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Case of hepatitis B virus reactivation after ibrutinib therapy in which the patient remained negative for hepatitis B surface antigens throughout the clinical course
Author(s) -
Tsuruya Kota,
Anzai Kazuya,
Shioyama Shunsuke,
Ito Ayano,
Arase Yoshitaka,
Hirose Shunji,
Tanaka Yasuhito,
Suzuki Hidekazu,
Kagawa Tatehiro
Publication year - 2021
Publication title -
hepatology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.123
H-Index - 75
eISSN - 1872-034X
pISSN - 1386-6346
DOI - 10.1111/hepr.13575
Subject(s) - hbsag , medicine , entecavir , hepatitis b virus , hbeag , immunology , hepatitis b , virology , antibody , gastroenterology , virus , lamivudine
A 71‐year‐old man was diagnosed with B‐cell chronic lymphocytic leukemia. He was negative for hepatitis B surface antigen (HBsAg), positive for antibodies against the hepatitis B surface and core, and negative for hepatitis B virus (HBV)‐DNA before starting chemotherapy. A total of 13 months after the initiation of ibrutinib (a Bruton's tyrosine kinase inhibitor), the patient's alanine aminotransferase levels suddenly increased to 427 U/L. As the level of serum HBV‐DNA increased to 5.2 logIU/mL, a diagnosis of HBV reactivation was made, whereas the patient remained negative for HBsAg. The patient's serum alanine aminotransferase levels normalized after the initiation of entecavir at a dose of 1 mg/day. However, it took >1 year to achieve an undetectable level of HBV‐DNA, even with an add‐on therapy of tenofovir disoproxil fumarate. Interestingly, the patient remained negative for HBsAg throughout the clinical course owing to triple HBsAg escape mutations: Q101K, M133L, and G145A.