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

Fractional exhaled nitric oxide (FENO) is a marker of airway inflammation. Measuring FENO at multiple flow rates enables calculation of NO parameters: bronchial NO output (J(aw)NO), 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. 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. FENO and other NO parameters were measured at baseline and after 1, 3 and 7 d of treatment with inhaled fluticasone propionate 250 mu g b.i.d. in 23 allergic children with a history of asthma-like symptoms. There was a decrease in J(aw)NO (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 d from the first dose of ICS. Also, CawNO seemed to reduce after 3 d (from 171 (89/328) to 79 (54/157) ppb, p = 0.041), while DawNO remained unchanged. Furthermore, CANO reduced during the 7 d treatment (from 3.0 (2.0/5.0) to 2.3 (1.9/2.6) ppb, p = 0.004). ICS treatment reduced FENO50 and J(aw)NO 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 J(aw)NO or FENO50, which are both determined also by DawNO that seems to be resistant to the treatment with ICS.

Automated summary

The study found that ICS treatment rapidly reduced FENO50 and J(aw)NO, likely due to the decrease in bronchial wall NO concentration while bronchial NO diffusion factor remained unchanged. This suggests that CawNO may be a more specific marker of airway inflammation and treatment response.