HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis

Abstract

Liver steatosis is a main histopathological feature of Hepatitis C (HCV) infection because of genotype 3. Steatosis and/or mechanisms underlying steatogenesis can contribute to hepatocarcinogenesis. The aim of this retrospective study was to assess the impact of infection with HCV genotype 3 on hepatocellular carcinoma (HCC) occurrence in patients with ongoing HCV cirrhosis. Three hundred and fifty-three consecutive patients (193 men, mean age 58 ± 13 years), with histologically proven HCV cirrhosis and persistent viral replication prospectively followed and screened for HCC between 1994 and 2007. Log-rank test and Cox model were used to compare the actuarial incidence of HCC between genotype subgroups. The patients infected with a genotype 3 (n = 25) as compared with those infected with other genotypes (n = 328) had a lower prothrombin activity [78 (interquartile range 60-85) vs 84 (71-195) %, P = 0.03] and higher rate of alcohol abuse (48%vs 29%, P = 0.046). During a median follow-up of 5.54 years [2.9-8.6], 11/25 patients (44%) and 87/328 patients (26%) with a genotype 3 and non-3 genotype, respectively, develop a HCC. HCC incidences were significantly different among the genotype subgroups (P = 0.001). The 5-year occurrence rate of HCC was 34% (95% CI, 1.3-6.3) and 17% (95% CI, 5.7-9.2) in genotype 3 and non-3 genotype groups, respectively (P = 0.002). In multivariate analysis, infection with a genotype 3 was independently associated with an increased risk of HCC occurrence [hazard ratio 3.54 (95% CI, 1.84-6.81), P = 0.0002], even after adjustment for prothrombin activity and alcohol abuse [3.58 (1.80-7.13); P = 0.003]. For patients with HCV cirrhosis and ongoing infection, infection with genotype 3 is independently associated with an increased risk of HCC development.

Management of Hepatitis C in the Indian Context: An Update

“…However experience from India has shown that genotype 3 is a comparatively difficult genotype to treat [25]. Studies have shown that this genotype is associated with higher steatosis, has a faster progression to fibrosis [26] and has higher incidence of hepatocellular carcinoma [27] along with a poorer treatment response as compared to genotype 2. In an attempt to follow the western guidelines, although it is often presumed that the Indian population would respond in a similar way as Americans or Japanese respond, but it has been shown to be otherwise [25].…”

HCV genotype 3: a wolf in sheep’s clothing

“…[4] Although HCV G3 was one of those genotypes who achieved a better sustained viral response (SVR) using pegylated interferon and ribavirin (PEG-IFN/Rbv) therapy, [5] the current effectiveness of the new DAAs against HCV G3 leaves a lot to be desired compared with the results obtained with other genotypes [6]. This is a major problem as compared with other genotypes, HCV G3 is associated with faster progression of fibrosis, [7,8] a greater risk for hepatocellular carcinoma (HCC), [8][9][10] and a higher mortality. [11] Why is it so pathogenic and resistant to treatment?…”

Meta-analysis of the Efficacy and Safety of Grazoprevir and Elbasvir for the Treatment of Hepatitis C Virus Infection

“…3,24,25) The prevalence of chronic HCV infection continues to rise in many countries, and it is a major cause of cirrhosis and hepatocellular carcinoma. 26,27) HCV-related cirrhosis remains the leading cause of liver transplantation in the US and accounts for nearly 40% of liver transplants in adults.…”