Approximately 2% to 5% of patients with chronic hepatitis C virus develop hepatocellular carcinoma every year. 

Although chronic hepatitis C virus (HCV) infection that is treated with antiviral therapy reduces the incidence of hepatocellular carcinoma (HCC), patients who achieve sustained virological response (SVR) are still at risk for HCC.

Stefano Brillanti, MD, of DIMEC, University of Bologna, and his colleagues evaluated the effect of therapy with direct acting antivirals on the development of HCC in patients with HCV-related liver cirrhosis and presented their findings at he 2016 International Liver Congress in Barcelona, Spain.


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“Direct acting antivirals have dramatically improved sustained virological response rates in cirrhotics,” said Dr Brillanti during a press conference on his study. “But at least until now, very little is known about the effect of these therapies on the possible development of hepatocellular carcinoma.”

The study included 344 consecutive, patients who did not have HIV (average age 63 years; 60.2% male) with Child-Pugh classification A or B cirrhosis. Patients were treated with different direct acting antivirals and followed for 24 weeks after therapy. Researchers assessed liver cirrhosis with transient elastography or liver histology. They used contrast-enhanced ultrasonography at baseline to exclude active HCC, and at 12 and 24 weeks post-treatment follow-up. Suspected HCC was confirmed or excluded by CT-scan or MRI.

After the 26-week follow-up, 26 patients (7.6%) had developed HCC. However, only 3.2% of patients without previous HCC developed HCC after treatment, and 29% of patients with a prior history developed HCC after the treatment.

Among the 59 patients with a history of previous HCC, those who developed HCC after treatment with direct acting antiviral therapy were typically younger (median age 56 vs 73) compared to the patients without a prior history of HCC. Patients with a history of HCC were also more frequently treatment experienced (88.2% vs 61.9%) and had more advanced liver fibrosis (Fibroscan, Kpa>21.5).

Dr Brillanti noted that SVR was obtained in 89% of the patient cohort. Patients were treated with different direct acting antivirals depending on the patient’s genotype, but there was no association between genotype and the occurrence of HCC.

“The history of previous HCC was the strongest predictor of the development of new HCC after therapy,” he concluded. “Cirrhotic patients should be closely monitored after treatment, and the biological significance of our findings needs to be better defined.”

Reference

1. Brillanti S. Abstract LBP506. Development of hepatocellular carcinoma in HCV cirrhotic patients treated with direct acting antivirals. Presented at the International Liver Congress; April 13-17, 2016; Barcelona,