Small airway dysfunction as predictor and marker for clinical response to biological therapy in severe eosinophilic asthma: a longitudinal observational study.
Aged
Antibodies, Monoclonal, Humanized
/ pharmacology
Asthma
/ diagnosis
Biological Therapy
/ methods
Female
Forced Expiratory Volume
/ drug effects
Humans
Longitudinal Studies
Male
Middle Aged
Predictive Value of Tests
Prospective Studies
Pulmonary Eosinophilia
/ diagnosis
Severity of Illness Index
Treatment Outcome
Anti-T2 biologics
Asthma control
FEV1
Small airways dysfunction
Journal
Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633
Informations de publication
Date de publication:
21 Oct 2020
21 Oct 2020
Historique:
received:
29
06
2020
accepted:
11
10
2020
entrez:
22
10
2020
pubmed:
23
10
2020
medline:
21
8
2021
Statut:
epublish
Résumé
Anti-T2 biological therapies have proven to effectively reduce acute exacerbations and daily doses of oral steroids in severe eosinophilic asthma. Despite the remarkable clinical efficacy, there are usually only moderate improvements in airflow limitation, suggesting that other measures of lung function like small airway dysfunction (SAD) might better reflect the clinical response. We aimed to investigate if measures of small airway function would predict and correlate with the clinical response to anti-T2 therapy. We studied data of patients who were previously included in the German prospective longitudinal All Age Asthma Cohort (ALLIANCE) that recruits asthma patients of all severity grades and inflammatory phenotypes. The selection criteria for this analysis were adult patients with severe eosinophilic asthma under treatment with anti-T2 biological agents. Asthma control was assessed by asthma control test (ACT) and number of severe exacerbations. Small airway function was assessed by the frequency dependence of resistance (FDR, R5-20)) derived from impulse oscillometry (IOS) and the mean forced expiratory flow between 25 and 75% of the forced vital capacity (FEF 20 patients were included (mean age, 59 ± 9 years; 60% female; mean body mass index (BMI), 27.6 ± 5.4 kg/m Our data suggest that severe SAD may represent a distinct phenotype of eosinophilic asthma that substantially improves under anti-T2 biological therapy. Measures of small airway function might be useful in selecting appropriate patients qualifying for anti-T2 biological therapy in addition to blood eosinophil count.
Sections du résumé
BACKGROUND
BACKGROUND
Anti-T2 biological therapies have proven to effectively reduce acute exacerbations and daily doses of oral steroids in severe eosinophilic asthma. Despite the remarkable clinical efficacy, there are usually only moderate improvements in airflow limitation, suggesting that other measures of lung function like small airway dysfunction (SAD) might better reflect the clinical response. We aimed to investigate if measures of small airway function would predict and correlate with the clinical response to anti-T2 therapy.
METHODS
METHODS
We studied data of patients who were previously included in the German prospective longitudinal All Age Asthma Cohort (ALLIANCE) that recruits asthma patients of all severity grades and inflammatory phenotypes. The selection criteria for this analysis were adult patients with severe eosinophilic asthma under treatment with anti-T2 biological agents. Asthma control was assessed by asthma control test (ACT) and number of severe exacerbations. Small airway function was assessed by the frequency dependence of resistance (FDR, R5-20)) derived from impulse oscillometry (IOS) and the mean forced expiratory flow between 25 and 75% of the forced vital capacity (FEF
RESULTS
RESULTS
20 patients were included (mean age, 59 ± 9 years; 60% female; mean body mass index (BMI), 27.6 ± 5.4 kg/m
CONCLUSION
CONCLUSIONS
Our data suggest that severe SAD may represent a distinct phenotype of eosinophilic asthma that substantially improves under anti-T2 biological therapy. Measures of small airway function might be useful in selecting appropriate patients qualifying for anti-T2 biological therapy in addition to blood eosinophil count.
Identifiants
pubmed: 33087134
doi: 10.1186/s12931-020-01543-5
pii: 10.1186/s12931-020-01543-5
pmc: PMC7579879
doi:
Substances chimiques
Antibodies, Monoclonal, Humanized
0
Types de publication
Letter
Observational Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
278Références
J Allergy Clin Immunol. 1997 Jul;100(1):44-51
pubmed: 9257786
N Engl J Med. 2017 Jun 22;376(25):2448-2458
pubmed: 28530840
Clin Exp Allergy. 2014 Apr;44(4):499-507
pubmed: 24341600
N Engl J Med. 2014 Sep 25;371(13):1198-207
pubmed: 25199059
Am J Respir Crit Care Med. 2017 Dec 1;196(11):1385-1395
pubmed: 28862877
BMC Pulm Med. 2018 Aug 20;18(1):140
pubmed: 30126401
Lancet Respir Med. 2015 Nov;3(11):849-58
pubmed: 26493938
Thorax. 2019 Apr;74(4):417-418
pubmed: 30315084
Am J Respir Crit Care Med. 2018 Dec 15;198(12):1578-1581
pubmed: 30156881
Respir Med. 2019 Mar;148:49-53
pubmed: 30827474
Eur Respir J. 2005 Sep;26(3):511-22
pubmed: 16135736
Lancet Respir Med. 2019 May;7(5):402-416
pubmed: 30876830
J Allergy Clin Immunol. 2009 Oct;124(4):719-23.e1
pubmed: 19767070
Am J Respir Crit Care Med. 1996 Jul;154(1):224-30
pubmed: 8680684
Eur Respir J. 2003 Dec;22(6):1026-41
pubmed: 14680096
J Allergy Clin Immunol. 2012 Feb;129(2):381-7, 387.e1
pubmed: 22188824
N Engl J Med. 2014 Sep 25;371(13):1189-97
pubmed: 25199060
PLoS One. 2013 May 15;8(5):e63366
pubmed: 23691036
Eur Respir J. 2005 Aug;26(2):319-38
pubmed: 16055882
Eur Respir J. 2020 Jan 2;55(1):
pubmed: 31558662
N Engl J Med. 2018 Jun 28;378(26):2475-2485
pubmed: 29782224
Am J Respir Crit Care Med. 2011 Sep 1;184(5):602-15
pubmed: 21885636
Eur Respir J. 2014 Feb;43(2):343-73
pubmed: 24337046
J Allergy Clin Immunol Pract. 2020 Jan;8(1):229-235.e3
pubmed: 31299351
Pulm Pharmacol Ther. 2020 Apr;61:101899
pubmed: 31972327
Eur Respir J. 2017 Jan 4;49(1):
pubmed: 28052957