Onset of action of inhaled glucocorticoids on bronchial and alveolar nitric oxide output.

INTRODUCTION Exhaled nitric oxide (FENO) is a marker of airway inflammation. Measuring FENO at multiple flow rates enables calculation of NO parameters: bronchial NO output (JawNO), bronchial wall (CawNO) and alveolar (CANO) NO concentrations, and bronchial diffusion factor of NO (DawNO). FENO is known to rapidly reduce after the commencement of inhaled corticosteroid (ICS) treatment. However, little is known on the effect of ICS on the other NO parameters. AIMS OF THE STUDY We assessed 1) the onset of action of ICS treatment on the NO parameters and 2) whether the changes in bronchial NO output are due to changes in bronchial wall NO concentration or diffusion factor. METHODS FENO and other NO parameters were measured at baseline and after 1, 3 and 7 days of treatment with inhaled fluticasone propionate 250 g b.i.d. in 23 allergic children with a history of asthma-like symptoms. RESULTS There was a decrease in JawNO (from 680 (244/1791) (median (1st/3rd quartile)) to 357 (165/753) pl s-1, p<0.001) and FENO50 (from 13.8 (7.5/35) to 8.3 (5.36/17.0) ppb, p<0.001) in 3 days from the first dose of ICS. Also, CawNO seemed to reduce after 3 days (from 171 (89/328) to 79 (54/157) ppb, p=0.041), while DawNO remained unchanged. Furthermore, CANO reduced during the 7 days treatment (from 3.0 (2.0/5.0) to 2.3 (1.9/2.6) ppb, p=0.004). CONCLUSION ICS treatment reduced FENO50 and JawNO rapidly and the decline was caused by decreased bronchial wall NO concentration while bronchial NO diffusion factor remained unchanged. These findings suggest that CawNO could be a more specific marker of airway inflammation and treatment response than JawNO or FENO50, which are both determined also by DawNO that seems to be resistant to the treatment with ICS.