Emergency liver resection for ruptured hepatocellular carcinoma complicating cirrhosis.

BACKGROUND/AIMS: From a consecutive series of 51 patients surgically treated from January 1993 to August 1997 for hepatocellular carcinoma (HCC) complicating cirrhosis, 6 subjects (12%) presented with acute hemoperitoneum due to spontaneous rupture of the tumor: 3 patients were suffering from chronic hepatitis C, 2 were affected by alcoholic cirrhosis, and one by chronic hepatitis B. The present paper reports experience of the treatment of ruptured HCC complicating cirrhosis in 6 patients undergoing emergency hepatectomy. METHODOLOGY: Hemoperitoneum was successfully diagnosed pre-operatively with the combination of abdominal ultrasound (US) and paracentesis. All subjects had a known history of chronic liver disease, but undiagnosed HCC. Child-Pugh classification assessed the hepatic functional reserve to predict operative risk. Surgical indication was based on hemodynamic instability and/or persistent bleeding. Time from admission to operation was recorded as well as tumor site, size and number, the site of bleeding, and the duration of surgery and hepatic devascularization. Tumor location was defined according to segmental anatomy. All patients underwent one-stage liver resection (segmentectomy VII-VIII in one patient; non-anatomical wedge resections in 5). Operative mortality was defined as death within 30 days of surgery. RESULTS: No intra-operative death occurred. In 4 patients the post-operative course was uneventful. Two patients died 2 weeks after surgery from liver failure (one patient) eventually complicated by renal failure (one patient). Three patients are alive and 2 of them disease-free at 24 months after surgery, whilst one patient has died from liver failure 21 months after surgery in the presence of intrahepatic recurrence of HCC. CONCLUSIONS: Present experience, combined with a literature review on 755 ruptured HCC cases, indicates that emergency liver resection is feasible in patients with limited tumor and preserved liver function (Child-Pugh A or B grade); surgical resection is the only procedure possibly associated with long-term survival, as shown by 4/6 patients of ours surviving more than 12 months, with 2 subjects disease-free at 24 months. Conservative management, such as surgical/radiological devascularization, packing or plication, can be conducted on high risk patients, though long-term survivors have not been reported.     

Lower incidence of hepatic failure than hepatocellular carcinoma in Japanese patients with chronic hepatitis C.

BACKGROUND: Previous studies have shown that the development of hepatic failure was found more frequently than that of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C in the United States and European countries. We investigated the status in Japan in a retrospective cohort study. METHODS: The incidences of HCC and hepatic failure were accessed in 459 patients with biopsy-proven C-viral chronic liver disease with a mean follow-up period of 8.9+/-3.2 years and the cause of death was also analyzed in the cohort. RESULTS: HCC developed in 63 patients, 46 of 355 interferon (IFN)-treated and 17 of 104 untreated patients. In contrast, the development of hepatic failure was found in 18 patients, 12 of 355 IFN-treated and six of 104 untreated patients. HCC developed in four of 116 with sustained virological response (SVR), and hepatic failure developed in one of them. Thirty-two of 63 patients developing HCC and eight of 18 patients developing hepatic failure died. CONCLUSIONS: Development of hepatic failure was less frequent than that of HCC in Japan. It is important for a favorable prognosis of patients with C viral chronic liver disease to achieve a higher SVR and thus inhibit the development of HCC in Japan.     

Risk of liver cirrhosis and hepatocellular carcinoma in subjects with hepatitis B and delta virus infection: A study from Kure, Japan

To investigate the effect of hepatitis delta virus (HDV) superinfection on the long-term outcome of Japanese subjects with chronic hepatitis B virus (HBV) infection, we examined the presence of antibodies to hepatitis delta antigen (anti-HD) in serial serum samples collected from 1127 subjects with chronic HBV infection. The subjects were followed for at least 36 months (mean: 121.3 months) between 1973 and 1991. Among 69 cases where anti-HD was detected, eight (12%) developed liver cirrhosis (LC) and six (9%) developed hepatocellular carcinoma (HCC). However, among 1058 cases without anti-HD, there were 43 patients (4%) who developed LC and 29 (3%) who developed HCC. The prevalence of LC and HCC was significantly higher among the cases with anti-HD than those without anti-HD. The proportion of LC and HCC per 1000 person years was 10.46 and 7.84, respectively among cases with anti-HD, and 4.05 and 2.73 among those without anti-HD, respectively. The overall relative risk of LC and HCC was 2.58 and 2.87, respectively; 95% confidence interval (CI): LC, 1.14–5.13; HCC, 1.03–6.23. These results indicate that in the Kure district in Japan, where HDV infection of persons infected with HBV is about 6%, such superinfection increases the risk of LC and HCC.     

