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Complement as the enabler of carfilzomib‐induced thrombotic microangiopathy
Author(s) -
Blasco Miquel,
MartínezRoca Alexandra,
RodríguezLobato Luis G.,
GarciaHerrera 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,
DiazRicart Maribel,
Palomo Marta
Publication year - 2021
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.16796
Subject(s) - thrombotic microangiopathy , carfilzomib , complement system , cd59 , medicine , complement membrane attack complex , multiple myeloma , alternative complement pathway , eculizumab , immunology , disease , oncology , antibody , lenalidomide
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.