Evidence map›Paper›PMID 37197769›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2023

Phenotype overlap in the natural history of asthma.

Fabio L M Ricciardolo, Giuseppe Guida, Francesca Bertolini, Antonino Di Stefano, Vitina Carriero

Abstract readReview
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing 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

37 citing papers in PubMed.

  1. Trial
  2. Review
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  4. Bronchodilator response is linked with uncontrolled moderate-to-severe childhood asthma and elevated IL-4 and IL-13.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  5. Review
  6. Sex chromosomes and gonadal sex interactions in airway and immune responses to allergen challenge.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Observational
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Fabio L M RicciardoloDepartment of Clinical and Biological Sciences, Severe Asthma and Rare Lung Disease Unit, San Luigi Gonzaga University Hospital, University of Turin, Turin, Italy fabioluigimassimo.ricciardolo@unito.it.ORCID https://orcid.org/0000-0003-1826-5018
Giuseppe GuidaDepartment of Clinical and Biological Sciences, Severe Asthma and Rare Lung Disease Unit, San Luigi Gonzaga University Hospital, University of Turin, Turin, Italy.ORCID https://orcid.org/0000-0003-3876-8587
Francesca BertoliniDepartment of Clinical and Biological Sciences, Severe Asthma and Rare Lung Disease Unit, San Luigi Gonzaga University Hospital, University of Turin, Turin, Italy.ORCID https://orcid.org/0000-0003-4390-0394
Antonino Di StefanoDepartment of Pneumology and Laboratory of Cytoimmunopathology of the Heart and Lung, Istituti Clinici Scientifici Maugeri SpA, IRCCS, Novara, Italy.
Vitina CarrieroDepartment of Clinical and Biological Sciences, Severe Asthma and Rare Lung Disease Unit, San Luigi Gonzaga University Hospital, University of Turin, Turin, Italy.ORCID https://orcid.org/0000-0003-1866-5206

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heterogeneity of asthma makes it challenging to unravel the pathophysiologic mechanisms of the disease. Despite the wealth of research identifying diverse phenotypes, many gaps still remain in our knowledge of the disease's complexity. A crucial aspect is the impact of airborne factors over a lifetime, which often results in a complex overlap of phenotypes associated with type 2 (T2), non-T2 and mixed inflammation. Evidence now shows overlaps between the phenotypes associated with T2, non-T2 and mixed T2/non-T2 inflammation. These interconnections could be induced by different determinants such as recurrent infections, environmental factors, T-helper plasticity and comorbidities, collectively resulting in a complex network of distinct pathways generally considered as mutually exclusive. In this scenario, we need to abandon the concept of asthma as a disease characterised by distinct traits grouped into static segregated categories. It is now evident that there are multiple interplays between the various physiologic, cellular and molecular features of asthma, and the overlap of phenotypes cannot be ignored.

Indexed as

AsthmaComorbidityHumansInflammationPhenotype

Identifiers

PMID37197769
PMCPMC10189644

What OpenQuestion holds

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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.