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 Printable version |
Treatment of Hepatitis B chronic infection |
Hépato-Gastro. Volume 17, Number 1, 75-80, janvier-février 2010, Mini-revue
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 Résumé
Article gratuit
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Author(s) : Stanislas Pol |
Summary : The potential severity of chronic hepatitis B virus (HBV) infection (the 20 % risk of developing cirrhosis with its carcinomatous and non carcinomatous complications) is directly related to HBV replication which induces necro-inflammation and fibrosis. There is a need to reduce viral replication. The immune mediated pathophysiology of chronic HBV infection explains the therapeutic approaches combining antiviral treatment (nucleos(t)idic analogues or Interferon) and immune stimulation (only Interferon is proven to be efficacious) to overcome the suboptimal HBV-specific lymphocytotoxicity. The aim of therapy is to achieve undetectable serum HBV DNA which results in reduction of virological breakthrough and resistance and complications of cirrhosis. Any HBV-infected patient with significant liver disease (A>1 and/or F>1 according to Metavir scoring system) and/or abnormal transaminase activity or viral replication should receive antiviral therapy with high genetic barrier, namely in 2009 Entecavir or Tenofovir. Their high antiviral efficacy and their fair resistance profile explain that the 2 main problems in treating HBV infection are adherence and safety since treatments should be long lasting if not definitive.The management of HBV-infected patients with chronic hepatitis will include : 1. inactivation of HBV replication mainly by analogues and 2. monitoring of drug safety : nephrotoxicity of long term treatments by nucleotidic analogues is now a concern which does not clearly modify the indications on the basis of a fair biochemical follow up. |
Keywords : Hepatitis B virus, chronic hepatitis, nucleos(t)idic analogue, nephrotoxicity, Fanconi syndrome |
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