Article

The effect of montelukast on exhaled nitric oxide of alveolar and bronchial origin in inhaled corticosteroid-treated asthma.

Asthma and Airway Centre, University Health Network, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.
Respiratory medicine (impact factor: 2.33). 10/2008; 103(2):296-300. DOI:10.1016/j.rmed.2008.08.007 pp.296-300
Source: PubMed

ABSTRACT Inhaled corticosteroid therapy suppresses nitric oxide levels (NO) of airway origin but not necessarily NO of alveolar or small airway origin. Systemic therapy with an oral anti-leukotriene agent may suppress NO production in distal airways and alveoli not reached by inhaled therapy.
Adult patients with mild asthma were treated for 3 weeks with inhaled fluticasone 250 microg twice daily then with inhaled fluticasone plus oral montelukast 10 mg daily for 3 additional weeks. We monitored exhaled NO (eNO), spirometry, lung volumes, and asthma symptoms scores at baseline and at the end of each treatment period. In a subset of patients, we continued with montelukast monotherapy and repeated these measurements.
In the 18 patients studied, pulmonary function parameters and asthma symptom scores were not altered significantly from baseline by any therapy. The total eNO at baseline was 55+/-35.3 ppb, dropping to 28.1+/-15.3 ppb (p=0.005) after 3 weeks of fluticasone and to 23.5+/-14 ppb (p=0.001 vs. baseline) after the addition of montelukast. The trend towards reduced total eNO with the combination therapy vs. monotherapy was not statistically significant. Alveolar eNO dropped from 4.2+/-2.4 at baseline to 3.0+/-1.5 (p=0.1) after fluticasone and then to 2.2+/-0.9 (p=0.08 vs. baseline) after fluticasone plus montelukast, increasing then to 3.8+/-1.8 after montelukast alone (p=0.6 vs. baseline).
Leukotriene receptor antagonists administered systemically might decrease small airway/alveolar sites of inflammation when combined to inhaled corticosteroid therapy.

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    Article: Impact of analysis interval on the multiple exhalation flow technique to partition exhaled nitric oxide.
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    ABSTRACT: Exhaled nitric oxide (eNO) is elevated in asthmatics and is a purported marker of airway inflammation. By measuring eNO at multiple flows and applying models of eNO exchange dynamics, the signal can be partitioned into its proximal airway [J' aw NO (nl/sec)] and distal airway/alveolar contributions [CA(NO)(ppb)]. Several studies have demonstrated the potential significance of such an approach in children with asthma. However, techniques to partition eNO are variable, limiting comparisons among studies. The objective of this study is to examine the impact of the analysis interval (time or volume) on eNO plateau concentrations and the estimation of J' aw NO and CA(NO). In 30 children with mild to moderate asthma, spirometry and eNO at multiple flows (50, 100, and 200 ml/sec) were measured. The plateau concentration of eNO at each flow was determined using two different methods of analysis: (1) constant time interval and (2) constant volume interval. For both methods of analysis, a two-compartment model with axial diffusion was used to characterize J' aw NO and CA(NO). At a flow of 200 ml/sec, the time interval analysis predicts values for eNO that are smaller than the volume interval analysis. As a result, there are significant differences in CA(NO) between the methods of analysis (volume > time). When using the multiple flow technique to partition eNO, the method of analysis (constant time vs. constant volume interval) significantly affects the estimation of CA(NO), and thus potentially the assessment and interpretation of distal lung inflammation.
    Pediatric Pulmonology 02/2010; 45(2):182-91. · 2.53 Impact Factor

Keywords

18 patients
 
3 additional weeks
 
3 weeks
 
Adult patients
 
airway origin
 
asthma symptom scores
 
asthma symptoms scores
 
combination therapy
 
inhaled corticosteroid therapy
 
inhaled fluticasone
 
inhaled fluticasone 250 microg
 
inhaled therapy
 
mild asthma
 
montelukast monotherapy
 
oral anti-leukotriene agent
 
oral montelukast 10 mg
 
pulmonary function parameters
 
small airway origin
 
Systemic therapy
 
treatment period