Hepatitis BLife Extension Suggestions
Conventional Treatment for Hepatitis B
Acute hepatitis B typically resolves on its own and may not require treatment (Liaw 2009). The goal of chronic hepatitis B treatment is to suppress HBV viral replication, which may limit hepatitis progression and may lower the risk of some complications, such as cirrhosis or cancer (Gish 2012).
Antiviral therapy. There are 7 drugs approved for treatment of chronic hepatitis (Mutimer 2012). Interferon (IFN) is a signal protein produced by infected or cancerous cells to bolster the immune response of neighboring cells (Marieb 2010). Interferon alpha (IFN-α) therapy is an approved antiviral for HBV and HCV infection. Both standard IFN-α and pegylated IFN-α (an IFN derivative with a longer half-life in the body) (Grimm 2011) are administered via subcutaneous injection (Nebbia 2012). INF-α, either alone or in combination with the nucleoside analog lamivudine, lowers viral load and normalizes ALT levels (Scaglione 2012). IFN alone may reduce the incidence of cirrhosis, hepatocellular carcinoma, and liver-related deaths (Scaglione 2012). Side effects of IFN include fatigue, flu-like symptoms, mood changes, bone marrow suppression, and development or exacerbation of autoimmune illnesses (Scaglione 2012). IFN-α may be better for achieving a sustained virological response than nucleotide analogs (see below) (Nebbia 2012).
Nucleotide and nucleoside analogs. Nucleotide and nucleoside analogs (NUCs; lamivudine, telbivudine, entecavir, adefovir dipivoxil, and tenofovir disoproxil fumarate) interfere with HBV viral replication. Trials of NUCs in HBV patients demonstrate a decrease in viral load, ALT levels, and hepatocellular carcinoma incidence, as well as the possible reversal of HBV-mediated cirrhosis. As oral medications, NUCs are more convenient to take than IFN, but the eventual development of resistance to these drugs limits their long-term utility. Side effects, which vary by drug, include myopathy and peripheral neuropathy (telbivudine), kidney toxicity and dysfunction (tenofovir and adefovir), decreased bone mineral density (tenofovir), and lactic acidosis in patients with liver disease (entecavir) (Scaglione 2012).