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Pulmonary Research Institute, Hospital Grosshansdorf, Center for Pneumology and Thoracic Surgery, D-22927, Grosshansdorf, Germany
CORRESPONDENCE: H. Magnussen, Pulmonary Research Institute, Hospital Grosshansdorf, Center for Pneumology and Thoracic Surgery, Wöhrendamm 80, D-22927, Grosshansdorf, Germany. Fax: 49 4102601379. E-mail: magnussen@pulmoresearch.de
Keywords: bronchial hyperresponsiveness, exhaled nitric oxide, fluticasone, induced sputum, montelukast
Received: May 11, 2001
Accepted May 7, 2002
Supported by GlaxoSmithKline, D-20354 Hamburg, Germany.
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 µg b.i.d.) on functional and inflammatory parameters in steroid-naïve patients with moderate asthma.
Forty patients (forced expiratory volume in one second (FEV1), 6080% predicted) were studied in a double-blind, randomised, crossover design. Treatment periods were separated by 38 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 ß2-agonists were allowed for relief of symptoms.
FEV1 increased by 0.50±0.07 L (mean±sem) after fluticasone and by 0.37±0.07 L after montelukast (p<0.001, each), and PC20 by 1.33±0.13 (p<0.001) and 0.15±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·s1) 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.
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