Presence of Active Hepatitis Associated with Liver Cirrhosis Is a Risk Factor for Mortality Caused by Posthepatectomy Liver Failure

The histologic activity of associated hepatitis was examined in 285 patients who underwent hepatectomy for hepatocellular carcinoma (HCC), to determine if the histologic activity is an independent risk factor for postoperative mortality due to liver failure. The proportion of patients with liver cirrhosis who died due to liver failure (6/180, 3.3%) was not different from that of patients with chronic hepatitis (2/68, 2.9%). However, mortality was higher in patients with liver cirrhosis and active hepatitis (4/46, 8.7%) than in those with cirrhosis and inactive hepatitis (2/134, 1.5%, P < 0.05). Such difference was not observed in the chronic hepatitis group. Multivariate analysis showed that clearance of indocyanine green at 15 min (ICGR15) and activity of hepatitis were two independent risk factors for postoperative mortality due to liver failure. In conclusion, histologic activity of associated hepatitis should be taken into account in hepatic resection of HCC in cirrhotic liver, in addition to the functional reserve of the liver.     

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Purpose  Hepatic vena cava disease (HVD), a form of Budd-Chiari syndrome, is caused by the obstruction of hepatic portion of the inferior vena cava. It is a chronic disease characterized by the development of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). As HVD occurred in areas with high incidence of hepatitis B virus (HBV) infection and some patients tested HBsAg positive, it was thought to be the cause of LC and HCC. To assess the pathogenesis of LC or HCC in HVD, a long-term follow-up study was done. Method  Fifty-six patients with HVD diagnosed by ultrasound (US) and confirmed by cavography in 31 and liver biopsy in 34 were followed up for an average of 14.8 ± 9 years. The occurrence of LC was diagnosed by US and/or liver biopsy and that of HCC by US, elevated level of α-fetoprotein, and liver biopsy or fine-needle aspiration cytology, or computed tomographic scan. Other risk factors for LC/HCC such as alcohol use and HBV and hepatitis C virus (HCV) infections were assayed. Results  Forty-four (78.5%) and 6 (10.7%) patients developed cirrhosis and HCC, respectively. LC/HCC occurred more frequently among those who had severe or frequent acute exacerbations (P = 0.017), but it was not related to alcohol use or HBV and HCV infections. Conclusion  HVD is independent risk factors for LC and HCC. Severe and/or recurrent loss of hepatocytes caused by hepatic venous outflow obstruction and/or thrombotic obstruction of small radicals of hepatic and portal veins that occurred during acute exacerbations was considered important in the pathogenesis of LC and HCC in HVD.     

Management before hepatectomy for hepatocellular carcinoma with cirrhosis

The global distribution of hepatocellular carcinoma (HCC) varies markedly among regions, and patients in East Asia and Central Africa account for about 80% of all cases. The risk factors are hepatitis B, hepatitis C, alcohol, and etc. The risk of carcinogenesis further increases with progression to hepatic cirrhosis in all liver disorders. Radical treatment of HCC by liver resection without causing liver failure has been established as a safe approach through selection of an appropriate range of resection of the damaged liver. This background indicates that both evaluation of hepatic functional reserve and measures against concomitant diseases such as thrombocytopenia accompanying portal hypertension, prevention of rupture of esophageal varices, reliable control of ascites, and improvement of hypoalbuminemia are important issues in liver resection in patients with hepatic cirrhosis. We review the latest information on perioperative management of liver resection in HCC patients with hepatic cirrhosis.     

