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Exhaled nitric oxide before and after montelukast sodium therapy in school-age children with chronic asthma: a
D L Bratton1, M J Lanz, N Miyazawa
1Departments of Pediatrics and Medicine, National Jewish Medical and Research Center, Denver, CO 80206, USA. brattond@njc.org
Insights
Exhaled nitric oxide (ENO) is elevated in children with asthma. Montelukast sodium treatment significantly reduced ENO, suggesting an anti-inflammatory effect in pediatric asthma management.
Area of Science:
- Pediatric Pulmonology
- Allergy and Immunology
- Respiratory Medicine
Background:
- Exhaled nitric oxide (ENO) serves as a key biomarker for airway inflammation in asthma.
- Asthma in children often presents with elevated ENO levels compared to healthy controls.
Purpose of the Study:
- To evaluate the effect of montelukast sodium on exhaled nitric oxide (ENO) levels in children with mild to moderate persistent asthma.
- To assess the anti-inflammatory role of leukotriene D4 receptor antagonism in pediatric asthma.
Main Methods:
- 12 children (6-11 years) with mild to moderate persistent asthma participated.
- ENO concentrations were measured before, during (4 weeks), and after (2 weeks) montelukast sodium treatment.
- Pulmonary function (FEV(1)) and albuterol use were also monitored.
Main Results:
- Baseline ENO was significantly higher in asthmatic children (83 ppb) versus controls (13 ppb).
- Montelukast sodium treatment significantly reduced ENO (to 58 ppb; P < 0.01), which increased upon withdrawal (69 ppb).
- No significant correlation was found between ENO changes and improvements in FEV(1) or reduced albuterol use.
Conclusions:
- Exhaled nitric oxide (ENO) is elevated in children with mild asthma.
- Montelukast sodium treatment effectively reduces ENO levels in pediatric asthma, indicating an anti-inflammatory action.
- ENO reduction occurs independently of significant changes in pulmonary function or bronchodilator use.
Abstract:
Exhaled nitric oxide (ENO) is a surrogate marker of airway inflammation in asthma. In 12 children aged 6-11 years with mild to moderate persistent asthma, ENO concentrations were measured before and after 4 weeks of treatment with montelukast sodium, a leukotriene receptor antagonist, and 2 weeks after withdrawal of therapy. Baseline ENO levels (mean and 95% confidence interval) were significantly elevated in patients with asthma compared to age-matched nonasthmatic control subjects, with levels of 83 (42-123) vs. 13 (11-15) ppb (P < 0.001). After treatment with montelukast sodium, there was a significant (P < 0.01) reduction in ENO to 58 (27-89) ppb which again rose to 69 (38-99) ppb 2 weeks after treatment was withdrawn. During treatment, the fall in ENO was accompanied by nonsignificant improvements in prebronchodilator forced expiratory volume in 1 s (FEV(1)) from 81-85% predicted or reductions in use of albuterol from a mean of 2.5 to 1.6 puffs/day. Individual ENO measurements and change in ENO concentrations with treatment did not correlate with either pulmonary function changes or use of bronchodilator. These data show that ENO is elevated in children with relatively mild asthma treated with bronchodilator alone, and that treatment with montelukast sodium for 4 weeks results in a significant reduction in ENO concentrations, even in the absence of significant changes in pulmonary function. These findings suggest an anti-inflammatory role for leukotriene D(4) receptor antagonism in the treatment of children with mild to moderate asthma.
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