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Upon exposure to hepatitis B virus (<jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content>), individuals with a vigorous and broad immune response develop acute self\u2010limited infection, which may result in acute hepatitis. However, with stringent testing for <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> and universal precautions, acute <jats:styled-content style=\"fixed-case\">HBV<\/jats:styled-content> is rather rare. Reactivation of HBV most often presents as acute hepatitis B (AVH\u2010B) and clinically, it is difficult to differentiate AVH\u2010B from reactivation of chronic hepatitis B (CHB) and it requires a high index of suspicion. In the presence of high <jats:styled-content style=\"fixed-case\">HBV DNA<\/jats:styled-content> (&gt;2\u00a0\u00d7\u00a010<jats:sup>4<\/jats:sup> IU\/ml) underlying liver disease should be investigated by liver biopsy, endoscopy and\/or imaging. The degree of liver failure often depends on the severity of acute insult and the stage of underlying chronic liver disease. Mutations in the HBV genome, immunosuppressive therapy and viral or drug induced injury are common causes of reactivation. As most patients with <jats:styled-content style=\"fixed-case\">AVH<\/jats:styled-content>\u2010B resolve the infection spontaneously, antiviral therapy is not indicated in them. However, the use of a potent oral nucleoside(tide) analogue is necessary as soon as possible in patients with <jats:styled-content style=\"fixed-case\">CHB<\/jats:styled-content> reactivation. Liver transplantation should be considered in patients who develop liver failure secondary to severe acute exacerbation. If this is not feasible, supportive therapy with the addition of granulocyte colony stimulating factor (GCSF) therapy could be beneficial.<\/jats:p>","DOI":"10.1111\/liv.12081","type":"journal-article","created":{"date-parts":[[2013,1,3]],"date-time":"2013-01-03T11:25:14Z","timestamp":1357212314000},"page":"164-175","source":"Crossref","is-referenced-by-count":77,"title":["Management of acute hepatitis B and reactivation of hepatitis B"],"prefix":"10.1111","volume":"33","author":[{"given":"Ankur","family":"Jindal","sequence":"first","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manoj","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shiv K.","family":"Sarin","sequence":"additional","affiliation":[{"name":"Department of Hepatology Institute of Liver and Biliary Sciences New Delhi India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,1,3]]},"reference":[{"key":"e_1_2_8_2_1","unstructured":"Hepatitis B: Fact sheets WHO. 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