Our data suggest that repeated exposure to ozone, at a peak ambient air level, can enhance both functional and inflammatory responses to inhaled allergen in subjects with pre-existing allergic airway diseases, and that these effects might reach a clinically relevant magnitude.
Whether leukotriene receptor antagonists exhibit adequate antiinflammatory 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 mg b.i.d.) on functional and inflammatory parameters in steroid-naïve patients with moderate asthma.Forty patients (forced expiratory volume in one second (FEV1), 60-80% predicted) were studied in a double-blind, randomised, crossover design. Treatment periods were separated by 3-8 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 b 2 -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 (pv0.001, each), and PC20 by 1.33¡0.13 (pv0.001) and 0.15¡0.17 (NS) doubling doses, respectively. Correspondingly, percentages of sputum eosinophils were reduced by factor 2.7 (pv0.01) and 1.4 (nonsignificant (NS)), and the levels of exhaled NO (at 50 mL?s -1 ) by factor 2.1 (pv0.01) 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.
Shunt derived from MMIMS inert gas retention data correlated well with R-S during breathing of oxygen. Shunt as derived by MMIMS was generally less than R-S.
This study assessed the effect of the leukotriene receptor antagonist montelukast on hypertonic saline-induced airway obstruction.A total of 29 patients with chronic obstructive pulmonary disease (forced expiratory volume in one second (FEV1), 42 ¡ 4% predicted) received either 10 mg montelukast and 3 h later placebo via metered-dose inhaler (MDI) (M), or placebo and 3h later 200 mg salbutamol (S), or two doses of placebo (P), in a randomised order. Patients inhaled salbutamol 1 h after MDI and the challenge was performed 15 min later (3% saline, 5 min). Data are given as per cent changes versus baseline.Compared to P, S caused significant bronchodilation in FEV1 (7.3%) and forced inspiratory volume in one second (FIV1) (4.5%), and M in FIV1 (1.5%). The salineinduced fall in FEV1 was lower after M (-5.8%), compared with S (-10.3%) and P (-13.1%). FEV1 (11.3%) and FIV1 (7.6%) was improved over baseline after recovery by M but not P and S. Recovery times regarding FEV1 (8.5 min) and FIV1 (15.2 min) were shortest after M, respective values for S being 16.8 and 20.4 min, and for P 15.9 and 21.2 min. Effects were strongest in patients with low baseline FEV1 and/or inhaled corticosteroids.Data from this study indicate beneficial effects of montelukast on hypertonic salineinduced airway responses in patients with chronic obstructive pulmonary disease, particularly those with severe disease. The major effect was an accelerated recovery leading to values above baseline. Eur Respir J 2003; 22: 926-930.
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