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 [
[1]
]. 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
[
[2]
]; 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
[3]
]. Fortunately, HBV reactivation after TKI therapy is rarely reported in patients
with resolved HBV infection [
[4]
]. 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 [
[5]
]. 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) [
[6]
] 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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Article info
Publication history
Published online: March 20, 2020
Accepted:
February 22,
2020
Received:
February 21,
2020
Identification
Copyright
© 2020 Elsevier Ltd. All rights reserved.