Laurits Frøssing1, Alexander Silberbrandt2, Anna Von Bülow2, Vibeke Backer3, Celeste Porsbjerg2. 1. Respiratory Research Unit, Department of Respiratory Medicine L, Copenhagen University Hospital, Bispbjerg and Frederiksberg, Denmark. Electronic address: froessing@dadlnet.dk. 2. Respiratory Research Unit, Department of Respiratory Medicine L, Copenhagen University Hospital, Bispbjerg and Frederiksberg, Denmark. 3. Center for Physical Activity Research, Copenhagen University Hospital, Rigshospitalet, Denmark.
Abstract
BACKGROUND: With the introduction of different targeted therapies for type 2 (T2)-high asthma, there is an urgent need for markers to guide the choice of treatment. T2-high asthma includes different clinical phenotypes of asthma, but the prevalence and impact of activation of different T2 inflammatory pathways is unknown. OBJECTIVE: To describe the level of coexpression of clinically available T2 inflammatory markers in patients with severe asthma, and the relationship with clinical characteristics and comorbidities. METHODS: Patients with severe asthma according to European Respiratory Society/American Thoracic Society guidelines were examined prospectively including sputum induction and grouped according to T2 biomarkers: blood eosinophilia (≥0.3 × 109/L), total IgE (≥150 U/mL), and fractional exhaled nitric oxide (≥25 parts per billion). RESULTS: We found 116 (70%) of the 166 patients to have at least 1 T2 biomarker elevated: 39% had 2 or more elevated biomarkers, whereas 31% had only 1 biomarker elevated. Concomitant airway and systemic eosinophilia was present in 28% of all patients, corresponding to half (53%) of the patients with either. Expression patterns of the T2 biomarkers were associated with differences in allergic sensitization and the coexistence of nasal polyposis. CONCLUSIONS: Most patients with severe asthma showed at least 1 T2 inflammatory trait. Coexpression of T2 biomarkers was highly heterogeneous, and different expression patterns were associated with distinct clinical characteristics.
BACKGROUND: With the introduction of different targeted therapies for type 2 (T2)-high asthma, there is an urgent need for markers to guide the choice of treatment. T2-high asthma includes different clinical phenotypes of asthma, but the prevalence and impact of activation of different T2 inflammatory pathways is unknown. OBJECTIVE: To describe the level of coexpression of clinically available T2 inflammatory markers in patients with severe asthma, and the relationship with clinical characteristics and comorbidities. METHODS: Patients with severe asthma according to European Respiratory Society/American Thoracic Society guidelines were examined prospectively including sputum induction and grouped according to T2 biomarkers: blood eosinophilia (≥0.3 × 109/L), total IgE (≥150 U/mL), and fractional exhaled nitric oxide (≥25 parts per billion). RESULTS: We found 116 (70%) of the 166 patients to have at least 1 T2 biomarker elevated: 39% had 2 or more elevated biomarkers, whereas 31% had only 1 biomarker elevated. Concomitant airway and systemic eosinophilia was present in 28% of all patients, corresponding to half (53%) of the patients with either. Expression patterns of the T2 biomarkers were associated with differences in allergic sensitization and the coexistence of nasal polyposis. CONCLUSIONS: Most patients with severe asthma showed at least 1 T2 inflammatory trait. Coexpression of T2 biomarkers was highly heterogeneous, and different expression patterns were associated with distinct clinical characteristics.