乙型和丙型肝炎病毒感染与肝细胞癌

为探讨乙型和丙型肝炎病毒（ＨＢＶ和ＨＣＶ）感染与肝细胞癌（肝癌）发生的关系，采用ＥＬＩＳＡ和聚合酶链反应（ＰＣＲ）对沈阳地区１１７例肝癌、１０７例肝硬化和４５例血液透析患者血清进行了ＨＢＶ和ＨＣＶ血清标志及ＨＢＶＤＮＡ和ＨＣＶＲＮＡ检测，并采用限制性片段长度多态性对其中７３例ＨＣＶＲＮＡ阳性血清进行了ＨＣＶ基因分型。结果，肝癌组ＨＢＶ感染率（６０７％）显著高于ＨＣＶ感染率（３３３％，Ｐ＜００１），肝硬化组ＨＢＶ感染率（４３９％）明显高于ＨＣＶ感染率（２９０％，Ｐ＜００５）；血液透析组ＨＢＶ和ＨＣＶ重叠感染率（２６７％）明显高于肝硬化组（１０３％，Ｐ＜００５）；各组均以ＨＣＶⅡ型为主（６５２％～８００％），ＨＣＶⅢ型次之（２００％～３１４％）。结果提示：沈阳地区肝癌的诱发因素仍以ＨＢＶ为主，血液透析患者ＨＢＶ和ＨＣＶ重叠感染的机会更大，ＨＣＶⅡ型感染在本地区ＨＣＶ相关性肝癌和肝硬化的发生中可能起主要作用。     

乙型用丙型肝炎病毒感染与肝细胞癌

为探讨乙型和丙型肝炎病毒（ＨＧＢＶ和ＨＣＶ）感染与肝细胞癌（肝癌）发生的关系采用ＥＬＩＳＡ和聚合酶链反应（ＰＣＲ）对沈阳地区１１７例肝癌、１０７便肝硬化和４５ 析患者血清进行了ＨＢＶ和ＨＣＶ血清标志及ＨＢＶＤＮＡ和ＨＣＶ ＲＮＡ检测，并采用性片段长度多态性对其中７３便ＨＣＶ ＲＮＡ阳性血清进行了ＨＣＶ基因分型。结果，肝癌组ＨＢＶ感染率（６０．７％）显著高于ＨＣＶ感染率（３３．５％，Ｐ〈０．０１），     

套式及免疫套式聚合酶链反应检测乙型肝炎表面抗原阴性肝病患者血清中乙型肝炎病毒DNA

为了更准确、简便而又快速地了解乙型肝炎表面抗原（ＨＢｓＡｇ）阴性肝病患者的病因，建立了套式和免疫套式聚合酶链反应（ＰＣＲ）检测血清中乙型肝炎病毒（ＨＢＶ）ＤＮＡ的技术，结合丙型肝炎病毒（ＨＣＶ）感染指标的检测，对ＨＢｓＡｇ阴性肝病患者的病因进行了研究。发现套式ＰＣＲ能将单次ＰＣＲ的敏感性稳定地提高１０００倍；免疫套式ＰＣＲ可检测到０．１～０．０１ｐｇ／Ｌ水平。检测ＨＢｓＡｇ阴性肝硬化２２例（Ａ组）、ＨＢｓＡｇ阴性慢性肝炎１３例（Ｂ组）、ＨＢｓＡｇ阴性和乙型肝炎病毒核心抗体（抗－ＨＢｃ）阳性正常对照组３０例（Ｃ组）及ＨＢｓＡｇ（＋）／ＨＢｅＡｇ（－）肝硬化患者１２例（Ｄ组），分别有４５．５％、３０．８％、１３．３％和１００％患者血清中ＨＢＶＤＮＡ阳性。ＨＢＶＤＮＡ在一些抗－ＨＢｓ（＋）肝病患者和所谓健康人的血清中也存在。Ａ、Ｂ两组检出有ＨＢＶ和（或）ＨＣＶ感染患者分别占８１．８％和５３．８％。提示套式和免疫套式ＰＣＲ是简便、快速而又高度敏感的检测方法；ＨＢＶ感染可能是引起ＨＢｓＡｇ阴性慢性肝病的重要原因，且ＨＢｓＡｇ阴性肝病病因大多与病毒感染有关；应该重新认识自然感染者血清中抗－ＨＢｓ的临床意义。     

