Recent advances in coeliac disease

Armstrong et al.
Current Opinion in Gastroenterology • March 2009
ISSN: 0267-1379 • Frequency: 6/year • Impact Factor: 3.877 • Subscribe Now

Special Author Introduction
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Hepatitis B virus (HBV) infection is a mayor cause of chronic liver disease. It is estimated that nearly two billion people are infected worldwide by HBV and that more than 350 million have persistent and chronic infection. HBV carriers have a high risk of developing chronic liver disease, cirrhosis and hepatocellular carcinoma.

Treatment of chronic hepatitis B virus infection is aimed at suppressing viral replication to the lowest possible level, and thereby to halt the progression of liver disease and prevent the onset of complications. Antiviral therapy, available for chronic HBV patients includes interferon and nucleos(t)ide analogues, such as lamivudine (LAM), adefovir dipivoxil (ADV) and entecavir (ETV). Prolonged treatment with nucleos(t)ide analogues can induce mutations in the reverse transcriptase domain of the polymerase gene and confer resistance to antiviral. The emergence of drug-resistant mutants is followed by increases in viral load and re-elevation of transaminase levels.

Preventing HBV antiviral drug resistance to nucleos(t)ide analogues and appropriate management when resistance occurs has become a major focus in the management of chronic hepatitis B. HBV antiviral drug resistance may be best prevented by using an agent or combination of agents with a high genetic barrier to resistance. Frequent assessment of quantitative serum HBV DNA remains the best approach to early detection of resistance, and antiviral therapy should be modified as soon as resistance is detected.

This article evaluate the therapy in chronic HBV infected patients with frequent measurements of DNA levels, characterize HBV genotypes, and determine the emergence of nucleos(t)ide analogues primary and secondary mutants before and during the therapy by direct sequencing.