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Tocilizumab for severe cytokine‐release syndrome after haploidentical donor transplantation in a patient with refractory Epstein‐Barr virus‐positive diffuse large B‐cell lymphoma
Author(s) -
Ureshino Hiroshi,
Ando Toshihiko,
Kizuka Haruna,
Kusaba Kana,
Sano Haruhiko,
Nishioka Atsujiro,
Itamura Hidekazu,
Shindo Takero,
Kubota Yasushi,
Kojima Kensuke,
Kimura Shinya
Publication year - 2018
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/hon.2481
Subject(s) - tocilizumab , cytokine release syndrome , medicine , immunosuppression , refractory (planetary science) , lymphoma , transplantation , immunology , cytokine , gastroenterology , chemotherapy , t cell , chimeric antigen receptor , immune system , rheumatoid arthritis , physics , astrobiology
It has been well documented that patients may develop cytokine‐release syndrome (CRS) following the administration of monoclonal antibodies, such as chimeric antigen receptor‐modified T cell. Cytokine‐release syndrome is a common complication in patients who have received haploidentical donor allogeneic haematopoietic cell transplantation (haplo‐HCT). Although severe CRS after haplo‐HCT is a potentially life‐threatening toxicity, a standard treatment has not been established. Cytokine blockade with tocilizumab, an anti‐IL‐6 receptor antibody, has been effective for the treatment of patients with CRS after chimeric antigen receptor‐modified T‐cell treatment and has also improved CRS after haplo‐HCT. A 46‐year‐old man was diagnosed with haemophagocytic syndrome associated with Epstein‐Barr virus‐positive diffuse large B‐cell lymphoma. Salvage chemotherapy was unsuccessful; consequently, he received haplo‐HCT. On day +4, he developed grade 3 CRS, subsequently high‐dose corticosteroid initiated. Nevertheless, on day +6, he developed grade 4 CRS, resulting in requirement for ventilator support and multiple vasopressors. Corticosteroid could not improve severe CRS; therefore, tocilizumab was administered on day +14. Serum C‐reactive protein level transiently decreased and weaned multiple vasopressors. Although CRS improved, he developed candidaemia; consequently, he died on day +34. Tocilizumab could transiently improve severe CRS after haplo‐HCT. Although tocilizumab may have led to the improvement of CRS, a remaining concern is whether it inhibited the patient's ability to mount antifungal immunity, leading to their demise.