Exploring the relevance and extent of small airways dysfunction in asthma (ATLANTIS): baseline data from a prospective cohort study.


Journal

The Lancet. Respiratory medicine
ISSN: 2213-2619
Titre abrégé: Lancet Respir Med
Pays: England
ID NLM: 101605555

Informations de publication

Date de publication:
05 2019
Historique:
received: 20 09 2018
revised: 26 11 2018
accepted: 18 12 2018
pubmed: 17 3 2019
medline: 21 4 2020
entrez: 17 3 2019
Statut: ppublish

Résumé

Small airways dysfunction (SAD) is well recognised in asthma, yet its role in the severity and control of asthma is unclear. This study aimed to assess which combination of biomarkers, physiological tests, and imaging markers best measure the presence and extent of SAD in patients with asthma. In this baseline assessment of a multinational prospective cohort study (the Assessment of Small Airways Involvement in Asthma [ATLANTIS] study), we recruited participants with and without asthma (defined as Global Initiative for Asthma severity stages 1-5) from general practices, the databases of chest physicians, and advertisements at 29 centres across nine countries (Brazil, China, Germany, Italy, Spain, the Netherlands, the UK, the USA, and Canada). All participants were aged 18-65 years, and participants with asthma had received a clinical diagnosis of asthma more than 6 months ago that had been confirmed by a chest physician. This diagnosis required support by objective evidence at baseline or during the past 5 years, which could be: positive airway hyperresponsiveness to methacholine, positive reversibility (a change in FEV Between June 30, 2014, and March 3, 2017, we recruited and evaluated 773 participants with asthma and 99 control participants. All physiological measures contributed to the clinical SAD model with the structural equation modelling analysis. The prevalence of SAD in asthma was dependent on the measure used; we found the lowest prevalence of SAD associated with acinar airway ventilation heterogeneity (S SAD is a complex and silent signature of asthma that is likely to be directly or indirectly captured by combinations of physiological tests, such as spirometry, body plethysmography, impulse oscillometry, and multiple breath nitrogen washout. SAD is present across patients with all severities of asthma, but it is particularly prevalent in severe disease. The clinical classification of SAD into two groups (a milder and a more severe group) by use of impulse oscillometry and spirometry, which are easy to use, is meaningful given its association with GINA severity stages, asthma control, quality of life, and exacerbations. Chiesi Farmaceutici SpA.

Sections du résumé

BACKGROUND
Small airways dysfunction (SAD) is well recognised in asthma, yet its role in the severity and control of asthma is unclear. This study aimed to assess which combination of biomarkers, physiological tests, and imaging markers best measure the presence and extent of SAD in patients with asthma.
METHODS
In this baseline assessment of a multinational prospective cohort study (the Assessment of Small Airways Involvement in Asthma [ATLANTIS] study), we recruited participants with and without asthma (defined as Global Initiative for Asthma severity stages 1-5) from general practices, the databases of chest physicians, and advertisements at 29 centres across nine countries (Brazil, China, Germany, Italy, Spain, the Netherlands, the UK, the USA, and Canada). All participants were aged 18-65 years, and participants with asthma had received a clinical diagnosis of asthma more than 6 months ago that had been confirmed by a chest physician. This diagnosis required support by objective evidence at baseline or during the past 5 years, which could be: positive airway hyperresponsiveness to methacholine, positive reversibility (a change in FEV
FINDINGS
Between June 30, 2014, and March 3, 2017, we recruited and evaluated 773 participants with asthma and 99 control participants. All physiological measures contributed to the clinical SAD model with the structural equation modelling analysis. The prevalence of SAD in asthma was dependent on the measure used; we found the lowest prevalence of SAD associated with acinar airway ventilation heterogeneity (S
INTERPRETATION
SAD is a complex and silent signature of asthma that is likely to be directly or indirectly captured by combinations of physiological tests, such as spirometry, body plethysmography, impulse oscillometry, and multiple breath nitrogen washout. SAD is present across patients with all severities of asthma, but it is particularly prevalent in severe disease. The clinical classification of SAD into two groups (a milder and a more severe group) by use of impulse oscillometry and spirometry, which are easy to use, is meaningful given its association with GINA severity stages, asthma control, quality of life, and exacerbations.
FUNDING
Chiesi Farmaceutici SpA.

Identifiants

pubmed: 30876830
pii: S2213-2600(19)30049-9
doi: 10.1016/S2213-2600(19)30049-9
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT02123667']

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

402-416

Investigateurs

Emilio Pizzichini (E)
Alberto Cukier (A)
Rafael Stelmach (R)
Ronald Olivenstein (R)
Qingling Zhang (Q)
Philipp Badorrek (P)
Christian Gessner (C)
Nicola Scichilone (N)
Alfredo Chetta (A)
Pierluigi Paggiaro (P)
Stefano Milleri (S)
Mariella D'Amato (M)
Antonio Spanevello (A)
Maria Pia Foschino (MP)
Willem Germen Boersma (WG)
Marielle Broeders (M)
J Sebastiaan Vroegop (JS)
Vicente Plaza Moral (V)
Ratko Djukanovic (R)
Omar Usmani (O)
Robert Schilz (R)
Richard Martin (R)
Nicola Hanania (N)

Commentaires et corrections

Type : CommentIn
Type : ErratumIn
Type : CommentIn
Type : CommentIn

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Dirkje S Postma (DS)

Department of Pulmonology, Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, Netherlands. Electronic address: d.s.postma@gmail.com.

Chris Brightling (C)

Institute for Lung Health, National Institute for Health Research Biomedical Research Centre, University of Leicester, Leicester, UK.

Simonetta Baldi (S)

Institute for Lung Health, National Institute for Health Research Biomedical Research Centre, University of Leicester, Leicester, UK; Department of Global Clinical Development, Chiesi SAS, Bois-Colombes, France.

Maarten Van den Berge (M)

Department of Pulmonology, Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Leonardo M Fabbri (LM)

Research Centre on Asthma and COPD, University of Ferrara, Ferrara, Italy; COPD Centre, Sahlgrenska University Hospital, Gothenburg, Sweden.

Alessandra Gagnatelli (A)

Department of Global Clinical Development, Chiesi Farmaceutici SpA, Parma, Italy.

Alberto Papi (A)

Research Centre on Asthma and COPD, University of Ferrara, Ferrara, Italy.

Thys Van der Molen (T)

Department of General Practice, Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, Netherlands.

Klaus F Rabe (KF)

LungenClinic, Grosshansdorf, Germany; Department of Medicine, Christian Albrechts University, Kiel, Germany; Airway Research Center North, German Center for Lung Research (DZL), Hannover, Germany.

Salman Siddiqui (S)

Institute for Lung Health, National Institute for Health Research Biomedical Research Centre, University of Leicester, Leicester, UK.

Dave Singh (D)

Centre for Respiratory Medicine and Allergy, University Hospital of South Manchester, University of Manchester, Manchester, UK.

Gabriele Nicolini (G)

Department of Global Clinical Development, Chiesi Farmaceutici SpA, Parma, Italy.

Monica Kraft (M)

University of Arizona College of Medicine, Department of Medicine, Tucson, AZ, USA.

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