Fixed Airflow Limitation in Severe Asthma: Rethinking the Role of Small Airway Disease

Small airway disease (SAD) remains a challenging and underrecognized driver of fixed airflow obstruction in severe asthma. Impulse oscillometry (IOS) provides valuable insight into peripheral airway dysfunction and allows characterization of different bronchodilator response patterns. We describe two cases of late-onset severe asthma with confirmed SAD by spirometry and IOS, unresponsive to systemic corticosteroids and to biologics, despite optimized high-dose extrafine triple inhaled therapy and adherence. Both patients exhibited persistent airflow obstruction and abnormal IOS parameters, suggesting a resistant SAD phenotype. Importantly, the role of corticosteroid challenge in this subgroup remains unclear, as it failed to predict subsequent biologic response. These observations highlight the clinical utility of IOS in diagnosing and monitoring SAD and reinforce the need for personalized therapeutic approaches to address this treatment-resistant endotype of severe asthma.

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Publication Details

Journal
Open Respiratory Archives
Published
2025-09-04
DOI
https://doi.org/10.1016/j.opresp.2025.100483
Primary Topic
Asthma and respiratory diseases
Type
article
Field-Weighted Citation Impact
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article

Fixed Airflow Limitation in Severe Asthma: Rethinking the Role of Small Airway Disease

Miguel Jiménez-Gómez, Ismael García‐Moguel, Rocío Magdalena Díaz-Campos
Open Respiratory Archives
Asthma and respiratory diseases
article

Fixed Airflow Limitation in Severe Asthma: Rethinking the Role of Small Airway Disease

Miguel Jiménez-Gómez, Ismael García‐Moguel, Rocío Magdalena Díaz-Campos
article en

Abstract

Small airway disease (SAD) remains a challenging and underrecognized driver of fixed airflow obstruction in severe asthma. Impulse oscillometry (IOS) provides valuable insight into peripheral airway dysfunction and allows characterization of different bronchodilator response patterns. We describe two cases of late-onset severe asthma with confirmed SAD by spirometry and IOS, unresponsive to systemic corticosteroids and to biologics, despite optimized high-dose extrafine triple inhaled therapy and adherence. Both patients exhibited persistent airflow obstruction and abnormal IOS parameters, suggesting a resistant SAD phenotype. Importantly, the role of corticosteroid challenge in this subgroup remains unclear, as it failed to predict subsequent biologic response. These observations highlight the clinical utility of IOS in diagnosing and monitoring SAD and reinforce the need for personalized therapeutic approaches to address this treatment-resistant endotype of severe asthma.

Open Respiratory ArchivesVol. 7(4)
Research Institute Hospital 12 de Octubre (ES)
Openalex Percentile: Top 70%
Asthma and respiratory diseases
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