Published online Mar 21, 2014. doi: 10.3748/wjg.v20.i11.2876
Revised: January 14, 2014
Accepted: February 17, 2014
Published online: March 21, 2014
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Liver cirrhosis (LC) is a critical stage of chronic liver disease, including that caused by hepatitis C virus (HCV). In the absence of antiviral therapy, 67%-91% of patients with HCV-related LC patients die of liver-related causes, including hepatocellular carcinoma (HCC) and liver failure. Among the therapeutic strategies used to prevent liver-related complications in these patients is standard therapy with pegylated interferon and ribavirin, which induces a sustained virological response (SVR) in 25% of HCV genotype 1-infected patients and in 69% of patients infected with genotypes 2 and 3. SVR in patients with HCV-related LC has been associated with reduced rates of hepatic decompensation, HCC, and mortality. More recently developed direct-acting antiviral agents have shown excellent antiviral efficacy, with preliminary data demonstrating that an interferon-free regimen that includes these direct-acting antiviral agents achieved SVR in more than 50% of patients with HCV genotype 1 LC. Branched-chain amino acid supplementation, improvement of insulin resistance, and the use of β-blockers for portal hypertension may also reduce liver-related complications. Here, we review advances in antiviral and adjunctive therapies for improved outcomes in patients with HCV-associated LC.
Core tip: Liver cirrhosis (LC) is the critical stage of hepatitis C virus (HCV)-related chronic liver disease. Many studies of HCV-related LC patients have indicated that sustained virological response (SVR) after interferon therapy is highly associated with reductions in hepatic decompensation, hepatocellular carcinoma incidence, and mortality. Furthermore, direct-acting antiviral agents have shown excellent antiviral efficacy. Preliminary data have indicated that an interferon-free regimen achieved SVR for more than 50% of patients with LC due to HCV genotype 1. Branched-chain amino acid supplementation, improvement of insulin resistance, and the use of β-blockers for portal hypertension may also contribute to a reduction in liver-related complications.