Abstract
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 /FVC ratio 1NO >2 ppb underwent a doubleblind randomised controlled crossover trial with an open label systemic steroidcomparator. Following a 2 wksteroid 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 openlabel, 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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CITATION STYLE
Short, P. M., Williamson, P. A., & Lipworth, B. J. (2011). P257 Effects of extra-fine inhaled and oral corticosteroids on alveolar nitric oxide in COPD. Thorax, 66(Suppl 4), A172–A172. https://doi.org/10.1136/thoraxjnl-2011-201054c.257
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