,共同参与肝癌的发病机制。     

2007年亚太肝病学会有关丙型肝炎诊断、处理和治疗的共识

1HCV感染与实验室检测1.1抗HCV检测应由获准的第三代或第四代酶联免疫试验(EIA)进行(Ⅱ-2)。1.2标本经获准EIA方法检测阴性者可报告为抗HCV阴性,但须注意,血液透析或重叠感染HIV的患者可出现HCVRNA阳性,而抗HCV阴性(Ⅱ-2)。     

抗HCV及HCV—RNA在丙型肝炎中的变化对丙型肝炎特异性诊断的影响

抗ＨＣＶ及ＨＣＶ－ＲＮＡ是目前丙型肝炎常用的方法，本文用ＰＣＲ方法及第二代ＥＬＩＳＡ试剂动态观察１００例疑诊内型肝炎患者ＨＣＶ－ＲＮＡ及抗ＨＣＶ，结果显示，上述两种仍为目前敏感性和特异性高的方法，同时发现动态观察可避免因抗ＨＣＶ产生较晚，ＨＣＶ－ＲＮＡ在血液中的阶段性及病毒基因变异对诊断的影响，从而提高诊断可靠性。     

逆转录双PCR法检测340例慢性肝病患者HCV感染及与HBV感染的关系

本文采用逆转录双PCR法对340不例同慢性肝病患者中的抗—HCV阳性血清进行HCV—RNA检测,66例抗HCV阳性血清检出55例HCV—RNA阳性,HCV—RNA阳性率为16.18％(55/340),在慢迁肝、慢活肝、肝硬化、慢重肝及肝细胞癌中HCV—RNA阳性率分别为10.98％(18/164)、20.59％(7/34)、36.67％(11/30),33.33％(1/3)及16.51％(18/109)。HCV感染在慢性肝病中主要是以与HBV合并感染形式存在,为10.88％(37/340),单一HCV感染仅为5.29％(18/340),结果提示HCV感染可加重慢性乙型肝炎的肝损害,促进病情向重症化发展,而其在肝细胞癌中的意义有待进一步研究。     

乙型和丙型肝炎病毒感染与慢性肝病

检测天津地区１１９例慢性肝病毒者ＨＢＶ、ＨＣＶ标志，并对其中２８例ＨＣＶＲＮＡ阳性血清进行基因分型。结果，ＨＢＶ感染率明显高于ＨＣＶ感染率（Ｐ〈０．０５），肝癌患者中ＨＢＶ、ＨＣＶ重叠感染率明显高于慢性肝炎（Ｐ〈０．０５）；各组均以ＨＣＶⅡ型为主。提示天津地区慢性肝病上前仍以ＨＢＶ感染为主；ＨＢＶ、ＨＣＶ重叠感染对肝癌的发生似有相加作用；ＨＣＶⅡ型感染在天津地区ＨＣＶ相关性曙性肝病中可以起主要作用     

Hepatitis C Virus Infection among Patients with Chronic Liver Disease in an Area Hyperendemic for Hepatitis B

Tsai J-F, Jeng J-E, Chang W-Y, Lin Z-Y, Tsai J-H. Hepatitis C virus infection among patients with chronic liver disease in an area hyperendemic for hepatitis B. Scand J Gastroenterol 1994;29:550-552.

Background: The prevalence of hepatitis C virus (HCV) infection was assessed in patients with nonalcoholic chronic liver disease (CLD).

Methods: Antibody levels to HCV (anti-HCV) were assessed in 100 pairs of CLD patients and healthy controls.

Results: The prevalence of anti-HCV was higher in patients (26.0%) than in controls (2.0% p = 0.0001). The patient group with anti-HCV was older (p equals; 0.0001) and had more smokers (p equals; 0.034), fewer hepatitis B surface antigen carriers (p equals; 0.0001), and more patients with active liver disease (p equals; 0.023) and a history of blood transfusion (p equals; 0.026). Multivariate analysis showed that anti-HCV (odds ratio, 8.1; 95% confidence intervals, 3.7-17.6) was strongly associated with CLD.

Conclusions: HCV infection is a risk factor of non-alcoholic CLD, and HCV causes more severe hepatocellular damage than HBV.     

酒精性肝病合并乙型肝炎病毒感染60例临床分析

目的 通过对郑州大学第一附属医院5年收治的60例酒精性肝病(ALD)合并乙型肝炎病毒(HBV)感染患者的临床资料分析,研究其临床特点和危险因素,以提高大众对酒精性肝病合并乙型肝炎病毒感染的认识及增加对戒酒等健康生活习惯的重视.方法 分析60例酒精性肝病合并乙型肝炎病毒感染患者的临床资料,并以100例单纯酒精性肝病患者、100例单纯乙型肝炎病毒感染患者为对照组,比较组间疾病严重程度,评价3组的治疗效果,分析酒精性肝病合并乙型肝炎病毒感染发病类型的危险因素.结果 (1)合并组实验室指标升高明显高于对照组(P＜0.05).(2)治疗4周后合并组治疗效果较两对照组差(P＜0.05).(3)通过Logistic回归分析表明,危险因素OR值为平均每日饮酒量＞HB-DNA定量＞饮酒年限＞吸烟＞年龄.结论 乙型肝炎病毒感染可加重酒精性肝病患者病情,降低治疗效果;每日饮酒量、饮酒年限、HBV-DNA定量、吸烟、年龄均为二者合并时的危险因素;因此对于酒精性肝病合并乙型肝炎病毒感染患者通过戒酒,培养良好生活方式是预防肝功能损伤加重、改善疾病疗效及预后的重要积极措施.     

