Hepatocellular carcinoma incidence in chronic hepatitis C patients according to sustained virological response (SVR) with interferon-based therapies and baseline characteristics

Introduction

Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death worldwide with increasing incidence. Effective antiviral treatment for chronic hepatitis C (CHC) became available in the last 7 years but despite the WHO Hepatitis elimination targets, they are not universally available today in all regions for all the patients, indicating still a bleak outlook for CHC-associated HCC in the next decades.

Aim

To assess the HCC incidence in relation to interferon (IFN)-based antiviral treatment response and baseline characteristics of a large cohort of chronic hepatitis C (CHC) patients from a single institution.

Methods

We retrospectively collected data of CHC patients, who were diagnosed between 1989 and 2011 and treated at the AKH-University Hospital of Vienna before the introduction of direct-acting antiviral (DAA) only therapy. We analysed the HCC incidence in patients with a sustained virological response (SVR) and without SVR according to the patients' baseline characteristics.

Results

Our study included 2134 patients, who were treated or not treated with IFN-based antiviral treatment and had long-term follow-up available. The overall HCC incidence in this cohort was 6.2% (132 HCC cases over a median follow-up period of 9 years). According to the baseline fibrosis stage, the overall HCC incidence was: 1.1% in patients with baseline fibrosis stage F0-2, 8.2% in F3 and 20.6% in F4 patients. The HCC incidence was significantly higher in non-SVR and no-treatment group as compared with SVR patients: 12.4% vs 1.9%, P < .0001, 7.3% vs 1.9%, P < .0001. In multivariate analysis, lower platelet count (odds ratio-OR = -0.1, 95% CI: 0.15-0.63), for the SVR group and presence of cirrhosis (OR = 3.6, 95% CI: 1.59-8.17), ALBI grade >=2 (OR = 2.3, 95% CI: 1.0-5.3) for the non-SVR group were independently associated with HCC occurrence. For the group of patients with no treatment, the only predictor for HCC was high baseline alpha-fetoprotein values (OR = 10.2, 95% CI: 2.2-47.9).

Conclusion

The achievement of SVR significantly reduces the risk for HCC occurrence during long-term follow-up. However, the risk remains high in successfully treated patients with low platelet count and in patients who did not achieve SVR with more advanced liver disease. These risk factors should be considered in decision-making of HCC surveillance in this settling.