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Liver Int. 2017 Oct;37(10):1526-1534. doi: 10.1111/liv.13452. Epub 2017 May 20.

Improved survival of patients with hepatocellular carcinoma and compensated hepatitis C virus-related cirrhosis who attained sustained virological response.

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Humanitas University and IRCCS Istituto Clinico Humanitas, Rozzano, Italy.
Gastroenterology and Hepatology Unit, Di.Bi.M.I.S., University of Palermo, Palermo, Italy.
Gastroenterology and Hepatology Unit, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy.
Department of Medicine, ASST Nord Milano, Milan, Italy.
Department of Internal Medicine, A.O. Santi Paolo e Carlo, Milan, Italy.
Department of Surgery and Integrated Diagnostics, University of Genoa, Genoa, Italy.
Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy.



Few studies examined the outcome of patients with hepatitis C virus (HCV)-related cirrhosis who developed hepatocellular carcinoma (HCC). The relative weight as determinant of death for cancer vs end-stage liver disease (ESLD) and the benefit of HCV eradication remain undefined. This multicentre, retrospective analysis evaluates overall survival (OS), rate of decompensation and tumour recurrence in compensated HCC patients treated with interferon (IFN) according to HCV status since HCC diagnosis.


Two groups of patients with HCV-related cirrhosis and HCC were followed since HCC diagnosis: (i) compensated cirrhotics with prior sustained virological response (SVR) on IFN-based regimens (N=19); (ii) compensated cirrhotics without SVR (viraemic) (N=156).


Over a median follow-up of 3.0 years since the onset of HCC, OS was longer for HCC patients with SVR than for viraemic patients (log-rank P=.004). The 5-year OS rate was 65.9% in patients with SVR vs 31.9% in viraemic patients. Similar trends were reported for hepatic decompensation (log-rank P=.01) and tumour recurrence (log-rank P=.01). These findings were confirmed at multivariable and propensity score analysis. At propensity analysis, 0/19 compensated patients with SVR died for ESLD vs 7/19 (37%) viraemic patients (P=.004). HCC mortality was similar in the two groups.


Hepatocellular carcinoma patients with prior SVR and compensated cirrhosis at the time of tumour diagnosis have prolonged OS than viraemic patients. Given the lack of cirrhosis progression, no SVR patient ultimately died for ESLD while this condition appears the main cause of death among viraemic patients.


hepatitis C virus; hepatocellular carcinoma; interferon; survival; sustained virological response

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