Lamivudine treatment in patients with decompensated hepatitis B cirrhosis: for whom and when?

Abstract

HRONIC C HEPATITIS B virus (HBV) infection is a global public health problem that affects approximately 300 million individuals. In many parts of the world, hepatitis B-related liver failure and hepatocellular carcinoma (HCC) are the leading causes of death (1,2). Several studies have demonstrated that the ChildTurcotte-Pugh (CTP) scoring system is reliable in the assessment of the severity of hepatic dysfunction and the prognosis of patients with cirrhosis (3,4). The 5year survival rate of patients with compensated HBV cirrhosis (CTP score of 5 or 6) is 80% compared to only 14% in patients with decompensated HBV cirrhosis (CTP score 87) (5,6). Clinical factors associated with a higher risk of developing cirrhosis and HCC include male sex, alcohol consumption, and co-infection with hepatitis C or D or human immunodeficiency virus (HIV) (7,s). Among patients with HBV cirrhosis, those with detectable HBV replication (hepatitis B e antigen+ [HBeAg] and/or HBV DNA+) have higher mortality than patients with low or undetectable HBV replication (9,lO). Therefore, it is reasonable to hypothesize that suppression or elimination of HBV replication in patients with advanced HBV cirrhosis may lead to clinical improvement. Interferon-a (IFN) and lamivudine treatment of patients with chronic hepatitis B lead to a sustained loss of replicative markers in 2&40% of treated patients (11-13). Although IFN can benefit some patients with compensated HBV cirrhosis, response to IFN is poor in patients with decompensated HBV cirrhosis. In the latter patients, IFN may also precipitate hepatic failure during flares in aminotransferase (ALT) levels as well as life-threatening infections (14,15). Thus, IFN is not