Evidence map›Paper›PMID 35251534›Full record

ReviewEuropean clinical respiratory journal2022

Eosinophilic airway diseases: basic science, clinical manifestations and future challenges.

Christer Janson, Leif Bjermer, Lauri Lehtimäki, Hannu Kankaanranta, Jussi Karjalainen, Alan Altraja, Valentyna Yasinska, Bernt Aarli, Madeleine Rådinger, Johan Hellgren and 3 more

Open access · goldAbstract readReview
In one paragraph

Review in European clinical respiratory journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
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

5 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
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

13 authors at 9 institutions in 5 countries.

Christer JansonDepartment of Medical Sciences: Respiratory, Allergy and Sleep Research, Uppsala University, Uppsala, Sweden.ORCID https://orcid.org/0000-0001-5093-6980
Leif BjermerDepartment of Respiratory Medicine and Allergology, Skane University Hospital, Lund, Sweden.
Lauri LehtimäkiFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID https://orcid.org/0000-0003-1586-4998
Hannu KankaanrantaFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.ORCID https://orcid.org/0000-0001-5258-0906
Jussi KarjalainenFaculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Alan AltrajaDepartment of Pulmonology, University of Tartu and Lung Clinic, Tartu University Hospital, Tartu, Estonia.
Valentyna YasinskaDepartment of Respiratory Medicine and Allergy, Karolinska University Hospital, Huddinge, Sweden.
Bernt AarliDepartment of Clinical Science, University of Bergen and Department of Thoracic Medicine, Haukeland University Hospital, Bergen, Norway.
Madeleine RådingerKrefting Research Centre, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Johan HellgrenDepartment of Otorhinolaryngology, University of Gothenburg, Gothenburg, Sweden.
Magnus LofdahlRespiratory Medical Affairs, GSK, Solna, Sweden.
Peter H HowarthRespiratory Medical Franchise, GSK, Brentford, Middlesex, UK.
Celeste PorsbjergDepartment of Respiratory Medicine, Bispebjerg Hospital and Copenhagen University, Copenhagen, Denmark.
Tampere University · FIUniversity of Gothenburg · SEBispebjerg Hospital · DKGlaxoSmithKline (Sweden) · SEHaukeland University Hospital · NOKarolinska University Hospital · SESkåne University Hospital · SETartu University Hospital · EEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eosinophils have a broad range of functions, both homeostatic and pathological, mediated through an array of cell surface receptors and specific secretory granules that promote interactions with their microenvironment. Eosinophil development, differentiation, activation, survival and recruitment are closely regulated by a number of type 2 cytokines, including interleukin (IL)-5, the key driver of eosinophilopoiesis. Evidence shows that type 2 inflammation, driven mainly by interleukin (IL)-4, IL-5 and IL-13, plays an important role in the pathophysiology of eosinophilic airway diseases, including asthma, chronic rhinosinusitis with nasal polyps, eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome. Several biologic therapies have been developed to suppress type 2 inflammation, namely mepolizumab, reslizumab, benralizumab, dupilumab, omalizumab and tezepelumab. While these therapies have been associated with clinical benefits in a range of eosinophilic diseases, their development has highlighted several challenges and directions for future research. These include the need for further information on disease progression and identification of treatable traits, including clinical characteristics or biomarkers that will improve the prediction of treatment response. The Nordic countries have a long tradition of collaboration using patient registries and Nordic asthma registries provide unique opportunities to address these research questions. One example of such a registry is the NORdic Dataset for aSThmA Research (NORDSTAR), a longitudinal population-based dataset containing all 3.3 million individuals with asthma from four Nordic countries (Denmark, Finland, Norway and Sweden). Large-scale, real-world registry data such as those from Nordic countries may provide important information regarding the progression of eosinophilic asthma, in addition to clinical characteristics or biomarkers that could allow targeted treatment and ensure optimal patient outcomes.

Indexed as

asthmachronic rhinosinusitis with nasal polypsEosinophileosinophilic granulomatosis with polyangiitishypereosinophilic syndromeNordicNORDSTARreal-worldregistrysevere asthma

Identifiers

PMID35251534
PMCPMC8896196
OpenAlexW4214865456

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.