Exploring trends and predictors of long-term asthma remission

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.

To identify clinical predictors and trends of long-term remission in a cohort of adults with mild to severe asthma.

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.

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.

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.