Basophil activation test for allergic and febrile non-haemolytic transfusion reactions among paediatric patients with haematological or oncological disease.


Journal

Vox sanguinis
ISSN: 1423-0410
Titre abrégé: Vox Sang
Pays: England
ID NLM: 0413606

Informations de publication

Date de publication:
Jan 2023
Historique:
revised: 09 09 2022
received: 21 06 2022
accepted: 18 09 2022
pubmed: 13 10 2022
medline: 17 1 2023
entrez: 12 10 2022
Statut: ppublish

Résumé

Allergic transfusion reactions (ATRs) and febrile non-haemolytic transfusion reactions (FNHTRs) are common, although their mechanisms remain unclear. Immunoglobulin E (IgE)-mediated type I hypersensitivity may be involved in the pathogenesis of ATR. A basophil activation test (BAT) may help elucidate this process. The BAT was based on peripheral blood samples from paediatric patients with a haematological or oncological disease and on samples of residual blood products transfused in each case. Dasatinib was used to evaluate whether basophil activation was mediated by an IgE-dependent pathway. Twenty-seven patients with and 19 patients without ATR/FNHTR were included in this study, respectively. The median BAT values associated with ATR- (n = 41) and FNHTR-causing (n = 5) blood products were 22.1% (range = 6.1%-77.0%) and 27.8% (range = 15.2%-47.8%), respectively, which were higher than the median value of 8.5% (range = 1.1%-40.9%) observed in blood products without a transfusion reaction. Dasatinib suppressed basophil activity. BAT values were comparable in patients with ATR regardless of severity. Meanwhile, BAT values analysed with blood products non-causal for ATR/FNHTR were higher in patients with ATR/FNHTR than in those without. The IgE-mediated type I hypersensitivity may be involved in the pathogenesis of ATR and FNHTR. BAT analyses may help elucidate the underlying mechanisms and identify patients at risk.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
Allergic transfusion reactions (ATRs) and febrile non-haemolytic transfusion reactions (FNHTRs) are common, although their mechanisms remain unclear. Immunoglobulin E (IgE)-mediated type I hypersensitivity may be involved in the pathogenesis of ATR. A basophil activation test (BAT) may help elucidate this process.
MATERIALS AND METHODS METHODS
The BAT was based on peripheral blood samples from paediatric patients with a haematological or oncological disease and on samples of residual blood products transfused in each case. Dasatinib was used to evaluate whether basophil activation was mediated by an IgE-dependent pathway.
RESULTS RESULTS
Twenty-seven patients with and 19 patients without ATR/FNHTR were included in this study, respectively. The median BAT values associated with ATR- (n = 41) and FNHTR-causing (n = 5) blood products were 22.1% (range = 6.1%-77.0%) and 27.8% (range = 15.2%-47.8%), respectively, which were higher than the median value of 8.5% (range = 1.1%-40.9%) observed in blood products without a transfusion reaction. Dasatinib suppressed basophil activity. BAT values were comparable in patients with ATR regardless of severity. Meanwhile, BAT values analysed with blood products non-causal for ATR/FNHTR were higher in patients with ATR/FNHTR than in those without.
CONCLUSION CONCLUSIONS
The IgE-mediated type I hypersensitivity may be involved in the pathogenesis of ATR and FNHTR. BAT analyses may help elucidate the underlying mechanisms and identify patients at risk.

Identifiants

pubmed: 36224113
doi: 10.1111/vox.13365
doi:

Substances chimiques

Dasatinib RBZ1571X5H
Immunoglobulin E 37341-29-0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

41-48

Informations de copyright

© 2022 International Society of Blood Transfusion.

Références

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Auteurs

Yoko Usami (Y)

Department of Laboratory Medicine, Shinshu University Hospital, Matsumoto, Japan.
Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.

Ryu Yanagisawa (R)

Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.
Division of Blood Transfusion, Shinshu University Hospital, Matsumoto, Japan.
Centre for Advanced Cell Therapy, Shinshu University Hospital, Matsumoto, Japan.

Ryo Kanai (R)

Division of Blood Transfusion, Shinshu University Hospital, Matsumoto, Japan.

Yuichiro Ide (Y)

Department of Laboratory Medicine, Shinshu University Hospital, Matsumoto, Japan.
Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.

Saori Konno (S)

Department of Laboratory Medicine, Shinshu University Hospital, Matsumoto, Japan.
Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.

Maria Iwama (M)

Department of Laboratory Medicine, Nagano Children's Hospital, Azumino, Japan.

Akiko Futatsugi (A)

Department of Laboratory Medicine, Nagano Children's Hospital, Azumino, Japan.

Tomoko Takeshita (T)

Department of Laboratory Medicine, Nagano Children's Hospital, Azumino, Japan.

Yu Furui (Y)

Department of Haematology and Oncology, Nagano Children's Hospital, Azumino, Japan.

Kazutoshi Komori (K)

Department of Haematology and Oncology, Nagano Children's Hospital, Azumino, Japan.

Takashi Kurata (T)

Department of Haematology and Oncology, Nagano Children's Hospital, Azumino, Japan.

Shoji Saito (S)

Department of Paediatrics, Shinshu University School of Medicine, Matsumoto, Japan.

Miyuki Tanaka (M)

Department of Paediatrics, Shinshu University School of Medicine, Matsumoto, Japan.

Yozo Nakazawa (Y)

Department of Paediatrics, Shinshu University School of Medicine, Matsumoto, Japan.

Kazuo Sakashita (K)

Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.
Department of Haematology and Oncology, Nagano Children's Hospital, Azumino, Japan.

Minoru Tozuka (M)

Life Science Research Centre, Nagano Children's Hospital, Azumino, Japan.
Department of Laboratory Medicine, Nagano Children's Hospital, Azumino, Japan.

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