作者@article {Kanniess853 = {Kanniess, fRichter, K. and B{\"o}hme, S. and J{\"o}rres, R.A. and Magnussen, H.}, title = {Montelukast versus fluticasone: effects on lung function, airway responsiveness and inflammation in moderate asthma}, volume = {20}, number = {4}, pages = {853--858}, year = {2002}, doi = {10.1183/09031936.02.00244602}, publisher = {European Respiratory Society}, abstract = {Whether leukotriene receptor antagonists exhibit adequate anti-inflammatory effects in the treatment of asthma is still a controversial issue. The aim of the present study was to perform a direct comparison of the effects of a 4-week treatment with either montelukast (10 mg, once a day) or low-dose inhaled fluticasone (100 {\textmu}g b.i.d.) on functional and inflammatory parameters in steroid-na{\"\i}ve patients with moderate asthma. Forty patients (forced expiratory volume in one second (FEV1), 60{\textendash}80\% predicted) were studied in a double-blind, randomised, crossover design. Treatment periods were separated by 3{\textendash}8 weeks of washout. At the beginning and end of each period, FEV1, airway responsiveness to inhaled methacholine (provocative concentration causing a 20\% fall in FEV1 (PC20)), the level of exhaled nitric oxide (NO) and sputum differential cell counts were determined. Only short-acting β2-agonists were allowed for relief of symptoms. FEV1 increased by 0.50{\textpm}0.07 L (mean{\textpm}sem) after fluticasone and by 0.37{\textpm}0.07 L after montelukast (p\<0.001, each), and PC20 by 1.33{\textpm}0.13 (p\<0.001) and 0.15{\textpm}0.17 (ns) doubling doses, respectively. Correspondingly, percentages of sputum eosinophils were reduced by factor 2.7 (p\<0.01) and 1.4 (nonsignificant (ns)), and the levels of exhaled NO (at 50 mL{\textperiodcentered}s-1) by factor 2.1 (p\<0.01) and 1.1 (ns). These data indicate a comparable bronchodilator action of montelukast and fluticasone in patients with moderate asthma, but additional attenuation of airway inflammation by fluticasone as detectable through noninvasive methods. Supported by GlaxoSmithKline, D-20354 Hamburg, Germany.}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/20/4/853}, eprint = {//www.qdcxjkg.com/content/20/4/853.full.pdf}, journal = {European Respiratory Journal} }