Persistence of Eosinophilic Asthma Endotype and Clinical Outcomes: A Real-World Observational Study

J Asthma Allergy. 2021 Jun 25;14:727-742. doi: 10.2147/JAA.S306416. eCollection 2021.

Abstract

Purpose: Eosinophil count elevations are predictive of adverse outcomes in patients with asthma, yet little is known regarding longitudinal eosinophil patterns and their association with clinical outcomes. The goal of this study was to assess associations between longitudinal persistence of eosinophil elevations and both clinical outcomes and health care resource utilization (HCRU).

Methods: Data were extracted from 2 databases in the United Kingdom. Patients included were aged ≥13 years, had active asthma, and had ≥3 blood eosinophil count (BEC) recordings. Patients were categorized by BEC as: never high (all BEC ≤300 cells/µL), intermittently high (≥1 BEC >300 cells/µL but <75% of BEC >300 cells/µL), or persistently high (≥75% of BEC >300 cells/µL). Asthma exacerbations, asthma control (risk domain, overall, and full), and HCRU were evaluated for 12 months after the last BEC.

Results: The study population comprised 148,021 patients. Persistently high, intermittently high, and never high eosinophil patterns were detected in 13.6%, 40.5%, and 45.9% of patients, respectively. Patients with ≥1 elevated BEC were at greater risk for severe asthma exacerbations, regardless of whether the elevation was persistent (rate ratio [RR]: 1.28 [95% CI 1.24-1.33]; P < 0.001) or intermittent (RR: 1.24 [95% CI 1.21-1.27]; P < 0.001), compared with patients with no eosinophil elevations. Full asthma control was achieved by <25% of patients across eosinophil pattern groups, and HCRU did not appreciably differ, although patients with persistently high BEC had the shortest hospital stay duration among the groups.

Conclusion: These data suggest that elevated blood eosinophils, regardless of persistency, signify increased risk of severe asthma exacerbations.

Keywords: asthma control; asthma exacerbation; biomarker; eosinophilia; phenotype; type 2 inflammation.

Grant support

This work was supported by AstraZeneca. A named author is an employee of AstraZeneca; therefore, AstraZeneca was involved in the study design; collection, analysis, and interpretation of data; and the development and review of the manuscript. The decision to submit the manuscript for publication was made by the authors.