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Case Reports
. 2024 Dec 1;16(12):e74902.
doi: 10.7759/cureus.74902. eCollection 2024 Dec.

Severe Immune Effector Cell-Associated Neurotoxicity Syndrome in a Patient With Multiple Myeloma Treated With Elranatamab

Affiliations
Case Reports

Severe Immune Effector Cell-Associated Neurotoxicity Syndrome in a Patient With Multiple Myeloma Treated With Elranatamab

Taku Kikuchi et al. Cureus. .

Abstract

Elranatamab is an effective drug for triple-class-exposed relapsed/refractory multiple myeloma (TCE-RRMM). In the pivotal study, only grade 1 or 2 immune effector cell-associated neurotoxicity syndrome (ICANS) were reported, and the risk factors for immune effector cell-associated neurotoxicity syndrome have not yet been clearly elucidated. This case report documents the first case of grade 4 ICANS in a patient treated with elranatamab, presenting alongside grade 1 cytokine release syndrome (CRS). The patient had a history of cerebral hemorrhage without residual neurological deficits, but its association with ICANS was unclear. High-dose methylprednisolone therapy was required to manage the condition. Magnetic resonance imaging (MRI) findings were negative for new abnormalities, indicating that previous cerebral events could contribute to the risk of ICANS. This case emphasizes the importance of close monitoring of neurological parameters and prompt intervention for patients receiving elranatamab, regardless of a history of neurological conditions or the presence of neurological symptoms at the time of treatment. As more patients are treated with elranatamab, understanding the risk factors for severe immune effector cell-associated neurotoxicity syndrome (ICANS) will be crucial to ensure timely management and improved patient outcomes. Clinicians should be aware of the potential for severe neurotoxicity, even in patients without current neurological deficits, and pay attention to detecting early symptoms and initiate appropriate treatment promptly.

Keywords: bispecific antibodies; bispecific t cell engager; complication of treatment; elranatamab; immune effector cell-associated neurotoxicity syndrome (icans); relapsed and refractory multiple myeloma.

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Conflict of interest statement

Human subjects: Consent for treatment and open access publication was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: Taku Kikuchi, Nobuhiro Tsukada, Tadao Ishida declare(s) personal fees from Janssen, Sanofi, Phizer, BMS. lecture fee. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Figures

Figure 1
Figure 1. Clinical course from diagnosis to elranatamab administration.
VRD; bortezomib, lenalidomide, and dexamethasone, DVD; daratumumab, bortezomib, and dexemethasone, IsaPD; isatuximab, pomalidomide, and dexamethasone, VTD-PACE; bortezomib, thalidomide, dexamethasone, cisplatin, doxorubicin, cyclophosphamide, and etoposide, ASCT; autologous stem cell transplantation, DKD; daratumumab, carfilzomib, and dexamethasone.
Figure 2
Figure 2. Treatment course following the initiation of elranatamab.
mPSL; methylprednisolone, Dex; dexamethasone, CRS; cytokine release syndrome, ICANS; immune effector cell-associated neurotoxicity syndrome.
Figure 3
Figure 3. Head magnetic resonance imaging before elranatamab therapy.
The arrow indicates hemosiderin deposition in the left thalamus, representing chronic changes from the previous cerebral hemorrhage.
Figure 4
Figure 4. Head magnetic resonance imaging during the state of confusion.
The arrow indicates hemosiderin deposition in the left thalamus, representing chronic changes from the previous cerebral hemorrhage.

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