丙型肝炎肝硬化相关肝细胞癌患者的临床特征及其危险因素

目的 分析丙型肝炎肝硬化相关肝细胞癌(HCC)患者的流行病学特征、临床特点和相关危险因素.方法 对89例丙型肝炎肝硬化患者进行长期随访观察,并对HCC发生的危险因素进行单因素和多因素分析.结果 在86.5(60～120)个月随访过程中,89例患者中35例发生HCC,第5、第10年HCC累计发生率分别为16.9%、40.4%.4例有丙型肝炎家族史、12例有HCC家族史和7例有饮酒史的患者均在随访中发生HCC.89例中50例存在肝脂肪变患者第5、第10年HCC累计发生率分别为24.6%、51.0%;39例无肝脂肪变的患者第5、第10年HCC累计发生率分别为8.7%、26.2%,两组间差异有统计学意义(P＜0.05),慢性丙型肝炎肝硬化患者肝脂肪变与肝硬化的严重程度相关,肝脂肪变患者抗病毒治疗持续应答率低于无脂肪变患者,两组间差异有统计学意义(P＜0.05).HCC患者的ALT和总胆红素水平高于非HCC患者,白蛋白水平低于非HCC患者,两组间差异有统计学意义(P＜0.05).多因素回归分析结果显示肝功能分级和肝脂肪变与HCC独立相关.结论 慢性丙型肝炎肝硬化是一个缓慢进行性疾病,HCC是其重要并发症,肝功能分级和肝脂肪变是HCC发生的高危因素,饮酒和HCC家族史对HCC的发生有一定影响.丙型肝炎肝硬化伴肝脂肪变的患者病情进展速度明显加快,应定期筛查以降低HCC发病的危险.     

The seroprevalence of anti-HTLV-1 antibodies in patients with various liver diseases

The prevalence of antibodies to human T-cell leukemia virus type 1 (HTLV-1), which is linked to the etiology of adult T-cell leukemia (ATL), was examined in 380 patients with various liver diseases in Kumamoto Prefecture, southwestern Japan, which is one of the most endemic area for HTLV-1. Eighteen patients with acute hepatitis (AH), 201 chronic hepatitis (CH), 93 liver cirrhosis (LC) 40 hepatocellular carcinoma (HCC) and 28 with other liver diseases were examined. Among these patients, 110 patients had histories of blood transfusion. HTLV-1 specific antibodies were assayed by the ELISA method and the Western blotting method. The rate of positive reaction was 8.9% in all, 5.6% in AH, 6.0% in CH, 10.8% in LC, 17.5% in HCC and 14.3% in the cases of other liver diseases. The prevalence of anti-HTLV-1 antibodies in about 62,000 healthy blood donors in this area was 4.7%. The overall sero-prevalence in the patient group was significantly higher (p less than 0.001), than in healthy blood donors, particularly in the LC and HCC groups. Although the occurrence increased with age, no difference between sex was observed. Patients who had received blood transfusions were found to have a higher rate (17.2%), than those who had not (5.9%), and healthy blood donors. No difference was found between the two groups regarding family history of liver disease. This study indicates that blood transfusions may be an important route to the HTLV-1 infection.     

Clinical evaluation of serum tissue inhibitor of metalloproteinases-1 levels in patients with liver diseases

Serum levels of the tissue inhibitor of metalloproteinases-1 (TIMP-1) were measured in 268 patients with liver diseases by means of a one-step sandwich enzyme immunoassay. In the cases of acute hepatitis, chronic active hepatitis (CAH), liver cirrhosis (LC) and hepatocellular carcinoma (HCC), the levels of TIMP-1 were higher than those of the control group. Tissue inhibitor of metalloproteinases-1 levels correlated with type III procollagen peptide and with type IV collagen, indicating TIMP-1 as a useful marker for hepatic fibrosis. Levels of TIMP-1 also correlated with aspartate aminotransserase and alanine aminotransferase levels and showed the highest levels in acute hepatitis. Thus, TIMP-1 might also reflect hepatic inflammation. Serum levels of α-fetoprotein and TIMP-1 had a significant positive correlation in patients with HCC. A cut-off level of TIMP-1 between LC and HCC was set at 440 ng/mL, having a low sensitivity and a high specificity. These results suggest the usefulness of TIMP-1 as a tumour marker in cases of HCC where α-fetoprotein levels are not elevated.     

