Objective: Leukotrienes (LTs) are involved in airway eosinophilic inflammation in patients with asthma. We examined the effects of a cysteinyl LT 1-receptor antagonist, montelukast, on sputum eosinophil levels, and the correlation between sputum eosinophils and bronchodilatation in patients with asthma.
Design: Double-blind, randomized, crossover study.
Setting: University hospital and private hospital.
Patients: Twenty-nine patients with mild-to-moderate asthma.
Interventions: Montelukast, 10 mg, and placebo tablet, once daily, each for 4 weeks.
Measurements: Sputum eosinophils analyzed using hypertonic saline solution-induced sputum and airway hyperresponsiveness to histamine were evaluated before and after treatment. In addition, morning and evening peak expiratory flow (PEF), asthma symptoms, and peripheral blood eosinophil levels were assessed.
Results: The percentage of eosinophils in sputum decreased from 24.6 ± 12.3% at baseline to 15.1 ± 11.8% after montelukast treatment, for a change of − 9.5 ± 12.7% (n = 20). During placebo administration, the percentage of eosinophils fell from 21.3 ± 12.1% to 21.0 ± 11.5%, resulting in a decrease of − 0.3 ± 10.8% (n = 20). There was a statistically significant difference in the change in sputum eosinophil levels between these two periods (p < 0.005). The number of peripheral blood eosinophils also significantly decreased after montelukast treatment (314.1 ± 237.6/mL) compared with placebo (413.1 ± 232.1/mL; p < 0.005, n = 21). Although morning and evening PEF values were significantly improved from baseline after montelukast treatment (p < 0.01, n = 20), asthma symptoms and airway responsiveness to histamine were not significantly altered. Furthermore, there was no significant correlation between the decrease in sputum eosinophils and the increase in PEF.
Conclusion: These results suggest that montelukast has anti-inflammatory effects on the airway in patients with asthma, and that its bronchodilatory effect is not solely dependent on a decrease in airway eosinophilia.