非酒精性脂肪肝及其合并亚临床型乙肝病毒感染的病理和免疫研究

目的 探讨非酒精性脂肪肝(NAFLD)与NAFLD合并亚临床型乙肝病毒感染的病理与免疫特征.方法 选取2007年6月至2009年12月南京军区福州总医院门诊及住院NAFLD及NAFLD合并亚临床型乙肝病毒感染患者共47例,其中NAFLD组(A组)33例,NAFLD合并亚临床型乙肝病毒感染组(B组)14例.所有病例均行肝...     

难治性慢性肝炎与丙型及乙型肝炎病毒感染的关系

选择肝功能异常的慢性肝炎患者143例,采用常用药物治疗6个月,以肝功能不能复常为难治性慢性肝炎,其中慢迁肝26/56例(46.4%),慢活肝25/49例(51.0%),肝硬化29/38例(76.3%).经丙型及乙型肝炎病毒标志检测分析,26例慢迁肝中抗 HCV 阳性率46.2%,明显高于恢复组的16.7%(P<0.025);25例慢活肝中 HBV 复制标志阳性率68.0%,明显高于恢复组的29.2%(P<0.01);29例肝硬化中,HBV 复制标志阳性率58.6%,也明显高于恢复组的11.1%(P<0.05)。提示 HCV 感染可能是慢迁肝难治的重要因素,HBV 复制是慢活肝、肝硬化难治的重要因素。     

Hepatitis C Virus Recurrence in Living Donor Liver Transplant Recipients

Recurrence of hepatitis C virus (HCV) after liver transplantation (LT) is a universal phenomenon. Recent reports have suggested an earlier and more aggressive recurrence in the living donor liver transplant (LDLT) population. The aim of this study was to compare the histological recurrence of HCV after LDLT versus deceased donor transplantation (DDT). Twenty-nine patients underwent LT for HCV-related end-stage liver disease at our institution between April 2001 and March 2003 (42 months). Twenty patients underwent DDT, and nine patients LDLT. Laboratory data were collected on a weekly to biweekly basis and HCV PCR was performed before LT and 3-4 months and yearly post-LT. Liver biopsies were performed as needed and per institutional protocol at 7 days, at 4 months, and yearly thereafter. All biopsies were evaluated by a single pathologist and scored for rejection (Banff score) and chronic hepatitis (Ishak score system). The predominant genotype in the DDT and LDLT groups was genotype 1 (DDT = 70%, LDLT = 79%). HCV RNA titers pre-LT and 3-4 months after LT did not differ. The incidence of rejection was higher in the DDT group (P < 0.05). There was a trend toward improved Ishak stage and grade in the LDLT group at 4 and 12 months post-LT, however, this trend did not reach statistical significance. No histological difference in the recurrence or severity rate was observed at 4 or 12 months post-LT in the DDT group vs. the LDLT group.     

Chronic Hepatitis B Infection with Low Level Viremia Correlates with the Progression of the Liver Disease

Background and AimsCurrently, insufficient clinical data are available to address whether low-level viremia (LLV) observed during antiviral treatment will adversely affect the clinical outcome or whether treatment strategies should be altered if LLV occurs. This study compared the clinical outcomes of patients with a maintained virological response (MVR) and patients who experienced LLV and their treatment strategies.MethodsA retrospective cohort of 674 patients with chronic hepatitis B virus (HBV) infection who received antiviral treatment for more than 12 months was analyzed for the development of end-stage liver disease and treatment strategies during the follow-up period. End-stage liver disease included decompensated liver cirrhosis and hepatocellular carcinoma (HCC).ResultsDuring a median 42-month follow-up, end-stage liver disease developed more frequently in patients who experienced LLV than in those who experienced MVR (7.73% and 15.85% vs. 0.77% and 5.52% at 5 and 10 years, respectively; p=0.000). The trend was consistent after propensity score matching. In the high-risk group of four HCC risk models, LLV patients had a higher risk of HCC development (p<0.05). By Cox proportional hazard model analysis, LLV was an independent risk factor for end-stage liver disease and HCC (hazard ratio [HR]=6.280, confidence interval [CI]=2.081–18.951, p=0.001; HR=5.108, CI=1.392–18.737, respectively; p=0.014). Patients achieved a lower rate of end-stage liver disease by adjusting treatment compared to continuing the original treatment once LLV occurred (p<0.05).ConclusionsLLV is an independent risk factor for end-stage liver disease and HCC, and treatment adjustments can be considered.     

Clinical Significance of Hepatitis GB Virus C Infection in Alcoholic Liver Disease

Recently, hepatitis GB virus C (HGBV-C) has been recovered from patients with non-A-E hepatitis. However, it has been unclear whether HGBV-C may be related to the development of alcoholic liver disease (ALD) or not. In this study, we determined HGBV-C RNA in sera from alcoholic patients without markers for hepatitis C and B viruses to evaluate the role of HGBV-C in ALD. Serum samples were obtained from 68 patients with ALD and 40 nonalcoholic patients with chronic type C liver disease. HGBV-C RNA was detected in only 3 of 68 (4.4%) patients with ALD, in 2 of 27 patients with hepatic fibrosis, and in 1 of 5 patients with chronic hepatitis. There was no HGBV-C RNA in sera from patients with fatty liver, alcoholic hepatitis, or cirrhosis. Serum levels of AST, ALT, and γ-glutamyltranspeptidase in alcoholic patients with, as well as without, HGBV-C RNA decreased to normal levels after abstinence. In addition, an inflammatory change was not observed in liver biopsy specimens obtained from two HGBV-C-positive patients with alcoholic hepatic fibrosis. Our results clearly suggest that the prevalence of HGBV-C infection in patients with ALD is rare and that HGBV-C may not play an important role in the development of liver disease in alcoholics.