Exploring trends and predictors of long-term asthma remission
- PMID: 41112189
- PMCID: PMC12528878
- DOI: 10.1016/j.waojou.2025.101127
Exploring trends and predictors of long-term asthma remission
Abstract
Rationale: Asthma remission is a state of low to no disease activity. To date, little is known about predictors and the achievability of long-term asthma remission.
Objective: To identify clinical predictors and trends of long-term remission in a cohort of adults with mild to severe asthma.
Methods: This study included 203 adults with mild to severe asthma from the All Age Asthma Cohort, followed over 6 years. Participants attended 5 visits, during which type 2 inflammation markers (blood and sputum eosinophils, fractional exhaled nitric oxide), lung function measurements (oscillometry, spirometry), atopy and systemic comorbidities were assessed. Clinical remission was defined by an Asthma Control Test score of ≥20 plus the absence of both severe exacerbations and systemic corticosteroid use in the past 12 months, and normal or stable lung function. Long-term remission was defined as remission lasting at least 3 consecutive years, while short-term remission lasted 1 or 2 consecutive years.
Results: The frequencies of long-term, short-term, and no remission were 27%, 34%, and 39%, respectively. 16% of all patients with severe asthma achieved long-term remission, compared to 65% of those with mild-to-moderate disease. Over one-third of all patients never achieved remission and had persistent T2 markers despite high-dose ICS. Predictors of no asthma remission included number of persistent T2-markers (OR:0.26, CI: 0.11, 0.61), frequency dependence of resistance (FDR, R5-R20Hz; OR:0.36, CI: 0.15, 0.82), FEV1/FVC (OR:0.16, CI: 0.06, 0.37), GERD (OR:0.23, CI: 0.1, 0.5), CVD (OR:0.44, CI: 0.22, 0.87), dyslipidemia (OR:0.38, CI: 0.13, 1.05), whereas sensitization to house dust mite was associated with a higher remission rate (OR:2.06, CI: 1.03, 4.17). During long-term follow-up, significant adjusted predictors of no remission were sputum eosinophils, small airway dysfunction, and airflow obstruction.
Conclusion: This study highlights a substantial unmet need in achieving long-term remission, particularly in patients with persistent type 2 inflammation and impaired lung function, prompting re-evaluation of targeting T2 inflammation earlier to prevent lung function impairment.
Keywords: Asthma; Biological therapy; Comorbidity; Disease remission; Eosinophils; Longitudinal studies; Predictive value of tests; Type 2 inflammation.
© 2025 The Author(s).
Conflict of interest statement
Vera Veith, and Mustafa Abdo report no conflict of interest. Frauke Pedersen, Henrik Watz, Anne-Marie Kirsten, Folke Brinkmann, and Nicole Maison report no relevant conflict of interest. Matthias V. Kopp declares funding from the 10.13039/100009068University of Bern, consulting fees from 10.13039/100004339Sanofi Aventis GmbH and 10.13039/100009946Allergopharma GmbH, honoraria from 10.13039/100004339Sanofi Aventis GmbH, Infectopharm GmbH, and 10.13039/100009946Allergopharma GmbH, participation on an advisory board for 10.13039/100009946Allergopharma GmbH, and a leadership role in the Society of Pediatric Pulmonology. Anna-Maria Dittrich reports grants to institution from Vertex and 10.13039/501100024065OM Pharma, grants from 10.13039/501100002347BMBF and 10.13039/501100001659DFG and personal fees from Glaxo-Smith-Kline, 10.13039/100004336Novartis and Vertex outside of submitted work. Gesine Hansen declares funding from the 10.13039/501100010564German Center for Lung Research (DZL; 10.13039/501100002347BMBF) with grant payments made to 10.13039/501100005624Hannover Medical School, and the 10.13039/501100001659German Research Foundation (10.13039/501100001659DFG), EXC 2155 ‘RESIST’, as well as consulting fees from 10.13039/100004339Sanofi GmbH and lecture fees from MedUpdate and 10.13039/100006483AbbVie. Bianca Schaub reports grants from the 10.13039/501100002347BMBF (German center for lung research, CPC-Munich, 10.13039/501100010564DZL 82DZL033C2, Combat Lung diseases FP4), the German Center for Child and Adolescent 10.13039/100018696Health (DZKJ; 10.13039/501100005722LMU/10.13039/501100005722LMU Klinikum: 01GL2406A), from 10.13039/501100001659DFG (DFG-SCHA 997/8–1 (BS); DFG-SCHA 997/9–1, DFG-SCHA-997/10–1, DFG-SCHA-997/11–1. BS reports consulting fees from 10.13039/100004330GlaxoSmithKline, 10.13039/100004336Novartis, Astra Zeneca, Sanofi; payment/honoraria and participation on a Data Safety Monitoring Board or Advisory Board from 10.13039/100004339Sanofi. Erika von Mutius reports receiving research support, consulting fees, travel funding, honoraria, and patent-related royalties from multiple academic, governmental, and commercial entities, including 10.13039/501100024065OM Pharma S.A., Elsevier, 10.13039/100004325AstraZeneca, and the 10.13039/501100000780European Commission, with no other conflicts of interest declared. Klaus F. Rabe received medical writing support from 10.13039/100019719Chiesi and, in the past 36 months, has received consulting fees, honoraria, or served on advisory boards for 10.13039/100004325AstraZeneca, 10.13039/100008349Boehringer Ingelheim, 10.13039/100019719Chiesi, 10.13039/100004339Sanofi & 10.13039/100009857Regeneron, 10.13039/100008322CSL Behring, 10.13039/100004330GlaxoSmithKline, 10.13039/501100022535Berlin Chemie, and Menarini. Thomas Bahmer received an unrestricted research grant from the 10.13039/501100002347BMBF for the 10.13039/501100010564DZL ALLIANCE cohort, as well as 10.13039/501100002347BMBF funding for NAPKON and 10.13039/501100003107BMG funding for COVIDOM+; in the past 36 months, the author has received consulting fees from Thieme, HealthHero, and Pohl Boskamp, and honoraria from 10.13039/100004319Pfizer, 10.13039/100030732MSD, GSK, 10.13039/100004325AstraZeneca, and 10.13039/100019719Chiesi.
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