Asthmatics with concordant eosinophilic disease classified according to their serum IgE status.


Journal

Respiratory medicine and research
ISSN: 2590-0412
Titre abrégé: Respir Med Res
Pays: France
ID NLM: 101746324

Informations de publication

Date de publication:
May 2021
Historique:
received: 21 03 2020
revised: 14 10 2020
accepted: 01 11 2020
pubmed: 1 1 2021
medline: 29 10 2021
entrez: 31 12 2020
Statut: ppublish

Résumé

Eosinophilic inflammation has long been associated with asthma. Looking at systemic and airway eosinophilia, we have recently identified a group of patients exhibiting diffuse eosinophilic inflammation. Among the mechanisms governing eosinophilic inflammation, IgE-mediated mast cell activation is a key event leading to eosinophilia in atopic asthmatics. We conducted a retrospective study on our asthma clinic database containing more than 1500 patients and identified 205 asthmatics with successful sputum induction and concordant eosinophilic phenotype. This phenotype was defined as a sputum eosinophil count≥3% and a blood eosinophils concentration≥400cells/mm The largest group of asthmatics displaying concordant eosinophilic phenotype had a raised total serum IgE and atopy (45%). IgE-low non-atopic concordant eosinophilic asthma was a predominantly late onset disease, exhibited a more intense airway eosinophilic inflammation (P<0.05), required more often maintenance treatment with oral corticosteroids (P<0.05) but, surprisingly, had a reduced level of bronchial hyperresponsiveness to methacholine (P<0.05) despite similar baseline airway calibre impairment. The more severe airway eosinophilic inflammation in IgE-low non-atopic asthmatics despite similar treatment with ICS and a higher burden of OCS points to a certain corticosteroid resistance in this asthma phenotype.

Sections du résumé

BACKGROUND BACKGROUND
Eosinophilic inflammation has long been associated with asthma. Looking at systemic and airway eosinophilia, we have recently identified a group of patients exhibiting diffuse eosinophilic inflammation. Among the mechanisms governing eosinophilic inflammation, IgE-mediated mast cell activation is a key event leading to eosinophilia in atopic asthmatics.
METHODS METHODS
We conducted a retrospective study on our asthma clinic database containing more than 1500 patients and identified 205 asthmatics with successful sputum induction and concordant eosinophilic phenotype. This phenotype was defined as a sputum eosinophil count≥3% and a blood eosinophils concentration≥400cells/mm
RESULTS RESULTS
The largest group of asthmatics displaying concordant eosinophilic phenotype had a raised total serum IgE and atopy (45%). IgE-low non-atopic concordant eosinophilic asthma was a predominantly late onset disease, exhibited a more intense airway eosinophilic inflammation (P<0.05), required more often maintenance treatment with oral corticosteroids (P<0.05) but, surprisingly, had a reduced level of bronchial hyperresponsiveness to methacholine (P<0.05) despite similar baseline airway calibre impairment.
CONCLUSION CONCLUSIONS
The more severe airway eosinophilic inflammation in IgE-low non-atopic asthmatics despite similar treatment with ICS and a higher burden of OCS points to a certain corticosteroid resistance in this asthma phenotype.

Identifiants

pubmed: 33383519
pii: S2590-0412(20)30053-2
doi: 10.1016/j.resmer.2020.100797
pii:
doi:

Substances chimiques

Immunoglobulin E 37341-29-0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

100797

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

Auteurs

S Gerday (S)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium. Electronic address: sgerday@doct.uliege.be.

F Schleich (F)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium.

M Henket (M)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium.

F Guissard (F)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium.

V Paulus (V)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium.

R Louis (R)

Department of Pulmonary Medicine, CHU Sart-Tilman, Liege, GIGA I(3) Research Group, University of Liege, 4000 Liege, Belgium.

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Classifications MeSH