血液透析患者血液中丙型及乙型肝炎病毒的检测

为了解血液透析患者血液中丙型肝炎病毒（ＨＣＶ）及乙型肝炎病毒（ＨＢＶ）的感染情况，对２２例维持性血液透析患者应用逆转录聚合酶链反应及酶联免疫吸附实验，检测了血清中ＨＣＶＲＮＡ及其抗体水平；同时采用斑点杂交及固相放射免疫法检测了血清中ＨＢＶＤＮＡ及其血清标志物。结果显示，２７％的血液透析患者血清ＨＣＶ抗体阳性，其中３３％的患者血清存在ＨＣＶＲＮＡ。在血清ＨＣＶ抗体阴性的１６例患者中，也有１例（６％）血清ＨＣＶＲＮＡ阳性。在２２例血液透析患者中，３例（１４％）血清ＨＢＶＤＮＡ阳性（ＨＢｅＡｇ也均阳性）。其余１９例ＨＢＶＤＮＡ阴性患者（ＨＢｅＡｇ均阴性），有１２例（６３％）血清抗－ＨＢｃ阳性。在７例血清ＨＣＶＲＮＡ或（和）抗－ＨＣＶ阳性者，５例有既往或现在ＨＢＶ感染的证据，但未见ＨＣＶＲＮＡ与ＨＢＶＤＮＡ同时存在者。提示在相当数量的血液透析患者体内存在肝炎病毒血症，应加强对血液透析患者肝炎病毒感染的监测及预防工作     

肝细胞癌患者乙、丙和丁型肝炎病毒感染状况

为探讨乙型、丙型和丁型肝炎病毒（ＨＢＶ，ＨＣＶ和ＨＤＶ）感染对肝细胞癌（肝癌）发生的意义，本文作者采用ＥＬＩＳＡ和聚合酶链反应法对７２例广东籍肝癌患者ＨＢＶ、ＨＣＶ和ＨＤＶ血清标志以及血浆ＨＢＶＤＮＡ和ＨＣＶＲＮＡ进行了检测。ＨＢｓＡｇ和抗－ＨＣＶ阳性率分别为８４．７％和１８．１％，显著高于１２８名健康对照者。ＨＢｓＡｇ和／或ＨＢＶＤＮＡ总阳性率为９３．１％，抗－ＨＣＶ和／或ＨＣＶＲＮＡ阳性率为２７．８％，ＨＢＶ和ＨＣＶ重叠感染率为２２．２％。其中６１例ＨＢｓＡｇ阳性肝癌的ＨＤＶ血清标志检出率为１４．８％，明显高于６１例ＨＢｓＡｇ阳性的肝炎对照者。结果表明，广州地区肝癌的发生，主要与ＨＢＶ和ＨＣＶ感染密切相关外，且可能与ＨＤＶ感染有关。     

重叠HCV感染对HBV／C基因热点变异的影响

为探讨乙型肝炎病毒（ＨＢＶ）重叠丙型肝炎病毒（ＨＣＶ）感染时ＨＣＶ对ＨＢＶ复制和基因变异的影响，采用套式聚合酶链反应（ＰＣＲ）与限制性片段长度多态性（ＲＦＬＰ）相结合。对１９例ＨＢＶ感染重叠ＨＣＶ感染（Ａ组）和３１例单独ＨＢＶ感染（Ｂ组）的慢怀肝病患者分析前Ｃ区密码２８终止是（Ａ８３）和Ｃ密码９７异亮氨酸变为亮氨酸变异Ｌ９７）。结果显示Ａ组第一次ＰＣＲ阳性率（１６％）明显低于Ｂ组（６５％）（Ｐ，０     

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     

肝硬变和原发性肝癌患者HCV与HBV标志物分析

目的探讨肝硬变（ＬＣ），原发性肝癌（ＨＣＣ）发生和发展与ＨＣＶ及ＨＢＶ感染的关系．方法ＨＣＣ２８例，ＬＣ４８例和对照组５０例，用ＥＬＩＳＡ法同步检测ＨＢＶ及ＨＣＶ的６项血清标志物（Ｍ）．结果ＨＣＣ，ＬＣ及对照组ＨＢＶ＿Ｍ的阳性率分别为７５０％，８１３％和４００％；ＨＣＶ＿Ｍ的阳性率分别为７１％，２０８％和２０％．ＨＣＣ，ＬＣ中ＨＢＶ＿Ｍ阴性患者ＨＣＶ＿Ｍ阳性率为１２５％．ＨＣＶ与ＨＢＶ重叠感染者占ＨＣＣ和ＬＣ全部患者的１３２％．结论ＨＣＣ，ＬＣ发生和发展与ＨＢＶ及ＨＣＶ病毒感染密切相关，重叠感染者肝功能损害及临床失代偿程度更严重．     

