A young man presents with HBsAg positive anti HBcIgM positive, HBeAg negative and normal levels ofAST and ALT. He is asymptomatic. What is the next line of management.
Management of chronic hepatitis B Treatments are still limited, as no drug is consistently able to eradicate hepatitis B infection completely (i.e. render the patient HBsAg-negative). The goals of treatment are HBeAg seroconversion, reduction in HBV-DNA and normalisation of the LFTs. The indication for treatment is a high viral load in the presence of active hepatitis, as demonstrated by elevated serum transaminases and/or histological evidence of inflammation and fibrosis. The oral antiviral agents are more effective in reducing viral loads in patients with e antigen-negative chronic hepatitis B than in those with e antigen-positive chronic hepatitis B, as the pre-treatment viral loads are lower. Most patients with chronic hepatitis B are asymptomatic and develop complications, such as cirrhosis and hepatocellular carcinoma, only after many years . Cirrhosis develops in 15-20% of patients with chronic HBV over 5-20 years. This propoion is higher in those who are e antigen-positive. Two different types of drug are used to treat hepatitis B: direct-acting nucleoside/nucleotide analogues and pegylated interferon-alfa. Direct-acting nucleoside/nucleotide antiviral agents Orally administered nucleoside/nucleotide antiviral agents are the mainstay of therapy. These act by inhibiting the reverse transcription of pre-genomic RNA to HBV-DNA by HBV-DNA polymerase but do not directly affect the covalently closed circular DNA (cccDNA) template for viral replication, and so relapse is common if treatment is withdrawn. One major concern is the selection of antiviral-resistant mutations with long-term treatment. This is paicularly impoant with some of the older agents, such as lamivudine, as mutations induced by previous antiviral exposure may also induce resistance to newer agents. Entecavir and tenofovir (see below) are potent antivirals with a high barrier to genetic resistance and so are the most appropriate first-line agents. Lamivudine Although effective, long-term therapy is often complicated by the development of HBV-DNA polymerase mutants (e.g. the 'YMDD variant'), which lead to viral resistance. These occur after approximately 9 months and are characterised by a rise in viral load during treatment. Outside resource-limited settings, this agent is now seldom used for the treatment of HBV but may be used to prevent reactivation of HBV in previously infected, HBsAg-negative patients if they are undergoing chemotherapy . Ref Davidson edition23rd pg 876
Wait and Watch
Lamivudin
Immunoglobulin
Liver Transplant
G.I.T