CASE REPORT: GUILLAIN BARRÉ SYNDROME AFTER ANTI-BCMA CART-CELL THERAPY
- 1Universidade de Brasília (UnB), Brasília, DF, Brazil
- 2Hospital DF Star, Brasília, DF, Brazil
Abstract
Introduction: Guillain-Barré syndrome (GBS) is a rare autoimmune neuropathy that has emerged as an uncommon and still poorly characterized non-ICANS neurotoxicity associated with CAR T-cell therapies. Objectives: To report a case of GBS following anti-BCMA CART-cell terapy, highlighting the importance of early recognition and the potential prognostic impact of this condition. CASE REPORT: An 79-year-old was diagnosed with IgA/kappa multiple myeloma (R-ISS II) in 2024. He received first-line daratumumab, lenalidomide and dexamethasone (DRd), with biochemical progression after one year, followed by second-line bortezomib, pomalidomide, and dexamethasone (VPd), which was discontinued due to toxicity, and subsequently underwent anti-BCMA CAR T-cell therapy with ciltacabtagene autoleucel. On day +7, the course was notable for grade 2 cytokine release syndrome, which resolved with a single dose of tocilizumab. On day +22, he developed right peripheral facial palsy, left oculomotor nerve involvement, lower limb paraparesis, and neuropathic pain. Diagnostic workup, including neuroimaging, cerebrospinal fluid analysis, revealed albuminocytologic dissociation and electroneuromyography demonstrated acute motor and sensory neuropathy (AMSAN), consistent with GBS. He was treated with intravenous immunoglobulin and dexamethasone, with limited response, followed by plasma exchange, resulting in clinical stabilization and partial improvement. The patient evolved with incomplete recovery and was referred for rehabilitation. Discussion: GBS is a rare neurological complication associated with ciltacabtagene autoleucel, representing a spectrum of non-ICANS neurotoxicities distinct from classic ICANS. It typically has a delayed onset (5–78 days after infusion, mean ∼27 days) and often presents with early cranial nerve involvement, particularly facial nerve palsy, which may precede symmetric ascending weakness, paresthesias, areflexia, and, in severe cases, respiratory failure. Notably, 60% of patients exhibited facial nerve involvement, with cranial neuropathies frequently preceding peripheral symptoms ‒ an atypical presentation that differs from classical GBS. The pathophysiology appears to be related to systemic immune activation and cytokine-mediated collateral injury, rather than direct CAR-T cell attack. Diagnosis is based on albuminocytologic dissociation in cerebrospinal fluid, neuroimaging findings and electroneuromyography. The main treatment is intravenous immunoglobulin, with corticosteroids, plasmapheresis, or targeted therapies used in refractory cases; however, response rates may be lower than in classic GBS, with the possibility of persistent neurological deficits. Conclusion: Late neurological adverse events with ciltacabtagene autoleucel require ongoing surveillance beyond early post-infusion. Early recognition of delayed or atypical neurotoxicity enables prompt intervention and may reduce severe or irreversible outcomes.
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BibTeX
@article{amorim2026case,
title = {{CASE REPORT: GUILLAIN BARRÉ SYNDROME AFTER ANTI-BCMA CART-CELL THERAPY}},
author = {Maria Eduarda SANTOS DE AMORIM and Eduarda RODRIGUES MARTINS and Laís CONTREIRAS BRITO and Matheus Henrique DA SILVA DURÃES and Valéria DE LEMOS BRANDÃO and Paulo Henrique ALVES SOARES},
journal = {Hematology, Transfusion and Cell Therapy},
year = {2026},
month = oct,
doi = {10.1016/j.htct.2026.108457},
url = {https://doi.org/10.1016/j.htct.2026.108457},
note = {CC BY},
}
RIS
TY - JOUR
TI - CASE REPORT: GUILLAIN BARRÉ SYNDROME AFTER ANTI-BCMA CART-CELL THERAPY
AU - Maria Eduarda SANTOS DE AMORIM
AU - Eduarda RODRIGUES MARTINS
AU - Laís CONTREIRAS BRITO
AU - Matheus Henrique DA SILVA DURÃES
AU - Valéria DE LEMOS BRANDÃO
AU - Paulo Henrique ALVES SOARES
PY - 2026
DA - 2026/10/23
JO - Hematology, Transfusion and Cell Therapy
DO - 10.1016/j.htct.2026.108457
UR - https://doi.org/10.1016/j.htct.2026.108457
AB - Introduction: Guillain-Barré syndrome (GBS) is a rare autoimmune neuropathy that has emerged as an uncommon and still poorly characterized non-ICANS neurotoxicity associated with CAR T-cell therapies. Objectives: To report a case of GBS following anti-BCMA CART-cell terapy, highlighting the importance of early recognition and the potential prognostic impact of this condition. CASE REPORT: An 79-year-old was diagnosed with IgA/kappa multiple myeloma (R-ISS II) in 2024. He received first-line daratumumab, lenalidomide and dexamethasone (DRd), with biochemical progression after one year, followed by second-line bortezomib, pomalidomide, and dexamethasone (VPd), which was discontinued due to toxicity, and subsequently underwent anti-BCMA CAR T-cell therapy with ciltacabtagene autoleucel. On day +7, the course was notable for grade 2 cytokine release syndrome, which resolved with a single dose of tocilizumab. On day +22, he developed right peripheral facial palsy, left oculomotor nerve involvement, lower limb paraparesis, and neuropathic pain. Diagnostic workup, including neuroimaging, cerebrospinal fluid analysis, revealed albuminocytologic dissociation and electroneuromyography demonstrated acute motor and sensory neuropathy (AMSAN), consistent with GBS. He was treated with intravenous immunoglobulin and dexamethasone, with limited response, followed by plasma exchange, resulting in clinical stabilization and partial improvement. The patient evolved with incomplete recovery and was referred for rehabilitation. Discussion: GBS is a rare neurological complication associated with ciltacabtagene autoleucel, representing a spectrum of non-ICANS neurotoxicities distinct from classic ICANS. It typically has a delayed onset (5–78 days after infusion, mean ∼27 days) and often presents with early cranial nerve involvement, particularly facial nerve palsy, which may precede symmetric ascending weakness, paresthesias, areflexia, and, in severe cases, respiratory failure. Notably, 60% of patients exhibited facial nerve involvement, with cranial neuropathies frequently preceding peripheral symptoms ‒ an atypical presentation that differs from classical GBS. The pathophysiology appears to be related to systemic immune activation and cytokine-mediated collateral injury, rather than direct CAR-T cell attack. Diagnosis is based on albuminocytologic dissociation in cerebrospinal fluid, neuroimaging findings and electroneuromyography. The main treatment is intravenous immunoglobulin, with corticosteroids, plasmapheresis, or targeted therapies used in refractory cases; however, response rates may be lower than in classic GBS, with the possibility of persistent neurological deficits. Conclusion: Late neurological adverse events with ciltacabtagene autoleucel require ongoing surveillance beyond early post-infusion. Early recognition of delayed or atypical neurotoxicity enables prompt intervention and may reduce severe or irreversible outcomes.
SN - 2531-1379
SN - 2531-1387
ER -