Abstract

Introduction: It has recently been reported that hepatitis B (HBV) reactivation in patients with lymphoma who are hepatitis B surface antigen (HBsAg)-negative during or after cytotoxic therapy occurs after the use of rituximab and stem cell transplantation. However, clinical data on HBV reactivation in multiple myeloma (MM) patients has not been extensively reported. Bortezomib, a selective proteasome inhibitor, has had remarkable activity in relapsed multiple myeloma (MM). Although well-tolerated, reactivation of viral infections may emerge as a problem in this setting (2). We present a case of MM who developed HBV after bortezomib therapy. Case: A 73-year-old Russian female who had history of marginal cell lymphoma was monitored without needing therapy. Three years later, she developed MM requiring vertebral decompression and focal radiation. While on therapy renal failure ensued and she was started on bortezomib and doxorubicin. After five cycles, this was switched to lenalidomide. Prior to therapy, she was seropositive for anti HBs and HBc with negative HBsAg, indicating a prior natural infection. Her aminotransferase level was normal. She was serially monitored for hepatitis serology at dialysis, with seroconversion one month after change in therapy. Tenofovir was started, and patient recovered her immune status within a few months of therapy. Naranjo adverse drug reaction probability score was 5. Discussion: Bortezomib has significant risk of reactivation of infection by the varicella zoster virus, and acyclovir prophylaxis is recommended. A single case report describes reactivation of HBV after 10 cycles of bortezomib. Bortezomib-associated late hepatitis B reactivation appears to be a unique event that requires further confirmation. The contribution of one cycle of lenalidomide to this seroconversion is unknown.

Highlights

  • It has recently been reported that hepatitis B (HBV) reactivation often occurs after the use of rituximab and stem cell transplantation in patients with lymphoma who are hepatitis B surface antigen (HBsAg) negative

  • An estimated 800,000–1.4 million people in the United States suffer from chronic hepatitis B infection

  • It has been linked to an offense that offsets the host’s immunity and permits viral activity. This can be induced by exposure to immunosuppressants or host immunodeficiency, chemotherapy with rituximab, immune modulation using prednisone, or infliximab for autoimmune conditions

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Summary

Background

An estimated 800,000–1.4 million people in the United States suffer from chronic hepatitis B infection. It has been linked to an offense that offsets the host’s immunity and permits viral activity. This can be induced by exposure to immunosuppressants or host immunodeficiency, chemotherapy with rituximab, immune modulation using prednisone, or infliximab for autoimmune conditions. LEN has immunomodulatory, antiangiogenic, and apoptotic properties [4]. Both of these agents have remarkable activity in multiple myeloma (MM) with manageable toxicity profiles, but reactivation of viral infections can emerge as a problem [5]. Literature is scarce on HBV reactivation induced by immunosuppressive chemotherapy in MM patients. We present a MM patient who developed HBV reactivation after BOR and LEN therapy

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