Follow-up study of 582 liver cirrhosis patients for 26 years in Japan

A long-term follow-up study of liver cirrhosis (LC) was performed in 582 patients diagnosed by peritoneoscopy and liver biopsy in the 26 years from 1958 to 1984. The etiology of LC consisted of hepatitis B virus (HBV) in 21%, alcoholic in 39% and cryptogenic in 39%. Fifty-nine percent of patients had died. Causes of death were hepatocellular carcinoma (HCC 44%), liver failure (30%), rupture of esophageal varices (14%), gastrointestinal bleeding (4%) and non-liver-related causes (8%). HCC accounted for increasing percentages (68%) since 1980. In all groups classified by the etiology, the causes of death had the same order in incidence. The age of onset of LC increased by 10 years from 42 to 52 years old and the age of death by 15 years from 43 to 58 in the 26-year period. The cumulative survival rate improved over the period. The 50% survival year was 7.9 in total patients, and 7.0, 8.5 and 10.0 in the three periods 1958-64, 1965-74 and 1975-84, respectively. It was 9.5, 6.3 and 9.8 in HBV, alcoholic and cryptogenic, respectively. LC patients survived 40-44% of the life expectancy of the general population in Japan in all age groups. Cox's multiregression life-table method selected three important prognostic factors from 7 parameters: a poor prognosis with a history of heavy alcohol consumption and old age at onset, and a better prognosis with recent onset.     

Contribution of Hepatitis C Virus to the Progression of Alcoholic Liver Disease

Background: We determined hepatitis C virus (HCV) antibody, HCV RNA, and genotype in patients with alcoholic liver disease and studied the involvement of HCV in alcoholic liver disease. Additionally, we used the histological activity index (HAI) to study the influence of HCV on the severity of inflammation. Methods: The subjects were 143 patients with alcoholic liver disease: 7 with fatty liver (FL), 18 with hepatic fibrosis (HF), 24 with alcoholic hepatitis (ALH), 39 with chronic hepatitis (CH), 42 with liver cirrhosis (LC), and 13 with hepatocellular carcinoma (HCC). The HCV RNA positivity rate in each type of disease was 0/7 (0%), 1/18 (6%), 2/24 (8%), 27/39 (69%), 24/42 (57%), and 7/13 (54%), respectively. It was high in the advanced hepatic lesions. Results: Clinically, the serum hepatic function tests after abstinence from drinking improved significantly in the HCV RNA negative patients compared with the positive patients. The proportion of genotype II in each type of disease was 0/0, 0/1 (0%), 1/2 (50%), 18/27 (67%), 18/24 (75%), and 7/7 (100%), respectively. It became high with the advance of pathophysiology. The HCV RNA amount stood at 7.5 ± 0.4 [log (copies/ml)] in CH, 7.9 ± 0.4 in LC, and 8.4 ± 0.8 in HCC, with a statistically significant difference between CH and HCC. However, we found no changes in the HCV RNA amount due to abstinence from drinking. The HAI score was high in the HCV RNA positive patients, but several cases in the HCV RNA negative group showed severe inflammatory changes. Therefore, judging the presence or absence of HCV RNA with the HAI score alone was considered difficult. Conclusions:: These results suggest that HCV, particularly genotype II, plays an important role in the advance of disease to LC and HCC in heavy drinkers.     

Hepatitis C-related liver cirrhosis-strategies for the prevention of hepatic decompensation,hepatocarcinogenesis,and mortality

Liver cirrhosis(LC)is a critical stage of chronic liver disease,including that caused by hepatitis C virus(HCV).In the absence of antiviral therapy,67%-91%of patients with HCV-related LC patients die of liver-related causes,including hepatocellular carcinoma(HCC)and liver failure.Among the therapeutic strategies used to prevent liver-related complications in these patients is standard therapy with pegylated interferon and ribavirin,which induces a sustained virological response(SVR)in 25%of HCV genotype 1-infected patients and in 69% of patients infected with genotypes 2 and 3.SVR in patients with HCV-related LC has been associated with reduced rates of hepatic decompensation,HCC,and mortality.More recently developed direct-acting antiviral agents have shown excellent antiviral efficacy,with preliminary data demonstrating that an interferon-free regimen that includes these direct-acting antiviral agents achieved SVR in more than 50%of patients with HCV genotype 1 LC.Branched-chain amino acid supplementation,improvement of insulin resistance,and the use ofβ-blockers for portal hypertension may also reduce liverrelated complications.Here,we review advances in antiviral and adjunctive therapies for improved outcomes in patients with HCV-associated LC.     

