Journal of pharmaceutical health care and sciences · 2025
A case of hepatitis B virus reactivation after elranatamab therapy in a patient with multiple myeloma.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Nishimura Naoaki, Nakashima Hajime, Yoshikuni Kenji, Numata Akihiko, Ogawa Ryosuke
Аннотация
BACKGROUND: Multiple myeloma is an incurable hematologic malignancy. Although novel treatments have improved outcomes, many patients continue to relapse and eventually develop treatment resistance. Elranatamab, a bispecific antibody, has demonstrated promising efficacy in patients with relapsed/refractory multiple myeloma. However, clinical experience with elranatamab remains limited, and its immunomodulatory effects may increase the risk of opportunistic infections and viral reactivation. Here, we describe hepatitis B virus (HBV) reactivation in a patient with resolved HBV infection who was treated with elranatamab.
CASE PRESENTATION: A 76-year-old man with resolved HBV infection and treatment-resistant multiple myeloma received elranatamab. HBV DNA was not detected prior to treatment. On day 17 after initiation, an outpatient specimen returned as detectable but below the assay's lower limit of quantification (< 1.0 log10 IU/mL). Elranatamab was discontinued due to hypotension, and the patient was subsequently hospitalized one week later with pneumonia. On day 78 after initiation, HBV DNA increased to 3.6 log10 IU/mL with transaminase elevation; tenofovir alafenamide 25 mg once daily was started the same day, after which HBV DNA declined to below the lower limit of quantification.
CONCLUSIONS: Although elranatamab-specific information on HBV reactivation is limited, this case highlights a clinically relevant risk. Clinicians should remain vigilant for reactivation in patients receiving elranatamab, particularly those with resolved infection. Regular HBV DNA monitoring and prompt initiation of nucleos(t)ide analog therapy are essential to prevent severe complications, including fulminant hepatitis. Additionally, in the context of profound hypogammaglobulinemia during or after elranatamab, intravenous immunoglobulin may be considered to mitigate infection risk.
CASE PRESENTATION: A 76-year-old man with resolved HBV infection and treatment-resistant multiple myeloma received elranatamab. HBV DNA was not detected prior to treatment. On day 17 after initiation, an outpatient specimen returned as detectable but below the assay's lower limit of quantification (< 1.0 log10 IU/mL). Elranatamab was discontinued due to hypotension, and the patient was subsequently hospitalized one week later with pneumonia. On day 78 after initiation, HBV DNA increased to 3.6 log10 IU/mL with transaminase elevation; tenofovir alafenamide 25 mg once daily was started the same day, after which HBV DNA declined to below the lower limit of quantification.
CONCLUSIONS: Although elranatamab-specific information on HBV reactivation is limited, this case highlights a clinically relevant risk. Clinicians should remain vigilant for reactivation in patients receiving elranatamab, particularly those with resolved infection. Regular HBV DNA monitoring and prompt initiation of nucleos(t)ide analog therapy are essential to prevent severe complications, including fulminant hepatitis. Additionally, in the context of profound hypogammaglobulinemia during or after elranatamab, intravenous immunoglobulin may be considered to mitigate infection risk.