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Volume 27 Issue 6
December 2012

    Chunchen Wu, Hui Shi, Yun YunWang, Mengji Lu, Yang Xu and Xinwen Chen. A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy *[J]. Virologica Sinica, 2012, 27(6): 369-372. doi: 10.1007/s12250-012-3284-3
    Citation: Chunchen Wu, Hui Shi, Yun YunWang, Mengji Lu, Yang Xu, Xinwen Chen. A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy * .VIROLOGICA SINICA, 2012, 27(6) : 369-372.  http://dx.doi.org/10.1007/s12250-012-3284-3
    shu

    A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy

    cstr: 32224.14.s12250-012-3284-3
    • 1.

      State Key Lab of Virology, Wuhan Institute of Virology，Chinese Academy of Sciences, Wuhan 430071, China; 2Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China; 3Institute of Virology, University Hospital of Essen, Essen D45122, Germany

    • 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.

    A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy *

    • 1.

      State Key Lab of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China

    • 2.

      Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

    • 3.

      Institute of Virology, University Hospital of Essen, Essen D45122, Germany

    • Corresponding author: Chunchen Wu, wucc@wh.iov.cn Yang Xu, xuyangs@gmail.com
    • Received Date: 11 September 2012
      Accepted Date: 05 November 2012

      Fund Project: National Basic Research Priorities Program of China 2011CB 106303The Fundamental Research Funds for the Central Universities 2012QN140The National Natural Science Foundation of China 31200699

    • 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.
    • 加载中

      1. Dienstag J L, Schiff E R, Wright T L, et al. 1999. Lamivudine as initial treatment for chronic hepatitis b in the united states. N Engl J Med, 341(17): 1256-1263.
          doi: 10.1056/NEJM199910213411702

      2. Ferreira R, Carvalheiro J, Torres J, et al. 2012. Fatal hepatitis b reactivation treated with entecavir in an isolated anti-hbs positive lymphoma patient: A case report and literature review. Saudi J Gastroenterol, 18(4): 277-281.
          doi: 10.4103/1319-3767.98436

      3. Fukushima N, Mizuta T, Tanaka M, et al. 2009. Retrospective and prospective studies of hepatitis b virus reactivation in malignant lymphoma with occult hbv carrier. Ann Oncol, 20(12): 2013-2017.
          doi: 10.1093/annonc/mdp230

      4. Kim I K, Kim B G, Kim W, et al. 2012. Clinical prediction of failure of lamivudine prophylaxis for patients with hepatitis b infection undergoing cytotoxic chemotherapy for malignancy. Antimicrob Agents Chemother. 56(11): 5511-5519.
          doi: 10.1128/AAC.00821-12

      5. Kondili L A, Osman H, Mutimer D. 2004. The use of lamivudine for patients with acute hepatitis b (a series of cases). J Viral Hepat, 11(5): 427-431.
          doi: 10.1111/jvh.2004.11.issue-5

      6. Lai C L, Chien R N, Leung N W, et al. 1998. A one-year trial of lamivudine for chronic hepatitis b. Asia hepatitis lamivudine study group. N Engl J Med, 339(2): 61-68.
          doi: 10.1056/NEJM199807093390201

      7. Lee I C, Huang Y H, Chu C J, et al. 2010. Hepatitis b virus reactivation after 23 months of rituximab-based chemotherapy in an hbsag-negative, anti-hbs-positive patient with follicular lymphoma. J Chin Med Assoc, 73(3): 156-160.
          doi: 10.1016/S1726-4901(10)70031-9

      8. Lu M, Lorentz T. 2003. De novo infection in a renal transplant recipient caused by novel mutants of hepatitis b virus despite the presence of protective anti-hepatitis b surface antibody. J Infect Dis, 187(8): 1323-1326.
          doi: 10.1086/jid.2003.187.issue-8

      9. Matsue K, Kimura S, Takanashi Y, et al. 2010. Reactivation of hepatitis b virus after rituximab-containing treatment in patients with cd20-positive b-cell lymphoma. Cancer, 116(20): 4769-4776.
          doi: 10.1002/cncr.v116:20

      10. Miyake Y, Iwasaki Y, Takaki A, et al. 2008. Lamivudine treatment improves the prognosis of fulminant hepatitis b. Intern Med, 47(14): 1293-1299.
          doi: 10.2169/internalmedicine.47.1061

      11. Norder H, CouroucCouroucé A M, Coursaget P, et al. 2004. Genetic diversity of hepatitis B virus strains derived worldwide: genotypes, subgenotypes, and HBsAg subtypes. Intervirology, 47(6):289-309.
          doi: 10.1159/000080872

      12. Schmilovitz-Weiss H, Ben-Ari Z, Sikuler E, et al. 2004. Lamivudine treatment for acute severe hepatitis b: A pilot study. Liver Int, 24(6): 547-551.
          doi: 10.1111/liv.2004.24.issue-6

      13. Tillmann H L, Hadem J, Leifeld L, et al. 2006. Safety and efficacy of lamivudine in patients with severe acute or fulminant hepatitis b, a multicenter experience. J Viral Hepat, 13(4): 256-263.
          doi: 10.1111/jvh.2006.13.issue-4

      14. Yeo W, Chan T C, Leung N W, et al. 2009. Hepatitis b virus reactivation in lymphoma patients with prior resolved hepatitis b undergoing anticancer therapy with or without rituximab. J Clin Oncol, 27(4): 605-611.
          doi: 10.1200/JCO.2008.18.0182

      15. Yuen M F, Sablon E, Hui C K, et al. 2001. Factors associated with hepatitis b virus DNA breakthrough in patients receiving prolonged lamivudine therapy. Hepatology, 34(4 Pt 1): 785-791.

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      A Case of Hepatitis B Reactivation due to the Hepatitis B Virus Escape Mutant in a Patient undergoing Chemotherapy *

        Corresponding author: Chunchen Wu, wucc@wh.iov.cn
        Corresponding author: Yang Xu, xuyangs@gmail.com
      • 1. State Key Lab of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China
      • 2. Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
      • 3. Institute of Virology, University Hospital of Essen, Essen D45122, Germany
      • Received Date: 11 September 2012
      • Accepted Date: 05 November 2012
      Fund Project:  National Basic Research Priorities Program of China 2011CB 106303The Fundamental Research Funds for the Central Universities 2012QN140The National Natural Science Foundation of China 31200699

      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.

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