Impact of liver disease severity and etiology on the occurrence of diabetes mellitus in patients with liver cirrhosis

The association between liver cirrhosis (LC) and diabetes mellitus (DM) is well known. However, the impact of the severity or etiology of LC on the occurrence of DM is relatively unknown. We aimed to determine the prevalence and clinical correlates of DM in a large cohort of patients with cirrhosis. A total of 1,068 patients with LC were included in this cross sectional study (CIRCE study). The diagnosis of cirrhosis irrespective of its etiology was based on histological confirmation by liver biopsy or, in the absence of biopsy, on typical clinical, morphological and biological data. Data related to the cirrhosis etiology: alcohol, viral markers of hepatitis B, C, iron load parameters and autoimmune markers were collected for each patient. Venous blood samples were taken in the morning after 12-h overnight fasting. There were 383 patients with cirrhosis associated with hepatocellular carcinoma (HCC). DM was found in 412 (39.7 %) patients. Patients with DM were older and more likely to be overweight and male, with a family history of DM and a diagnosis of HCC. DM was not associated with a history of stroke or myocardial infarction. Cirrhosis secondary to hepatitis infection was less strongly associated with DM than with NASH or alcoholic cirrhosis. The severity of LC was not associated with DM. In multivariate analysis, the factors associated with DM were age, BMI, a family history of DM, and statin use. There was a significant interaction between HCC and cirrhosis etiology for the risk of DM. Cirrhosis secondary to hepatitis was associated with a lesser presence of DM only in patients with HCC (interaction p = 0.0015). LC was strongly associated with DM, with around 40 % of diabetic patients. In the group of patients with LC without HCC, diabetes was not associated with the etiology of cirrhosis.     

乙型肝炎肝衰竭患者预后影响因素研究

目的探讨影响乙型肝炎肝衰竭患者预后的相关因素。方法回顾性分析2008年3月-2013年10月福建医科大学孟超肝胆医院肝病科确诊为乙型肝炎肝衰竭患者500例,统计在治疗随访中肝衰竭预后好转或者病情加重的例数,并结合临床检查,采用Pearson单因素分析及Logistic回归分析确定影响乙型肝炎肝衰竭患者预后的相关危险因素。结果 Pearson单因素分析提示患者出现预后病情恶化与血清总胆红素(TBIL)、直接胆红素(DBIL)、白蛋白(ALB)、除乙肝外其他肝病病史、凝血酶原时间(PT)、肺部并发感染、肝性脑病、电解质紊乱、血肌酐、入院后抗病毒治疗情况、胆碱酯酶、血脂、血清纳指标有关(P0.05);Logistic回归分析提示,除乙肝外其他肝病病史、PT延长、肺部并发感染、出现肝性脑病、入院后未接受正规抗病毒治疗是乙型肝炎肝衰竭患者预后不良的危险因素(P0.05)。结论除乙肝外其他肝病病史、PT延长、肺部并发感染是影响乙型肝炎肝衰竭预后的危险因素,入院后对患者进行正规的抗病毒治疗有利于改善患者的预后。     

Which patients with hepatitis C develop liver complications?

To identify variables that are independent predictors of adverse outcomes in chronic hepatitis C, we analyzed a cohort of 455 patients followed for a median of 4.7 years. Associations were sought between demographic and behavioral factors, hepatitis C virus (HCV) genotype, liver histology and liver tests at entry, and development of liver complications, hepatocellular carcinoma (HCC), hepatic transplantation and liver-related death. Independent predictors were identified by multivariate analysis. The following were associated with a significantly higher rate of liver complications: age; birth in Asia, Europe, Mediterranean region, or Egypt; transmission by blood transfusion or sporadic cases; HCV genotypes 1b and 4 (compared with 1/1a); fibrosis stage 3 or 4 (cirrhosis); serum albumin; bilirubin; prothrombin time; and alpha-fetoprotein. However, the only independent predictors of liver-related complications were sporadic transmission (P <.001), advanced fibrosis (P =.004), and low albumin (P <.001). The corresponding independent risk factors for HCC were male gender (P =. 07), sporadic transmission (P <.001), and albumin (P <.001); bilirubin (P =.02) was an additional predictor of transplantation or liver-related death. It is concluded that only patients with advanced hepatic fibrosis or cirrhosis, are at risk of developing hepatic complications of chronic hepatitis C during 5-year follow-up. Among such patients, abnormalities in serum albumin, bilirubin, or prothrombin time indicate a high probability of complications. Patients without definite risk factors for HCV (sporadic cases) are at higher risk of complications, possibly because of interaction between older age, duration of infection, country of birth, and HCV genotypes 1b and 4.     

