Published online Jun 21, 2014. doi: 10.3748/wjg.v20.i23.7306
Revised: January 2, 2014
Accepted: April 1, 2014
Published online: June 21, 2014
Processing time: 236 Days and 3.5 Hours
Chronic hepatitis B infection is associated with the development of cirrhosis, hepatocellular carcinoma, and finally liver-related mortality. Each year, approximately, 2%-5% of patients with hepatitis B virus (HBV)-related compensated cirrhosis develop decompensation, with additional clinical manifestations, such as ascites, jaundice, hepatic encephalopathy, and gastrointestinal bleeding. The outcome of decompensated HBV-related cirrhosis is poor, with a 5-year survival of 14%-35% compared to 84% in patients with compensated cirrhosis. Because the risk of disease progression is closely linked to a patient’s serum HBV DNA level, antiviral therapy may suppress viral replication, stabilize liver function and improve survival. This article briefly reviews the role that antiviral therapy plays in cirrhosis complications, particularly, in decompensation and acute-on-chronic liver failure.
Core tip: The goals of antiviral therapy in hepatitis B virus-related cirrhosis would be to improve the hepatic disease severity, improve the clinical symptoms and quality of life, and prolong patient’s survival. Despite the limitations, antiviral therapy with nucleos(t)ide in patients with HBV-related cirrhosis can prevent the development of complications from cirrhosis, particularly, decompensation and acute-on-chronic liver failure (ACLF). Early antiviral treatment is important for patients with severe decompensated cirrhosis and ACLF. Thus, physicians could treat these patients using lamivudine with careful monitoring for the development of resistance or using the most potent antiviral agent, such as entecavir or tenofovir.