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 [
]. 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 [
- Lok A.S.
- McMahon B.J.
Chronic hepatitis B.
Hepatology. 2007; 45: 507-539https://doi.org/10.1002/hep.21513
]; therefore, TKI has been categorised and placed into a class of moderate risk of reactivation [
- Voican C.
- Mir O.
- Loulergue P.
- et al.
Hepatitis B virus reactivation in patients with solid tumors receiving systemic anticancer treatment.
Ann Oncol. 2016; (mdw414)https://doi.org/10.1093/annonc/mdw414
]. Fortunately, HBV reactivation after TKI therapy is rarely reported in patients with resolved HBV infection [
- Loomba R.
- Liang T.J.
Hepatitis B reactivation associated with immune suppressive and biological modifier therapies: current concepts, management strategies, and future directions.
Gastroenterology. 2017; 152: 1297-1309https://doi.org/10.1053/j.gastro.2017.02.009
]. 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 [
- Chang C.-S.
- Tsai C.-Y.
- Yan S.-L.
Hepatitis B reactivation in patients receiving targeted therapies.
Hematology. 2017; 22: 592-598https://doi.org/10.1080/10245332.2017.1321882
]. 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) [
- 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.
Eur J Canc. 2019; 117: 107-115https://doi.org/10.1016/j.ejca.2019.05.032
] 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.
- 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.
Ann Gastroenterol. 2018; 31: 480https://doi.org/10.20524/aog.2018.0266
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- Chronic hepatitis B.Hepatology. 2007; 45: 507-539https://doi.org/10.1002/hep.21513
- Hepatitis B virus reactivation in patients with solid tumors receiving systemic anticancer treatment.Ann Oncol. 2016; (mdw414)https://doi.org/10.1093/annonc/mdw414
- Hepatitis B reactivation associated with immune suppressive and biological modifier therapies: current concepts, management strategies, and future directions.Gastroenterology. 2017; 152: 1297-1309https://doi.org/10.1053/j.gastro.2017.02.009
- Hepatitis B reactivation in patients receiving targeted therapies.Hematology. 2017; 22: 592-598https://doi.org/10.1080/10245332.2017.1321882
- Incidence of hepatitis B reactivation during epidermal growth factor receptor tyrosine kinase inhibitor treatment in non–small-cell lung cancer patients.Eur J Canc. 2019; 117: 107-115https://doi.org/10.1016/j.ejca.2019.05.032
- Hepatitis B virus reactivation in HBsAg-negative, anti-HBc-positive patients receiving immunosuppressive therapy: a systematic review.Ann Gastroenterol. 2018; 31: 480https://doi.org/10.20524/aog.2018.0266
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Published online: March 20, 2020
Accepted: February 22, 2020
Received: February 21, 2020
© 2020 Elsevier Ltd. All rights reserved.