title: The effect of montelukast on exhaled nitric oxide of alveolar and bronchial origin in inhaled corticosteroid-treated asthma.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  Leukotriene receptor antagonists administered systemically might decrease small airway/alveolar sites of inflammation when combined to inhaled corticosteroid therapy.
authors.affiliation: Asthma and Airway Centre, University Health Network, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada. leandro.fritscher@uhn.on.ca
authors.forename: Leandro G
authors.initials: LG
authors.lastname: Fritscher
authors.forename: Marcelo T
authors.initials: MT
authors.lastname: Rodrigues
authors.forename: Noe
authors.initials: N
authors.lastname: Zamel
authors.forename: Kenneth R
authors.initials: KR
authors.lastname: Chapman
mesh_terms: D000085:Acetates / Q000008:administration & dosage* / Q000493:pharmacokinetics; D000280:Administration, Inhalation; D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000493:pharmacokinetics; D000328:Adult; D000730:Androstadienes / Q000008:administration & dosage / Q000494:pharmacology; D018927:Anti-Asthmatic Agents / Q000008:administration & dosage / Q000494:pharmacology; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism*; D001980:Bronchi / Q000187:drug effects / Q000378:metabolism*; D003521:Cyclopropanes; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume / Q000187:drug effects; D006801:Humans; D020024:Leukotriene Antagonists / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D011446:Prospective Studies; D011804:Quinolines / Q000008:administration & dosage* / Q000493:pharmacokinetics; D013440:Sulfides
chemical_list: D000085:Acetates; D000305:Adrenal Cortex Hormones; D000730:Androstadienes; D018927:Anti-Asthmatic Agents; D003521:Cyclopropanes; D020024:Leukotriene Antagonists; D011804:Quinolines; D013440:Sulfides; D009569:Nitric Oxide; D000068298:Fluticasone; C093875:montelukast