Hepatitis C virus and hepatocellular carcinoma

The sequential development of cirrhosis and hepatocellular carcinoma (HCC) in patients with transfusion-associated hepatitis was a clue leading to the identification of hepatitis C virus (HCV) as a risk factor for HCC. The incidence of HCV-related liver cancer is increasing in many developed countries: tumours arise in older patients, are almost invariably associated with cirrhosis and often have a less aggressive course than is seen in HCC related to other aetiological factors. Most HCCs grow as a single hepatic nodule for several years before generating satellite or distant tumour nodules. Tumour progression and hepatic failure are the leading causes of death. HCV might promote cancer through cirrhosis, which is per se an important risk factor for this tumour. HCV might also have oncogenic properties by interacting with cellular genes that regulate cell growth and differentiation. The primary prevention of HCC through vaccination against HCV is not yet available. The treatment of patients with chronic hepatitis C with interferon might attenuate the risk of HCC.     

Artificial intelligence for hepatitis evaluation

Recently, increasing attention has been paid to the application of artificial intelligence (AI) to the diagnosis of diverse hepatic diseases, which comprises traditional machine learning and deep learning. Recent studies have shown the possible value of AI based data mining in predicting the incidence of hepatitis, classifying the different stages of hepatitis, diagnosing or screening for hepatitis, forecasting the progression of hepatitis, and predicting response to antiviral drugs in chronic hepatitis C patients. More importantly, AI based on radiology has been proven to be useful in predicting hepatitis and liver fibrosis as well as grading hepatocellular carcinoma (HCC) and differentiating it from benign liver tumors. It can predict the risk of vascular invasion of HCC, the risk of hepatic encephalopathy secondary to hepatitis B related cirrhosis, and the risk of liver failure after hepatectomy in HCC patients. In this review, we summarize the application of AI in hepatitis, and identify the challenges and future perspectives.     

湖北地区乙型肝炎病毒基因型分布与临床的相关性

目的 了解湖北地区乙型肝炎病毒(HBV)基因型的分布及其与临床的相关性。 方法 选择湖北地区HBV DNA阳性的慢性HBV感染者190例,其中乙型肝炎表面抗原(HBsAg)携带者52例、慢性乙型肝炎56例、重型肝炎32例、肝硬化22例、原发性肝癌28例,应用多对型特异性引物-聚合酶链反应检测HBV的基因型。 结果 多对HBV型特异性引物法可快速准确鉴定HBV的基因型。190份HBV DNA阳性血清标本中,B基因型140例(73.7％),C基因型42例(22.1％),BC混合型8例(4.2％),未发现A、D和E基因型;B基因型在重型肝炎和肝癌患者中占绝对优势,分别为87.5％和89.3％,显著高于HBsAg携带者的67.3％;B基因型患者血清丙氨酸氨基转移酶水平(253.1±306.7)U／L高于C基因型患者的(154.1±192.9)U／L,差异有统计学意义(P<0.05);除HBsAg携带者外的慢性HBV感染者中,B基因型患者血清抗-HBe阳性率50.5％(53／105)显著高于C基因型的18.5％(5／27),P<0.01。 结论 多对型特异性引物同时进行聚合酶链反应的基因分型方法可用于HBV基因型的流行病学调查;湖北地区存在HBV的B、C和BC混合基因型,B型为本地区的优势基因型并在严重肝病和肝癌中的比例较高,基因型的分布可能有较大的地区差异。     

Prognostic effects of causative virus in hepatocellular carcinoma according to the Japan integrated staging (JIS) score

Background The Japan integrated staging (JIS) score is recognized to be useful in managing hepatocellular carcinoma (HCC). We evaluated the effects of the causative virus in patients stratified by this system. Methods We compared clinicopathologic features, cumulative and tumor-free survival rates, and causes of death between 301 hepatitis C virus-positive patients (HCV group) and 60 hepatitis B virus-positive patients (HBV group). Results Among patients with low JIS scores (0 or 1), the proportions of patients with high aspartate and alanine aminotranferase activities, moderate-to-severe active hepatitis, and with cirrhosis were significantly higher in the HCV than in the HBV group. Among patients with high JIS scores (2 to 4), the proportion with moderate-to-severe active hepatitis was also significantly higher in the HCV group. In patients with low JIS scores, those in the HCV group had significantly lower tumor-free and cumulative survival rates than those in the HBV group. Although no patient in the HBV group died of causes other than liver disease (HCC or hepatic failure), some patients in the HCV group died of causes other than liver disease. The proportion of patients who died because of HCC recurrence tended to be higher among patients with high JIS scores than among patients with a low JIS score. Conclusions The effects of viral status on survival outcomes are greatest in patients with JIS scores of 0 or 1.