重型病毒性肝炎患者病原学及预后的研究

对９４例重型病毒性肝炎进行了病毒标志的研究，并分析了几种影响重型肝炎预后的因素。结果发现：单纯ＨＢｖ感染４２例（４４．７％）；混合感染共５０例（５３．２％），其中ＨＢＶ与ＨＣＶｌ９例（２０．２％）．ＨＢＶ与ＮＤＶ１３例（１３．８％），ＨＢＶ与ＨＣＶ、ＨＤＶＩ０例（１０．６％）ＨＡＶ与ＫＢＶ３例（３．２％），ＨＡＶ与ＨＢＵ、ＨＣＶ３例（３．２％）ＨＡＶ与ＨＢｖ、ＨＤＶＩ例（１．１％）．ＮＡＶ与ＨＢＶ、ＨＣＶ、ＨＤＶ１例（１．１％）；病毒标志均阴性者２例（２．１％）。ＨＢＶ、ＨＣＶ和ＨＤＶ混合感染者病情重，病死率高。血清总胆红素越高，凝血酶原活性越低，其病死率越高；有并发症者的预后差，而ＡＭＰ升高者的预后较好；重肝的预后可能与年龄、性别无关。     

巨脾型晚期血吸虫病与HBV及HCV感染的研究

本文作者对１２４例临床诊断为巨脾型晚期血吸虫病（晚血）的患者作了肝组织病理、ＨＢＶ和ＨＣＶ标志检测及随访观察。病理诊断为血吸虫病性肝纤维化７８例（６２．９％），血吸虫病性肝纤维化合并肝炎３１例（２５％），门脉性肝硬化１５例（１２．１％），三组患者ＨＢｓＡｇ及ＨＣＶ标志检出率分别为３５．９％、６４．５％及９３．３％，提示肝细胞病变及其严重程度与肝炎病毒感染有密切关系。以血吸虫病性肝纤维化为基本病变的１０９例中，ＨＢｓＡｇ或ＨＣＶ标志阳性组病死率为２２．９％（１１／４８），显著高于阴性组１．６％（１／６１）。１８例死亡患者中，ＨＢｓＡｇ和／或ＨＣＶ标志阳性１７例，占９４．４％。最常见的死亡原因是肝功能衰竭，第二位是原发性肝癌（ＨＣＣ）。ＨＢＶ及ＨＣＶ感染是发生肝衰竭及ＨＣＣ的关键因素，与晚血患者的死亡密切相关。     

HCV HBV感染与肝细胞性肝癌

调查了肝癌高发地区不同肝病患者中丙型肝炎病毒(HCV)感染率。慢性肝病患者绝大多数已被乙型肝炎病毒(HBV)感染。HCV第二代抗体阳性率,肝癌7.3％,肝硬化6.6％,慢性肝炎6.6％和急性肝炎3.4％。两种病毒的复合感染率,肝癌5.1％,肝硬化1.7％,慢性肝炎3.9％和急性肝炎1.1％。在38例HCV抗体阳性的慢性肝病患者中,ALT异常84.2％,有输血史者占57.9％,HCV-RNA阳性率为71.1％。本研究的资料分析提示,在肝癌高发地区尽管HCV抗体阳性率较低,但HCV感染也是肝癌发生的重要病因之一。     

Occult hepatitis B virus infection is not associated with disease progression of chronic hepatitis C virus infection

