Introduction and Objectives Alveolar nitric oxide or (CANO), has been used as a surrogate marker of distal airway inflammation, which isimportant in COPD. Coarse particle inhaled corticosteroids (ICS) have been shown not to suppress CANO. We evaluated whether extra-fine particlesize inhaled corticosteroids (HFA-BDP) or systemic oral corticosteroids could suppress CANO in COPD.
Methods COPD patients with a smoking pack history >15 years, FEV1/FVC ratio <0.7, FEV1<80% predicted with small airways inflammation characterised by CANO >2 ppb underwent a double-blind randomised controlled crossover trial with an open label systemic steroid comparator. Following a 2 wk steroid washout period, patients were randomised to 3 weeks, 100 mcg HFA-BDP twice daily and then 3 weeks 400 mcg HFA-BDP twice daily or matched placebos with subsequent crossover. All patients then received 1 week open-label, 25 mg/day prednisolone. Spirometry, bodyplethysmography, impulse oscillometry, plasma cortisol and exhaled nitric oxide were recorded. CANO was corrected for axial diffusion.
Results 16 patients completed per protocol. Compared to respective placebo there were no significant differences seen with either dose of HFA-BDP. Oral prednisolone caused a significant reduction in FENO and J'awNO but not CANO. Plasma cortisol was significantly suppressed by oral prednisolone compared to all other treatments. There was no suppression seen with HFA-BDP at either dose verses placebo.
Conclusions While CANO remains a biomarker of interest in COPD, it is not suppressed by systemic or extra-fine particle ICS. Hence CANO is unlikely to be a useful marker for monitoring response of small airway disease to therapies in COPD.
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