ReviewEuropean respiratory review : an official journal of the European Respiratory Society2025
Persistent airway obstruction in severe eosinophilic asthma: targeting interleukin-5 and eosinophils.
Review in European respiratory review : an official journal of the European Respiratory Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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.
Who cites it
1 citing paper in PubMed.
- Is blood eosinophilia a treatable trait in chronic obstructive airway diseases?Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large proportion of patients (40-60%) with severe asthma present with persistent airway obstruction (PAO). Patients with severe eosinophilic asthma (SEA) and PAO appear to be an underrepresented group in clinical guidance, despite being associated with considerable healthcare and economic burden. High levels of eosinophils drive airway inflammation, obstruction and hyperresponsiveness, which are key characteristics of SEA and can increase the risk of PAO and subsequent irreversible worsening of lung function. Available clinical and real-world data must examine the effectiveness of biologic treatment targeting SEA in PAO to identify any data gaps that might help further define such patients and optimise their management. However, clinical trials of SEA frequently exclude the enrolment of patients with PAO. Eosinophils are activated and recruited to airways in response to different cytokines, particularly interleukin-5 (IL-5), produced
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