AIM To clarify the prevalence of occult hepatitis B virus(HBV) infection(OBI) and the association between OBI and liver disease progression, defined as development of liver cirrhosis or hepatocellular carcinoma(HCC), worsening of Child-Pugh class, or mortality in cases of chronic hepatitis C virus(HCV) infection. METHODS This prospective cohort study enrolled 174 patients with chronic HCV infection(chronic hepatitis, n = 83; cirrhosis, n = 47; HCC, n = 44), and evaluated disease progression during a mean follow-up of 38.7 mo. OBI was defined as HBV DNA positivity in 2 or moredifferent viral genomic regions by nested polymerase chain reaction using 4 sets of primers in the S, C, P and X open reading frame of the HBV genome. RESULTS The overall OBI prevalence in chronic HCV patients at enrollment was 18.4%, with 16.9%, 25.5% and 13.6% in the chronic hepatitis C, liver cirrhosis and HCC groups, respectively(P = 0.845). During follow-up, 52 patients showed disease progression, which was independently associated with aspartate aminotransferase 40 IU/L, Child-Pugh score and sustained virologic response(SVR), but not with OBI positivity. In 136 patients who were not in the SVR state during the study period, OBI positivity was associated with neither disease progression, nor HCC development. CONCLUSION The prevalence of OBI in chronic HCV patients was 18.4%, and OBI was not associated with disease progression in South Koreans.     

Current therapy for hepatitis C or D or immunodeficiency virus concurrent infection with chronic hepatitis B

Concurrent hepatitis C virus (HCV), hepatitis delta virus (HDV), or human immunodeficiency virus (HIV) infection with chronic hepatitis B virus (HBV) appears to increase the risk of progressive liver disease including liver cirrhosis and hepatocellular carcinoma. There is a 10% prevalence of HCV infection in chronic HBV or HDV infection. Serological evidence of previous exposure to HBV is found in more than 80% of HIV-positive patients in the high risk group. Notably, the most recently acquired virus tends to suppress the pre-existing virus. In chronic HBV infection acquired perinatally or in early childhood, usually HCV is dominant and may suppress or even displace HBV and HDV. Less frequently, HBV or HDV suppresses HCV. It is generally agreed that the dominant virus should be identified in order to make appropriate treatment decisions. Studies with standard interferon (IFN) to treat patients with HCV dominantly dual HBV/HCV infection have showed only limited virological response. But high dose of IFN has been demonstrated with better response rate. Combined ribavirin with standard or pegylated IFN therapy could achieve a sustained HCV clearance rate comparable with those infected with HCV alone. On the contrary, patients with HBV dominantly dual viral infection might indicate more appropriate addition of lamivudine to IFN than ribavirin. Additionally, patients with concurrent infection of HBV and HDV, IFN seems to be the only effective agent. However, the efficacy of IFN is related to the dose. High dose of IFN [9 MU tiw (thrice per week)] and longer treatment duration (at least 2 years) have been shown to achieve adequate virological response. In patients with concurrently infected HBV and HIV, anti-HBV therapy should be considered for all patients with evidence of liver disease, irrespective of the CD4 cell count. In patients not requiring antiretroviral therapy, HBV therapy should be preferentially based on IFN, adefovir, or telbivudine. In contrast, in patients with CD4 cell counts <350 cells/μl or those already on antiretroviral therapy, agents with double anti-HBV and anti-HIV activity are preferred. At present, the evidence of therapeutic efficacy is not sufficient to make a recommendation in treating patients with dual HBV/HCV or HBV/HDV or HBV/HIV infection. Further studies of the well-designed, larger scale are needed to elucidate the role of different regimens or combination in the treatment of dual viral infection.     

Prevalence of hepatitis C virus antibodies in chronic liver disease and hepatocellular carcinoma patients in India

The prevalence of antibodies to hepatitis C virus (HCV) was investigated in 129 patients with chronic liver disease (85 with chronic active hepatitis and 44 with cirrhosis) and 53 patients with hepatocellular carcinoma. The commercially available second generation anti-HCV enzyme immunoassay kit was used. Antibodies to hepatitis C virus were detected in 16.2% of the patients with chronic liver disease and in 15.1% with hepatocellular carcinoma. Of the HCV positive patients in all groups 51.7% were positive for hepatitis B virus (HBV) markers indicating present or past infection. Prevalence of HBV markers in all the three groups (CAH, cirrhosis and HCC) was higher as compared with anti-HCV prevalence. These results suggest that HCV infection may not be a major cause of chronic liver disease and hepatocellular carcinoma in India and indicate the presence of other aetiological agents.     

