S9 Inhaled and systemic corticosteroid response in moderate-to-severe asthma assessed by extended exhaled nitric oxide and lung function

Abstract

Introduction and Objectives: Alveolar nitric oxide (CANO) has been proposed as a potential biomarker of small airway inflammation in severe asthma. We wished to investigate the effects on CANO of the addition of coarse or fine particle inhaled corticosteroids to standard therapy in severe asthma. Methods: Severe asthmatics taking =1600 mg/daybudesonide or equivalent performed a randomised open-label crossover study. Subjects with FEV11, 58 (13)% predicted; residual volume, 193 (100)% predicted; mannitol PD10 177 (2.8) mg. There was no significant difference between FPSM and any add-on therapy for CANO. FPSM/BDP and FPSM/PRED suppressed JawNO and FENO compared to FPSM alone. There was no significant difference between treatments for pulmonary function or bronchial challenge. ECP, e-selectin and ICAM-1 were significantly suppressed by FPSM/ PRED compared to FPSM and FPSM/FP but not FPSM/BDP. Plasma cortisol was significantly suppressed by FPSM/PRED only. Conclusion: In severe asthma, alveolar nitric oxide is insensitive to changes in dose and delivery of inhaled corticosteroids and is not suppressed by systemic corticosteroids. Additional inhaled HFABDP caused reductions in FENO and JawNO without adrenal suppression. Oral prednisolone reduced FENO and JawNO with suppression of systemic inflammatory markers and urinary cortisol