Effects of inhaled corticosteroids on exhaled leukotrienes and prostanoids in asthmatic children

Lipid mediators play an important pathophysiologic role in atopic asthmatic children, but their role in the airways of atopic nonasthmatic children is unknown. We sought (1) to measure leukotriene (LT) E 4, LTB 4, 8-isoprostane, prostaglandin E 2, and thromboxane B 2 concentrations in exhaled breath condensate in atopic asthmatic and atopic nonasthmatic children; (2) to measure exhaled nitric oxide (NO) as an independent marker of airway inflammation; and (3) to study the effect of inhaled corticosteroids on exhaled eicosanoids. Twenty healthy children, 20 atopic nonasthmatic children, 30 steroid-naive atopic asthmatic children, and 25 atopic asthmatic children receiving inhaled corticosteroids were included in a cross-sectional study. An open-label study with inhaled fluticasone (100 μg twice a day for 4 weeks) was undertaken in 14 steroid-naive atopic asthmatic children. Compared with control subjects, exhaled LTE 4 ( P < .001), LTB 4 ( P < .001), and 8-isoprostane ( P < .001) levels were increased in both steroid-naive and steroid-treated atopic asthmatic children but not in atopic nonasthmatic children (LTE 4, P = .14; LTB 4, P = .23; and 8-isoprostane, P = .52). Exhaled NO levels were increased in steroid-naive atopic asthmatic children ( P < .001) and, to a lesser extent, in atopic nonasthmatic children ( P < .01). Inhaled fluticasone reduced exhaled NO (53%, P < .0001) and, to a lesser extent, LTE 4 (18%, P