Previous hepatitis B virus infection is associated with worse disease stage and occult hepatitis B virus infection has low prevalence and pathogenicity in hepatitis C virus‐positive patients

Abstract: Background: Anti‐hepatitis C virus (anti‐HCV) patients with chronic liver disease (CLD) frequently show markers of previous hepatitis B virus (HBV) infection. Moreover, they may carry occult HBV infection. These features might influence clinical and biochemical features as well as stage of disease. Aim: To assess the prevalence and clinical associations of previous (positivity for anti‐HBs and/or anti‐HBc antibodies) and occult HBV infection (positivity for HBV‐DNA by nested‐PCR) in the serum of anti‐HCV‐positive, HCV‐RNA‐positive, HBsAg‐negative patients with various degrees of CLD seen at a tertiary referral centre. Patients: A total of 119 patients fulfilled the inclusion criteria (84 chronic hepatitis and 35 liver cirrhosis). Results: Forty‐eight patients (40.3%) showed markers of previous HBV infection. This feature was more frequent (P = 0.02) among cirrhotics (57%) as compared to chronic hepatitis patients (33%). Chronic hepatitis patients positive for markers of previous HBV infection had worse histology as compared to negative ones (grading: 6.4 ± 2.7 versus 4.6 ± 3.0, P = 0.004; staging: 1.6 ± 1.2 versus 1.0 ± 1.0, P = 0.01). Eight patients were positive for HBV‐DNA in serum (6.7%). No difference in the presence of occult HBV infection was seen between various degrees of liver disease (7.1% of chronic hepatitis, 5.7% of cirrhosis) and among patients who were positive (10.4%) or negative (4.2%) for markers of previous HBV infection. No significant biochemical, virological, or histological difference was observed between age, age at infection, duration of infection, marker patterns of previous HBV infection‐matched HBV‐DNA‐positive and negative chronic hepatitis patients. Conclusions: Our findings suggest that previous HBV infection among anti‐HCV patients is associated with worse disease stage. In these patients, the prevalence of occult HBV infection is low and there is no difference in distribution among patients with or without markers of previous HBV infection. Furthermore, it does not seem to be associated with disease stage. Lastly, at least among patients with chronic hepatitis, it does not seem to affect the severity of disease.     

Impact of comorbidities on the severity of chronic hepatitis B at presentation

AIM: To evaluate the clinical relevance of each cofactor on clinical presentation of chronic hepatitis B.METHODS: Out of 1366 hepatitis B surface antigen (HBsAg) positive subjects consecutively observed in 79 Italian hospitals, 53 (4.3%) showed as the only cofactor hepatitis D virus (HDV) infection [hepatitis B virus (HBV)/HDV group], 130 (9.5%) hepatitis C virus (HCV) (group HBV/HCV), 6 (0.4%) human immunodeficiency virus (HIV) (group HBV/HIV), 138 (10.2%) alcohol abuse (group HBV/alcohol); 109 (8.0%) subjects had at least two cofactors and 924 were in the cofactor-free (CF) group.RESULTS: Compared with patients in group CF those in group HBV/alcohol were older and more frequently had cirrhosis (P < 0.001), those in group HBV/HDV were younger (P < 0.001), more frequently resided in the south of the country and had cirrhosis (P <0.001), those in group HBV/HCV were older (P < 0.001) and more frequently had cirrhosis (P < 0.001). These cofactors were all independent predictors of liver cirrhosis in HBsAg positive patients. Multivariate analysis showed that an older age [odds ratio (OR) 1.06, 95% CI: 1.05-1.08], alcohol abuse with more than 8 drinks daily (OR 2.89, 95% CI: 1.81-4.62) and anti-HDV positivity (OR 3.48, 95% CI: 2.16-5.58) are all independently associated with liver cirrhosis. This association was found also for anti-HCV positivity in univariate analysis, but it was no longer associated (OR 1.23, 95% CI: 0.84-1.80) at multivariate analysis.CONCLUSION: Older age, HDV infection and alcohol abuse are the major determinants of severe liver disease in chronic HBV infection, while HCV replication plays a lesser role in the severity of hepatic damage.     

Prevalence of antibodies to hepatitis C virus among Saudi patients with chronic liver diseases.

