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Reactivation of hepatitis B is a well-recognized complication in hepatitis B virus (HBV) infected patients undergoing cancer chemotherapy [2]. HBV reactivation usually occurs with fulminant hepatitis and hepatic failure in patients with hematological malignancies who receive anthracycline, rituximab, and steroids treatment as anticancer therapy [4, 7, 9, 14]. The nucleoside analogue, lamivudine (LMV) can significantly decrease HBV DNA and serum transaminases levels, as well as restore tissue function in compensated chronic hepatitis B infection [1, 6]. The safety and efficacy of LMV treatment for patients with severe acute or fulminant hepatitis B has been extensively documented [5, 12, 13], and most studies consider that LMV treatment can improve the survival rate of severe acute or fulminant hepatitis B patients [10, 13]. Moreover, LMV and interferon as prophylactic antiviral agents can significantly reduce the incidence of HBV reactivation and the overall morbidity of cancer patients with HBV positive undergoing chemotherapy [3]. This strategy may, however, fail.
Here we report a surface antigen of an HBV (HBsAg) positive cancer patient who developed fulminant exacerbation of chronic hepatitis B despite the administration of antiviral therapy with LMV after cytotoxic chemotherapy. The sequence analysis of this antigen revealed multiple mutation sites in HBV genotype C.
A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy *
- Received Date: 11 September 2012
- Accepted Date: 05 November 2012
Abstract: A 62-year-old man had chronic hepatitis B virus (HBV) infection and was diagnosed with liver cirrhosis. At the time of diagnosis the patient’s virologic markers were positive for hepatitis B surface antigen (HBsAg), antibody to hepatitis B e antigen (anti-HBe) and antibody to hepatitis B core antigen (anti-HBc), while antibody to hepatitis B surface antigen (anti-HBs) and HBV DNA were negative. Later the patient received chemotherapy for malignancy. However, this was interrupted due to elevated liver enzymes. At the same time HBV DNA became positive. Lamivudine (LMV) therapy was administered immediately. However, the levels of serum aminotransferase and total bilirubin (TB) were still rising. Finally the patient died of fulminant hepatic failure. A sequence revealed HBV genotype C (HBsAg subtype adw) with immune escape mutations, F8L, S34L, F41S, G44V, F93C, V96G, L110I, C149Y and F161Y. The high morbidity and mortality of this complication is one of the major obstacles to completing the standard treatment for malignancy in HBV carriers. Therefore, the relative risk of antiviral prophylactic failure should be further assessed and the the optimal strategy for antiviral prophylaxis in HBsAg-positive patients with oncologic and hematologic malignancies undergoing chemotherapy should be revised.