Does interferon therapy prevent hepatocellular carcinoma in patients with chronic viral hepatitis?

Centro A.M. e A. Migliavacca, Unità Operativa di Gastroenterologia 1, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Università degli Studi di Milano, Milano, Italy.
Gastroentérologie Clinique et Biologique (Impact Factor: 1.64). 03/2011; 35(6-7):455-64. DOI: 10.1016/j.clinre.2011.02.008
Source: PubMed


Chronic hepatitis C and B are well-recognized and potentially preventable risk factors for hepatocellular carcinoma (HCC) development. Clinical and epidemiological studies suggest that therapy with interferon-α may reduce the overall risk of HCC development in patients with chronic hepatitis C, who achieve sustained virological response, but even in those who fail to eradicate the infection. In chronic hepatitis B, interferon therapy reduces the risk of HCC development in HBeAg-positive and cirrhotic patients who achieve persistent suppression of viral replication, while in HBeAg-negative patients the beneficial effect of interferon-α is not definitively confirmed. The preventive role of interferon-α after potentially curative treatment for HCC in both chronic hepatitis B and C is uncertain due to methodological flaws of the existing studies and prospective randomized controlled trials with pegylated interferon-α are needed to clarify this issue.


Available from: Elena Vezali, Jul 17, 2014
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    • "Chronic hepatitis C (CHC) is one of the leading causes of hepatocellular carcinoma (HCC) [1-3]. Thus, an early eradication of hepatitis C virus (HCV) infection is a key point in order to stop the progression to cirrhosis and consequently to reduce the risk of developing HCC. "
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    ABSTRACT: Hepatitis C virus (HCV) infection is one of the major causes of hepatocellular carcinoma (HCC). Although predominant in cirrhotic HCV patients, the risk of HCC exists also in case of mere chronic hepatitis C (CHC). Thus the goal of the antiviral therapy is to obtain an early eradication of the HCV infection in order to reduce the risk of hepatocarcinogenesis. We report the case of a 61-year-old Caucasian male with CHC, who developed hemoperitoneum from HCC bleeding after having achieved sustained virological response (SVR). He underwent surgical resection and the histopathological examination showed a moderately-differentiated HCC in a slightly fibrotic liver. The patient has no tumor recurrence and keeps on doing well 18 months after surgery. This report, as many others, proves the existence of a residual risk of hepatocarcinogenesis in spite of obtaining an SVR in the absence of cirrhosis. Therefore, in our opinion, it is of primary importance to understand the underlying mechanisms of hepatocarcinogenesis and the major risk factors for HCC, in order to select those patients who most deserve a follow up. In this regard, we have proposed a different surveillance strategy according to the response to antiviral therapy, hepatic histology and the existence of one or more risk factors for HCC in SVR patients.
    Annals of Gastroenterology 04/2013; 26(1):80-83.
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    ABSTRACT: The management of chronic viral hepatitis C is evolving rapidly. Monotherapy with interferon, the accepted standard of treatment until recently, achieves only a modest sustained virological response rate of 15%. Combination treatment with alpha-2b interferon and ribavirin has been shown to increase sustained response rates to 40% in patients who have never been treated with interferon and to 50% in those who have relapsed following monotherapy with interferon. However, side effects, which have led to the discontinuation of combination treatment in a significant proportion of patients, must be carefully monitored. Treatment with interferon alpha-2b and ribavirin has now been approved in Canada, but the selection and monitoring of patients suitable for combination treatment requires special expertise. Although improvements in current therapeutic options may be possible with more frequent, higher doses or long-acting forms of interferon together with ribavirin, low sustained response rates (i.e., below 30%) for patients with hepatitis C virus genotype 1 emphasize the need for novel antiviral medications that will target the functional sites of the HCV genome.
    Canadian Medical Association Journal 04/2000; 162(6):827-33. · 5.96 Impact Factor
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    ABSTRACT: Objective:Chronic infection with hepatitis C may lead to 0842 the development of cirrhosis, liver failure, and hepatocellular carcinoma. However, not all patients progress to these endpoints. Ideally, clinicians could improve their capability of stratifying the risk and the time frame within which their patients will progress to these endpoints. The purpose of the present study was to construct statistical models predicting disease-progression for individual patients.Methods:Study endpoints were the development 0842 of hepatocellular carcinoma, liver transplantation, or death due to liver disease. The study cohort was 256 patients with hepatitis C acquired from either blood transfusion or use of intravenous drugs. During follow-up, 17 patients developed hepatocellular carcinoma, seven received liver transplantation, and 12 died from liver disease.Results:On multivariate analysis a history of0842 decompensation (relative risk [RR] 4.321, 95% confidence interval [CI] 1.777–10.511) and the serum albumin (RR 0.253, 95% CI 0.136–0.474) were independently associated with the study endpoints. Patients without a history of decompensation and with a serum albumin ≥4.1 mg/dl had a 3.2% chance of developing a study endpoint within 5 yr. Baseline genotype and quantitative RNA were not associated with development of the clinical endpoints, with the exception of patients coinfected with two or more genotypes.Conclusion:Thus, the serum 0842 albumin and a history of decompensation are useful for predicting the development of hepatocellular carcinoma, liver transplantation, and death due to liver disease among patients with hepatitis C.
    Liver Transplantation 05/2000; 6(3):379-81. DOI:10.1002/lt.500060328 · 4.24 Impact Factor
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