Editorial
Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2024; 30(25): 3147-3151
Published online Jul 7, 2024. doi: 10.3748/wjg.v30.i25.3147
Risk of hepatic decompensation from hepatitis B virus reactivation in hematological malignancy treatments
Michele Barone
Michele Barone, Section of Gastroenterology, Department of Precision and Regenerative Medicine -Jonian Area- University of Bari, Bari 70124, Italy
Author contributions: Barone M conceived and wrote this manuscript.
Conflict-of-interest statement: The author reports no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: Https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Michele Barone, MD, PhD, Adjunct Associate Professor, Section of Gastroenterology, Department of Precision and Regenerative Medicine -Jonian Area- University of Bari, Piazza G Cesare 11, Bari 70124, Italy. michele.barone@uniba.it
Received: March 25, 2024
Revised: May 20, 2024
Accepted: June 6, 2024
Published online: July 7, 2024
Processing time: 97 Days and 21 Hours
Abstract

In this editorial, we discussed the apparent discrepancy between the findings described by Colapietro et al, in their case report and data found in the literature. Colapietro et al reported a case of hepatitis B virus (HBV)-related hepatic decompensation in a patient with chronic myeloid leukemia and a previously resolved HBV infection who was receiving Bruton’s tyrosine kinase (BTK) inhibitor therapy. First of all, we recapitulated the main aspects of the immune system involved in the response to HBV infection in order to underline the role of the innate and adaptive response, focusing our attention on the protective role of anti-HBs. We then carefully analyzed literature data on the risk of HBV reactivation (HBVr) in patients with previous HBV infection who were treated with either tyrosine kinase inhibitors or BTK inhibitors for their hematologic malignancies. Based on literature data, we suggested that several factors may contribute to the different risks of HBVr: The type of hematologic malignancy; the type of therapy (BTK inhibitors, especially second-generation, seem to be at a higher risk of HBVr than those with tyrosine kinase inhibitors); previous exposure to an anti-CD20 as first-line therapy; and ethnicity and HBV genotype. Therefore, the warning regarding HBVr in the specific setting of patients with hematologic malignancies requires further investigation.

Keywords: Hematological malignancy; Hepatitis; Hepatitis B virus-DNA; Bruton’s tyrosine kinase; Previously resolved hepatitis B virus infection

Core Tip: All literature data on the risk of hepatitis B virus reactivation (HBVr) in patients with a previously resolved HBV infection and treated with tyrosine kinase inhibitors for their hematologic malignancies are based on retrospective studies. Different risks of HBVr in these patients may depend on the type of hematologic malignancy, the type of therapy (tyrosine kinase inhibitors or Bruton’s tyrosine kinase inhibitors), previous exposure to an anti-CD20 as first-line therapy, and both ethnicity and HBV genotype. Therefore, the warning regarding HBVr in this specific clinical setting requires further investigation.