InforMing the PAthway of COPD Treatment (IMPACT) trial: fibrinogen levels predict risk of moderate or severe exacerbations.


Journal

Respiratory research
ISSN: 1465-993X
Titre abrégé: Respir Res
Pays: England
ID NLM: 101090633

Informations de publication

Date de publication:
28 Apr 2021
Historique:
received: 15 12 2020
accepted: 05 04 2021
entrez: 29 4 2021
pubmed: 30 4 2021
medline: 24 11 2021
Statut: epublish

Résumé

Fibrinogen is the first qualified prognostic/predictive biomarker for exacerbations in patients with chronic obstructive pulmonary disease (COPD). The IMPACT trial investigated fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) triple therapy versus FF/VI and UMEC/VI in patients with symptomatic COPD at risk of exacerbations. This analysis used IMPACT trial data to examine the relationship between fibrinogen levels and exacerbation outcomes in patients with COPD. 8094 patients with a fibrinogen assessment at Week 16 were included, baseline fibrinogen data were not measured. Post hoc analyses were performed by fibrinogen quartiles and by 3.5 g/L threshold. Endpoints included on-treatment exacerbations and adverse events of special interest (AESIs). Rates of moderate, moderate/severe, and severe exacerbations were higher in the highest versus lowest fibrinogen quartile (0.75, 0.92 and 0.15 vs 0.67, 0.79 and 0.10, respectively). The rate ratios (95% confidence interval [CI]) for exacerbations in patients with fibrinogen levels ≥ 3.5 g/L versus those with fibrinogen levels < 3.5 g/L were 1.03 (0.95, 1.11) for moderate exacerbations, 1.08 (1.00, 1.15) for moderate/severe exacerbations, and 1.30 (1.10, 1.54) for severe exacerbations. There was an increased risk of moderate/severe exacerbation (hazard ratio [95% CI]: highest vs lowest quartile 1.16 [1.04, 1.228]; ≥ 3.5 g/L vs < 3.5 g/L: 1.09 [1.00, 1.16]) and severe exacerbation (1.35 [1.09, 1.69]; 1.27 [1.08, 1.47], respectively) with increasing fibrinogen level. Cardiovascular AESIs were highest in patients in the highest fibrinogen quartile. Rate and risk of exacerbations was higher in patients with higher fibrinogen levels. This supports the validity of fibrinogen as a predictive biomarker for COPD exacerbations, and highlights the potential use of fibrinogen as an enrichment strategy in trials examining exacerbation outcomes. NCT02164513.

Sections du résumé

BACKGROUND BACKGROUND
Fibrinogen is the first qualified prognostic/predictive biomarker for exacerbations in patients with chronic obstructive pulmonary disease (COPD). The IMPACT trial investigated fluticasone furoate/umeclidinium/vilanterol (FF/UMEC/VI) triple therapy versus FF/VI and UMEC/VI in patients with symptomatic COPD at risk of exacerbations. This analysis used IMPACT trial data to examine the relationship between fibrinogen levels and exacerbation outcomes in patients with COPD.
METHODS METHODS
8094 patients with a fibrinogen assessment at Week 16 were included, baseline fibrinogen data were not measured. Post hoc analyses were performed by fibrinogen quartiles and by 3.5 g/L threshold. Endpoints included on-treatment exacerbations and adverse events of special interest (AESIs).
RESULTS RESULTS
Rates of moderate, moderate/severe, and severe exacerbations were higher in the highest versus lowest fibrinogen quartile (0.75, 0.92 and 0.15 vs 0.67, 0.79 and 0.10, respectively). The rate ratios (95% confidence interval [CI]) for exacerbations in patients with fibrinogen levels ≥ 3.5 g/L versus those with fibrinogen levels < 3.5 g/L were 1.03 (0.95, 1.11) for moderate exacerbations, 1.08 (1.00, 1.15) for moderate/severe exacerbations, and 1.30 (1.10, 1.54) for severe exacerbations. There was an increased risk of moderate/severe exacerbation (hazard ratio [95% CI]: highest vs lowest quartile 1.16 [1.04, 1.228]; ≥ 3.5 g/L vs < 3.5 g/L: 1.09 [1.00, 1.16]) and severe exacerbation (1.35 [1.09, 1.69]; 1.27 [1.08, 1.47], respectively) with increasing fibrinogen level. Cardiovascular AESIs were highest in patients in the highest fibrinogen quartile.
CONCLUSIONS CONCLUSIONS
Rate and risk of exacerbations was higher in patients with higher fibrinogen levels. This supports the validity of fibrinogen as a predictive biomarker for COPD exacerbations, and highlights the potential use of fibrinogen as an enrichment strategy in trials examining exacerbation outcomes.
TRIAL REGISTRATION BACKGROUND
NCT02164513.

Identifiants

pubmed: 33910578
doi: 10.1186/s12931-021-01706-y
pii: 10.1186/s12931-021-01706-y
pmc: PMC8080358
doi:

Substances chimiques

Biomarkers 0
Bronchodilator Agents 0
Drug Combinations 0
Fibrinogen 9001-32-5

Banques de données

ClinicalTrials.gov
['NCT02164513']

Types de publication

Clinical Trial, Phase III Journal Article Multicenter Study Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

130

Subventions

Organisme : GlaxoSmithKline
ID : Study number: CTT116855

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Auteurs

Dave Singh (D)

Centre for Respiratory Medicine and Allergy, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, The University of Manchester, Manchester University NHS Foundation Trust, Manchester, UK.

Gerard J Criner (GJ)

Pulmonary and Critical Care Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.

Mark T Dransfield (MT)

Division of Pulmonary, Allergy, and Critical Care Medicine, Lung Health Center, University of Alabama at Birmingham, Birmingham, AL, USA.

David M G Halpin (DMG)

University of Exeter Medical School, College of Medicine and Health, University of Exeter, Exeter, UK.

MeiLan K Han (MK)

University of Michigan, Pulmonary & Critical Care, Ann Arbor, MI, USA.

Peter Lange (P)

Department of Public Health, University of Copenhagen, Copenhagen, Denmark.

Sally Lettis (S)

Biostatistics, GlaxoSmithKline, Stockley Park West, Uxbridge, Middlesex, UK.

David A Lipson (DA)

Clinical Sciences, GlaxoSmithKline, Collegeville, PA, USA.
Pulmonary, Allergy and Critical Care Division, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

David Mannino (D)

University of Kentucky College of Public Health, Lexington, KY, USA.

Neil Martin (N)

Global Medical Affairs, GlaxoSmithKline, Brentford, Middlesex, UK.
Institute for Lung Health, University of Leicester, Leicester, UK.

Fernando J Martinez (FJ)

Weill Cornell Medicine, New York, NY, USA.

Bruce E Miller (BE)

Clinical Sciences, GlaxoSmithKline, Collegeville, PA, USA.

Robert Wise (R)

Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Chang-Qing Zhu (CQ)

Biostatistics, GlaxoSmithKline, Stockley Park West, Uxbridge, Middlesex, UK.

David Lomas (D)

Division of Medicine, UCL Respiratory, Rayne Building, University College London, London, WC1E 6BN, UK. d.lomas@ucl.ac.uk.

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Classifications MeSH