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Letter to the Editor| Volume 130, P272-274, May 2020

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Hepatitis B flare during osimertinib targeted therapy in a lung cancer patient with a resolved hepatitis B virus infection

  • Po-Hsin Lee
    Affiliations
    Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan
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  • Teng-Yu Lee
    Affiliations
    Division of Gastroenterology & Hepatology, Taichung Veterans General Hospital, Taichung, Taiwan

    Department of Medicine, Chung Shan Medical University, Taichung, Taiwan
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  • Gee-Chen Chang
    Correspondence
    Corresponding author: Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, No. 1650, Sect. 4, Taiwan Boulevard, Taichung, 407 Taiwan.fax: +886 4 23741320.
    Affiliations
    Division of Chest Medicine, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan

    Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan

    Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan
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Published:March 20, 2020DOI:https://doi.org/10.1016/j.ejca.2020.02.026
      Chronic Hepatitis B Virus (HBV) infection is concerning public health issue worldwide. Acute HBV reactivation may occur and cause the development of fulminant hepatitis flare, hepatic failure, and death. Cytotoxic chemotherapy has been known to be a risk factor for HBV reactivation, in which 20–50% of patients may suffer from abrupt hepatitis flare [
      • Lok A.S.
      • McMahon B.J.
      Chronic hepatitis B.
      ]. In addition to chemotherapy, Tyrosine Kinase Inhibitors (TKIs), such as BCR–ABL TKI Imatinib and nilotinib, are also reported to be risk factors surrounding HBV reactivation [
      • Voican C.
      • Mir O.
      • Loulergue P.
      • et al.
      Hepatitis B virus reactivation in patients with solid tumors receiving systemic anticancer treatment.
      ]; therefore, TKI has been categorised and placed into a class of moderate risk of reactivation [
      • Loomba R.
      • Liang T.J.
      Hepatitis B reactivation associated with immune suppressive and biological modifier therapies: current concepts, management strategies, and future directions.
      ]. Fortunately, HBV reactivation after TKI therapy is rarely reported in patients with resolved HBV infection [
      • Chang C.-S.
      • Tsai C.-Y.
      • Yan S.-L.
      Hepatitis B reactivation in patients receiving targeted therapies.
      ]. However, not only has the chimeric oncogene (BCR–ABL) TKI, and Epidermal Growth Factor Receptor (EGFR)-TKI been reported to be a risk factor in HBV reactivation for HBV carriers [
      • Yao Z.-H.
      • Liao W.-Y.
      • Ho C.-C.
      • et al.
      Incidence of hepatitis B reactivation during epidermal growth factor receptor tyrosine kinase inhibitor treatment in non–small-cell lung cancer patients.
      ]. In this case report, we focus on a lung cancer patient with resolved HBV infection (positive hepatitis B core antibodies [anti-HBc], negative surface antigen of hepatitis B virus (HBsAg), and undetectable serum HBV DNA) [
      • Cholongitas E.
      • Haidich A.-B.
      • Apostolidou-Kiouti F.
      • Chalevas P.
      • Papatheodoridis G.V.
      Hepatitis B virus reactivation in HBsAg-negative, anti-HBc-positive patients receiving immunosuppressive therapy: a systematic review.
      ] who experienced HBV reactivation during epidermal growth factor receptor–tyrosine kinase inhibitor (EGFR-TKI) therapy. To the best of our knowledge, this is the first case of EGFR-TKI-induced HBV reactivation in a patient with resolved HBV infection.

      Keywords

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