Evidence map›Paper›PMID 27214328›Full record

ArticleClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology2016

Exacerbation risk in severe asthma is stratified by inflammatory phenotype using longitudinal measures of sputum eosinophils.

C J Walsh, T Zaihra, A Benedetti, C Fugère, R Olivenstein, C Lemière, Q Hamid, J G Martin

Abstract read
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In one paragraph

Article in Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Angiogenesis Factors as Emerging Circulating Biomarkers in Asthma.Allergy, asthma & immunology research · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Immune responses and exacerbations in severe asthma.Current opinion in immunology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. A bispecific antibody strategy to target multiple type 2 cytokines in asthma.The Journal of allergy and clinical immunology · 2018
    Article
  19. Article
  20. Sputum cell counts to manage prednisone-dependent asthma: effects on FEVAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

C J WalshDepartment of Medicine, Institute of Medical Sciences, Keenan Centre for Biomedical Research, Li Ka Shing Knowledge institute, St. Michael's Hospital, University of Toronto, Toronto, ON, Canada.
T ZaihraDepartment of Mathematics, SUNY-Brockport, Brockport, NY, USA.
A BenedettiRespiratory Epidemiology and Clinical Research Unit, McGill University Health Centre, Montreal, QC, Canada.
C FugèreMontreal Chest Institute and the Meakins-Christie Laboratories, Montreal, QC, Canada.
R OlivensteinMontreal Chest Institute and the Meakins-Christie Laboratories, Montreal, QC, Canada.
C LemièreResearch Centre, Hôpital du Sacré-Cœur de, Montreal, QC, Canada.
Q HamidMontreal Chest Institute and the Meakins-Christie Laboratories, Montreal, QC, Canada.
J G MartinDepartment of Medicine, McGill University, Montreal, QC, Canada. james.martin@mcgill.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAirway inflammatory phenotyping is increasingly applied to subjects with asthma. However, its relationship to clinical outcomes in difficult asthma is incompletely elucidated.

objectiveThe goal of our study was to determine the relationship between exacerbation rates and phenotypes of difficult asthma based on the longitudinal measures of sputum eosinophils and neutrophils.

methodsSubjects in the longitudinal observational study from two tertiary care centres that completed 1 year of observation and provided at least three sputum samples were classified by inflammatory phenotypes using previously established thresholds. Kaplan-Meier curves and univariable and multivariable Cox proportional hazard models were used to determine the association between inflammatory phenotypes and exacerbation rate.

resultsDuring the study, 115 exacerbations occurred in 73 severe asthmatic subjects. Subjects with the persistently eosinophilic phenotype had a significantly shorter time to first exacerbation and greater risk of exacerbation over a 1-year period than those with the non-eosinophilic phenotype based on the univariable and multivariable Cox proportional hazard model (hazard ratio [HR], 3.24; 95% confidence interval [CI], 1.35-7.72; adjusted HR, 3.90; 95% CI, 1.34-11.36). No significant differences in time to first exacerbation or exacerbation risk over a 1-year period were observed among the neutrophilic phenotypes.

conclusionsThe persistent eosinophilic phenotype is associated with increased exacerbation risk compared with the non-eosinophilic phenotype in severe asthma. No differences in time to first exacerbation or exacerbation risk over a 1-year period were detected among neutrophilic phenotypes.

Indexed as

AdultAgedAged, 80 and overAnti-Asthmatic AgentsAsthmaDisease ProgressionEosinophilsFemaleHumansInflammationKaplan-Meier EstimateLeukocyte CountLongitudinal StudiesMaleMiddle AgedNeutrophilsAnti-Asthmatic Agentsasthma exacerbationbiomarkerslongitudinal studysevere asthma

Identifiers

PMID27214328

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.