The prevalence of antibodies against hepatitis C virus (anti-HCV) was determined in 55 patients with chronic liver diseases including liver cirrhosis (42 patients), liver cirrhosis and hepatocellular carcinoma (8 patients), and chronic active hepatitis (4 patients). A total of 63.6% of these patients were positive for anti-HCV, a significantly higher prevalence than the rate of 3.9% observed in 488 asymptomatic volunteers. Of the 42 patients with liver cirrhosis 16 (38.1%) had positive anti-HCV without any markers of hepatitis B virus (HBV), while 12 (28.6%) had markers of neither HCV nor HBV infection. Our findings suggest that HCV infection may play a significant role in the pathogenesis of chronic liver disease in Saudi Arabia, which is an area of endemic HBV infection. Screening for anti HCV should be considered mandatory in patients with chronic liver disease (CLD) especially where the etiology appears obscure.     

Seroprevalence of anti-HAV among patients with chronic viral liver disease

AIM:To investigate the current seroprevalence of hepatitis A virus(HAV) antibodies in patients with chronic viral liver disease in Korea.We also tried to identify the factors affecting the prevalence of HAV antibodies. METHODS:We performed an analysis of the clinical records of 986 patients(mean age:49±9 years,714 males/272 females) with chronic hepatitis B virus(HBV) or hepatitis C virus(HCV) infection who had undergone HAV antibody testing between January 2008 and December 2009.RESULTS:The overall prevale...     

Impact of acute hepatitis C virus superinfection in patients with chronic hepatitis B virus infection

BACKGROUND & AIMS: Superinfection in patients with chronic hepatitis B virus (HBV) infection is not uncommon. Acute hepatitis delta virus (HDV) superinfection is associated with severe and/or progressive liver disease. The natural course following acute hepatitis C virus (HCV) superinfection has not been well studied. The aim of this study was to investigate the impact of acute HCV superinfection. METHODS: The clinical features during acute phase and long-term outcomes of acute HCV superinfection were studied and compared with a cohort of acute HDV superinfection and a matched control group of active chronic hepatitis B. RESULTS: Acute HCV superinfection typically occurs as acute icteric hepatitis. The severity is similar to acute HDV superinfection in that hepatic decompensation developed in 34% of patients, hepatitis failure occurred in 11%, and 10% died. During a follow-up period of 1-21 years, patients with acute HCV superinfection had a significantly higher cumulated incidence of cirrhosis (48% at 10 years) and hepatocellular carcinoma (14% at 10 years, 21% at 15 years, and 32% at 20 years) than acute HDV superinfection or active chronic hepatitis B. Hepatitis B surface antigen (HBsAg) seroclearance occurred earlier in HCV superinfected patients. Continuing hepatitis after HBsAg seroclearance was observed only in HCV superinfected patients. CONCLUSIONS: Acute HCV superinfection in patients with chronic HBV infection is clinically severe during its acute phase. The long-term prognosis following acute HCV superinfection is much worse than that following HDV superinfection or active hepatitis B in terms of continuing hepatitis activity after HBsAg loss and the development of cirrhosis or hepatocellular carcinoma.     

Hepatitis B and C virus infection as risk factors for liver cirrhosis and cirrhotic hepatocellular carcinoma: a case-control study

To investigate whether hepatitis B virus (HBV) and hepatitis C virus (HCV) infection are risk factors for liver cirrhosis and hepatocellular carcinoma (HCC), a case-control study of 102 cirrhotic HCC patients, 102 sex-matched and age-matched patients with liver cirrhosis, and 102 matched patients with non-hepatic disease controls was performed. The prevalences of hepatitis B surface antigen (HBsAg) and antibody to HCV (anti-HCV) in HCC (70.5%, 39.2%) and liver cirrhosis (74.5%, 27.4%) were higher than controls (16.6%, 10.5%) (P = 0.0001). In HBsAg-negative patients, the prevalence of anti-HCV in cirrhotic HCC (66.6%) and liver cirrhosis (46.1%) was higher than in controls (10.5%; P = 0.0001). There was no such difference in HBsAg-positive patients. Multivariate analysis revealed that both HBsAg and anti-HCV were important risk factors for HCC (odds ratio, 6.52 and 4.59, respectively) and liver cirrhosis (odds ratio, 4.22 and 2.29, respectively). There was no difference in odds ratio when HCC and liver cirrhosis were compared. Our result implies that both HBV and HCV are independent risk factors for cirrhotic HCC and liver cirrhosis in Taiwan.