Open AccessMontelukast reduces airway eosinophilic inflammation in asthma: a randomized, controlled trial
Author(s) -
Pizzichini E.,
Leff J.A.,
Reiss T.F.,
Hendeles L.,
Boulet LP.,
Wei L.X.,
Efthimiadis A.E.,
Zhang J.,
Hargreave F.E.
Publication year - 1999
Publication title -
european respiratory journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.021
H-Index - 241
eISSN - 1399-3003
pISSN - 0903-1936
DOI - 10.1034/j.1399-3003.1999.14a04.x
Subject(s) - medicine , montelukast , asthma , sputum , placebo , gastroenterology , eosinophilia , eosinophil , bronchial hyperresponsiveness , immunology , anesthesia , respiratory disease , pathology , lung , tuberculosis , alternative medicine
Leukotrienes are pro‐inflammatory mediators which may contribute to tissue, sputum, and blood eosinophilia seen in allergic and inflammatory diseases, including asthma. Montelukast is a cysteinyl leukotriene 1 (CysLT 1 ) receptor antagonist which improves asthma control; the aim of this study was to investigate its effect on induced sputum eosinophils. Montelukast 10 mg (n=19) or placebo (n=21) were administered orally once in the evening for 4 weeks to 40 chronic adult asthmatic patients, aged 19–64 yrs, in a double‐blind, randomized, parallel group study. Patients were included if, at prestudy, they had >5% sputum eosinophils, symptomatic asthma with a forced expiratory volume in one second ≥65% of the predicted value and were being treated only with “as needed” inhaled β 2 ‐agonists. In addition to sputum eosinophils, blood eosinophils and clinical endpoints were also assessed. Four weeks of montelukast treatment decreased sputum eosinophils from 7.5% to 3.9% (3.6% decrease, 95% confidence interval (CI) ‐16.6–0.4). In contrast, placebo treatment was associated with an increase in sputum eosinophils from 14.5% to 17.9% (3.4% increase, 95% CI ‐3.5–9.8). The least squares mean difference between groups (‐11.3%, 95% CI ‐21.1–‐1.4) was significant (p=0.026). Compared with placebo, montelukast significantly reduced blood eosinophils (p=0.009), asthma symptoms (p=0.001) and β 2 ‐agonist use (p<0.001) while significantly increasing morning peak expiratory flow (p=0.001). Montelukast was generally well tolerated in this study, with a safety profile similar to the placebo. These results demonstrate that montelukast decreases airway eosinophilic inflammation in addition to improving clinical parameters. Its efficacy in the treatment of chronic asthma may be due, in part, to the effect on airway inflammation.