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CLL-147 Chronic Hepatitis B Infection Management During Long-Term Follow-Up of Chronic Lymphocytic Leukemia (CLL) Treated With Multiple Lines of Chemoimmunotherapy, Including Ibrutinib
Hepatitis B virus (HBV) reactivation may occur in B cell dysfunction, especially in those B cells that have previously met with HBV surface antigen (HBsAg), despite prior acquired immunity. Ibrutinib is a Bruton's tyrosine kinase inhibitor (BTKi) that regulates B-cell signaling, resulting in B-...
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Published in: | Clinical lymphoma, myeloma and leukemia myeloma and leukemia, 2023-09, Vol.23, p.S322-S322 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Hepatitis B virus (HBV) reactivation may occur in B cell dysfunction, especially in those B cells that have previously met with HBV surface antigen (HBsAg), despite prior acquired immunity. Ibrutinib is a Bruton's tyrosine kinase inhibitor (BTKi) that regulates B-cell signaling, resulting in B-cell maturation. HBV reactivation during treatment with tyrosine kinase inhibitors is still a dilemma; there is little knowledge about how to protect against acute reactivation of HBV.
To present a case report of chronic HBV reactivation during ibrutinib treatment.
A 75-year-old man previously diagnosed with Rai stage 2 CLL and naturally immunized against HBV was admitted to our clinic. In May 2017, a rituximab + chlorambucil (R-Cl) protocol was administered with tenofovir disoproxil fumarate prophylaxis. After 6 cycles of chemotherapy, he was in remission. No HBV reactivation occurred during prophylaxis or the treatment-free follow-up interval. Three years after his last dose of chemotherapy, in September 2020, he had weight loss, rapidly growing lymphadenopathy, and anemia. Due to a relatively low performance status score, ibrutinib 420 mg/d was administered. After the ninth cycle of ibrutinib, elevated liver enzymes were detected. His HBV DNA level was increased, so entecavir was administered; after the third cycle, the HBV DNA level did not decrease enough, so his treatment was switched to tenofovir alafenamide fumarate (TAF). After 3 cycles of TAF, continued follow up for chronic inactive HBV and CLL.
Ibrutinib has a potential role in B-cell signaling, causing alteration of cellular immunity. On the other hand, ibrutinib also facilitates B-cell maturation, allowing immunomodulation of T cells, which are also considered amendatory for the immune system. Primary or secondary prophylaxis for HBV, especially for carriers before initiation of ibrutinib, is still controversial according to local and international guidelines. An individualized approach and risk assessment is still considered the best option for HBV prophylaxis. |
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ISSN: | 2152-2650 2152-2669 |
DOI: | 10.1016/S2152-2650(23)01100-X |