Persistence of hepatocellular carcinoma risk in hepatitis C patients with a response to IFN and cirrhosis regression.

Abstract

In patients with HCV-related cirrhosis, a sustained virological response may lead to cirrhosis regression. Whether histological changes translate into prevention of long-term complications, particularly hepatocellular carcinoma is still unknown. This was investigated in a cohort of histological cirrhotics who had been prospectively followed-up for 10years after the achievement of a sustained virological response to IFN. In all, 38 sustained virological response cirrhotics who underwent a liver biopsy 5years post-SVR were prospectively followed to assess the impact of cirrhosis regression on clinical endpoints. During a follow-up of 86 (30-96) months from liver biopsy, no patients developed clinical decompensation, whilst 5 (13%) developed hepatocellular carcinoma after 79 (7-88) months. The 8-year cumulative probability of hepatocellular carcinoma was 17%, without differences between patients with or without cirrhosis regression (19% [95% CI 6%-50%] vs 14% [95% CI 4%-44%], P=.88). Patients who developed or did not an hepatocellular carcinoma had similar rates of residual cirrhosis (P=1.0), collagen content (P=.48), METAVIR activity (P=.34), portal inflammation (P=.06) and steatosis (P=.17). At baseline, patients who developed an hepatocellular carcinoma had higher γGT (HR 1.03, 95% CI 1.00-1.06; P=.014) and glucose (HR 1.02, 95% CI 1.00-1.02; P=.012) values; moreover, they had increased Forns Score (HR 12.8, 95% CI 1.14-143.9; P=.039), Lok Index (HR 6.24, 95% CI 1.03-37.6; P=.046) and PLF (HR 19.3, 95% CI 1.72-217.6; P=.016) values. One regressor died of lung cancer. The 8-year cumulative survival probability was 97%, independently on cirrhosis regression (96% vs 100%, P=1.0) or hepatocellular carcinoma (100% vs 97%, P=1.0). Post-SVR cirrhosis regression does not prevent hepatocellular carcinoma occurrence.