Complement as the enabler of carfilzomib‐induced thrombotic microangiopathy

Summary Carfilzomib has been associated with the development of thrombotic microangiopathy (TMA) in relapsed/refractory multiple myeloma patients, a severe disease with no currently available aetiological treatment. We evaluated the potential role of terminal complement pathway in four patients with...

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Published in:British journal of haematology 2021-04, Vol.193 (1), p.181-187
Main Authors: Blasco, Miquel, Martínez‐Roca, Alexandra, Rodríguez‐Lobato, Luis G., Garcia‐Herrera, Adriana, Rosiñol, Laura, Castro, Pedro, Fernández, Sara, Quintana, Luis F., Cibeira, María T., Bladé, Joan, Fernández de Larrea, Carlos, Tovar, Natalia, Jimenez, Raquel, Poch, Esteban, Guillen, Elena, Campistol, Josep M., Carreras, Enric, Diaz‐Ricart, Maribel, Palomo, Marta
Format: Article
Language:English
Subjects:
C5b‐9 deposits
carfilzomib
Cell culture
drug‐induced thrombotic microangiopathy
eculizumab
Endothelial cells
Hematology
Membrane attack complex
Multiple myeloma
Thrombotic microangiopathy
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Summary:Summary Carfilzomib has been associated with the development of thrombotic microangiopathy (TMA) in relapsed/refractory multiple myeloma patients, a severe disease with no currently available aetiological treatment. We evaluated the potential role of terminal complement pathway in four patients with carfilzomib‐induced TMA. Membrane attack complex (C5b‐9) deposition on endothelial cells in culture exposed to plasma from patients during the acute phase of the disease suggests complement overactivation as a mechanism of potential endothelial damage in three out of four patients. If confirmed in larger cohorts, C5b‐9 evaluation will allow early identification of patients who could benefit from complement blockade and treatment monitoring.
ISSN:0007-1048
1365-2141
DOI:10.1111/bjh.16796