REVIEW ARTICLE Management of acute hepatitis B and reactivation of hepatitis B Ankur Jindal, Manoj Kumar and Shiv K. Sarin Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India Keywords Acute hepatitis B – Chronic hepatitis B – Hepatitis B reactivation – Antiviral drugs – Fulminant hepatitis – Hepatitis flare Abbreviations ACLR, acute-on-chronic liver failure; ALF, acute liver failure; AVH-B, acute hepatitis B; CHB, chronic hepatitis B; ESR1, oestrogen receptor alpha; GCSF, granulocyte-colony stimulating factor; HAV, hepatitis A virus; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis delta virus; HEV, hepatitis E virus; HIV, human immunodeficiency virus; NNRTI, non-nucleoside reverse transcriptase inhibitors; WHV woodchuck hepatitis virus. Correspondence Dr S K Sarin, MD, DM, Senior Professor, Hepatology, Institute of Liver & Biliary Sciences (ILBS), New Delhi, India Tel: +91 11 4630 0000 Fax: +91 11 2612 3504 e-mail: [email protected] DOI:10.1111/liv.12081 Abstract The natural course of hepatitis B virus infection and the resulting hepatic injury is determined by the degree of virus replication and the intensity of host immune response. Upon exposure to hepatitis B virus (HBV), individu- als with a vigorous and broad immune response develop acute self-limited infection, which may result in acute hepatitis. However, with stringent test- ing for HBV and universal precautions, acute HBV is rather rare. Reactiva- tion of HBV most often presents as acute hepatitis B (AVH-B) and clinically, it is difficult to differentiate AVH-B from reactivation of chronic hepatitis B (CHB) and it requires a high index of suspicion. In the presence of high HBV DNA (>2 9 10 4 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 AVH-B 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 CHB reactivation. Liver transplantation should be considered in patients who develop liver fail- ure 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. Hepatitis B virus (HBV) infection is the tenth leading cause of death worldwide (1). Almost 30% of the world population has been exposed to HBV and an estimated 400 million of these are chronically infected (2). The natural course of HBV infection is determined by the interplay between viral replication and the host immune response. Upon exposure to HBV, individuals with a vigorous and broad immune response to the virus develop an acute self-limited infection, which may result in acute hepatitis. An aberrant response can lead to fulminant hepatitis. Individuals who do not have a broad and vigorous immune response do not clear the virus, but develop persistent chronic hepatitis B virus. The virus persists in the body even after sero- logical recovery from acute hepatitis B; therefore, indi- viduals who have been exposed to HBV are at risk for reactivation [flare or exacerbation] of hepatitis when an immune imbalance occurs (3). The severity of the flare depends on the state of underlying liver disease. As patients with severe acute exacerbation of chronic hepatitis B may not have underlying cirrhosis, they may recover to relatively normal liver function in con- trast to those with end-stage cirrhosis. It is therefore important to recognize this clinical presentation of chronic hepatitis B. Although there is no consensus definition of reactiva- tion [flare or exacerbation] of hepatitis B is character- ized by sudden elevation of serum ALT levels. It usually refers to an abrupt increase in serum ALT to >5– 10 times the upper limit of normal or >3 times the baseline level (4). Reactivation of hepatitis in chronic HBV-infected patients is common and may be caused by a number of factors (Table 1). Reactivation of hepa- titis B virus (HBV) replication is a sudden increase or reappearance of serum HBV DNA in a patient with chronic or past HBV infection (5). This review will focus on management of acute hepa- titis B and reactivation of hepatitis B (flare or exacerba- tion) spontaneous or that owing to superimposed hepatotropic viruses. Acute hepatitis B During acute hepatitis B, manifestations range from subclinical or anicteric hepatitis to icteric and, in some cases, fulminant hepatitis. Liver International (2013) © 2012 John Wiley & Sons A/S 164 Liver International ISSN 1478-3223
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