Source: Annual Congress 2002 - Bronchial responsiveness in asthma and COPD
Disease area: Airway diseases

Abstract

Based on previous observations on potential mediators of airway obstruction in COPD (AJRCCM 164:1810, 2001), the present pilot study aimed at assessing the effect of the leukotriene receptor antagonist montelukast on the airway response elicited by hypertonic saline inhalation. Twenty patients with COPD (mean FEV₁, 44 (range, 22-61) %pred) were included. After initial lung function measurements including forced expiratory (FEV₁ ) and inspiratory (FIV₁ ) volumes, patients received either 10 mg montelukast and 3 h later placebo via MDI (M), or placebo and 3 h later 200 μg salbutamol (S), or placebo at both time points (P). 1 h after inhalation (4 h after start) lung function was measured again. Patients then inhaled additional 200 μg salbutamol and 15 min later 3 % saline from an ultrasonic nebuliser for 5 min; lung function was monitored over 40 min. Statistical analysis was performed by ANOVA. Mean changes relative to initial values as measured before administration of the oral medication were:

	bronchodilation at 4 h		maximum fall after 3 % saline		time needed for recovery to baseline
	(%)		(%)		(min)
	FEV1	FIV1	FEV1	FIV1	FEV1	FIV1
P	-2.1	-5.3	13.4	27.2	19.3	26.4
S	8.0	4.4	9.8	24.3	20.8	24.4
M	0.1	1.6	4.9	24.7	7.8	14.9

Compared to the time course observed after placebo, S caused bronchodilation in terms of FEV₁ and FIV₁ , and M in FIV₁ only. M but not S reduced the maximum saline-induced fall in FEV₁ (p<0.05). Recovery times for both FEV₁ and FIV₁ were shortest (p<0.05) after M. These data suggest that montelukast is capable of exerting bronchoprotective effects in COPD in the model of hypertonic saline-induced airway obstruction. Supported by a grant from MSD, Haar, Germany

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Citations should be made in the following way:
I. E. Zühlke, D. Nielsen-Gode, F. Kanniess, K. Richter, R. A. Jörres, H. Magnussen (Grosshansdorf, Germany). Montelukast attenuates the airway response to hypertonic saline in patients with moderate to severe COPD. Eur Respir J 2002; 20: Suppl. 38, 1204

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