Evidence map›Paper›PMID 40928297›Full record

ArticleClinical and translational allergy2025

Sputum Eosinophil and Macrophage Changes After Aspirin Challenge in Patients With Nonsteroidal Anti-Inflammatory Drug-Exacerbated Respiratory Disease.

Gabriela Trąd-Wójcik, Piotr Szatkowski, Adam Ćmiel, Radosław Kacorzyk, Adam Stępień, Lucyna Mastalerz

Abstract read
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Article in Clinical and translational allergy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Gabriela Trąd-WójcikSecond Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Piotr SzatkowskiSecond Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Adam ĆmielDepartment of Applied Mathematics, AGH University of Science and Technology, Krakow, Poland.
Radosław KacorzykSecond Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Adam StępieńSecond Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.
Lucyna MastalerzSecond Department of Internal Medicine, Jagiellonian University Medical College, Krakow, Poland.ORCID https://orcid.org/0000-0002-8994-0036

Funding

'Initiative of Excellence - Research University' Strategic Programme (ID.UJ)National Science Centre, Poland 2020/39/B/NZ5/02296National Science Centre, Poland UMO-2015/19/B/NZ5/00096
6 · The paper itself

Abstract

backgroundInduced sputum cell count is crucial for assessing airway inflammatory phenotypes. This study investigated how aspirin-induced bronchospasm affects sputum cell counts in patients with nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD), comparing systemic versus local aspirin administration.

methodsSeventy-eight patients with N-ERD and 39 with aspirin-tolerant asthma (ATA) participated. In the N-ERD group, induced sputum was collected before aspirin challenge and during aspirin-induced bronchospasm. We assessed changes in the percentages of eosinophils, neutrophils, lymphocytes, and macrophages, and airway inflammatory phenotypes classified by sputum cells into: (A) eosinophilic, neutrophilic, paucigranulocytic, and mixed; and (B) eosinophilic and noneosinophilic.

resultsBaseline sputum neutrophil percentage was lower in the N-ERD than in the ATA (32.9% ± 20.8% vs. 41.6% ± 22.5%; p = 0.02). Inflammatory phenotypes at baseline differed between groups in both classifications (A: p = 0.041; B: p = 0.044). In the N-ERD group, sputum eosinophil percentage decreased after both oral (8.9% ± 11.6% vs. 6.1% ± 8.9%, p = 0.009) and inhaled (10.4% ± 16.1% vs. 4.8% ± 6.3%, p = 0.045) challenges, without altering inflammatory phenotypes. The ATA group showed no changes. Sputum macrophage percentage dropped after oral challenge in both groups (N-ERD: 40.5% ± 18.5% vs. 35.6% ± 21.5%; p = 0.004; ATA: 36.5% ± 23.6% vs. 26.7% ± 20.4%; p = 0.0003). In the N-ERD group, baseline sputum lymphocyte and eosinophil percentages were inversely correlated with the provocative dose of aspirin that resulted in a 20% decrease in baseline forced expiratory volume in 1 s following oral aspirin challenge (R = -0.31, p = 0.02 and R = -0.33, p = 0.02, respectively).

conclusionIn N-ERD, sputum eosinophil percentage decreased after aspirin challenge regardless of administration route. In both N-ERD and ATA, sputum macrophage percentage decreased after oral aspirin challenge.

Indexed as

airway inflammatory phenotypesaspirin challengeaspirin hypersensitivityinduced sputum cellssputum eosinophil percentage

Identifiers

PMID40928297
PMCPMC12421734

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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 Socratic graph.