As compared with placebo, once-daily treatment with montelukast provided significant protection against exercise-induced asthma over a 12-week period. Tolerance to the medication and rebound worsening of lung function after discontinuation of treatment were not seen.
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 b 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 b 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.
Abstractleukotriene receptor antagonist provide further evidence of the role of leukotrienes Background -A study was undertaken to in the pathogenesis of exercise-induced determine whether montelukast, a new bronchoconstriction. potent cysteinyl leukotriene receptor (Thorax 1997;52:1030-1035 antagonist, attenuates exercise-induced bronchoconstriction. The relationship beKeywords: leukotriene receptor antagonist, exercisetween the urinary excretion of LTE 4 and induced bronchoconstriction, montelukast. exercise-induced bronchoconstriction was also investigated. Methods -Nineteen non-smoking asth-Cysteinyl leukotrienes, synthesised from matic patients with a forced expiratory arachidonic acid through the 5-lipoxygenase volume in one second (FEV 1 ) of [65% of pathway, have an important role in asthma. 1 the predicted value and a reproducible fall Leukotriene C 4 (LTC 4 ) is the dominant metain FEV 1 after exercise of at least 20% were bolite of arachidonic acid released in lung tissue enrolled. Subjects received placebo and but it is very unstable and quickly converted montelukast 100 mg once daily in the even-to leukotriene D 4 (LTD 4 ). In turn, LTD 4 is ing or 50 mg twice daily, each for two days, converted to a less potent metabolite, leukoin a three-period, randomised, double triene E 4 (LTE 4 ), which is excreted in the ilarly against exercise-induced broncho-available, selective, and potent cysteinyl leukoconstriction between plasma concentra-
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