Montelukast, a potent leukotriene receptor antagonist, causes dose-related improvements in chronic asthma

The leukotrienes are known to be important mediators of bronchial asthma, The ability of montelukast, a potent and selective CysLT(1) leukotriene receptor antagonist, to cause a dose-related improvement in chronic asthma was investigated in a placebo-controlled, multicentre, parallel-group study, After a two meek placebo run-in period, chronic asthmatic patients with a forced expiratory volume in one second (FEV1) 40-50% predicted with greater than or equal to 15% increase (absolute value) after beta(2)-agonist mere randomly assigned to one of four treatment groups (placebo or montelukast 2, 10, or 50 mg once daily in the evening) for a three week, double-blind treatment period. For patient-reported end-points (daytime symptom score, use of as needed inhaled beta(2) agonist, asthma-specific quality of life) and frequency of asthma exacerbations, montelukast 10 and 50 mg caused similar responses, superior to 2 mg and significantly (p<0.05; linear trend test) different from placebo, All three doses caused improvements in FEVI and morning and evening peak expiratory how rate (PEFR) that mere significantly (p<0.05) different from placebo, Differences (least square mean) between the pooled 10 and 50 mg montelukast treatment groups and placebo were: 7.1% change from baseline in FEV1, 19.23 L.min(-1) in morning PEFR, -0.29 in daytime asthma symptom score (absolute value), and -0.82 in beta(2)-agonist use (puff.day(-1)). The incidence of adverse experiences was neither dose-related nor different between montelukast and placebo treatments. We conclude that montelukast causes a dose-related improvement in patient-reported asthma end-points over the range 2-50 mg, Montelukast causes benefit to chronic asthmatic patients by improving asthma control end-points.