Montelukast added to budesonide in children with persistent asthma: a randomized, double-blind, crossover study.

OBJECTIVE: We tested the hypothesis that adding montelukast to budesonide would improve asthma control in children with inhaled glucocorticoid-dependent persistent asthma. STUDY DESIGN: In a multicenter, randomized, double-blind, crossover study, we compared the benefit of adding montelukast, 5 mg, or placebo once daily to budesonide, 200 microg, twice daily. RESULTS: After a 1-month run-in with budesonide, 200 microg, twice daily, 279 children were randomized to montelukast or placebo. The mean +/- SD age was 10.4 +/- 2.2 years, the mean forced expiratory volume in 1 second (FEV(1)) was 77.7% +/- 10.6% predicted, and reversibility was 18.1% +/- 12.9%. Compared with adding placebo to budesonide, adding montelukast produced significant improvements in mean percent change from baseline FEV(1) (P =.062 [P =.010 for per-protocol analysis]), mean absolute change from baseline FEV(1) (P =.040), mean increase from baseline in morning (P =.023) and evening (P =.012) peak expiratory flows, decrease in exacerbation days by approximately 23% (P <.001), decreased beta2-agonist use (P =.013), and reduced blood eosinophil counts (P <.001). The treatments did not differ significantly with regard to safety. CONCLUSIONS: Montelukast, 5 mg, added to budesonide improved asthma control significantly, indicated by a small additive effect on lung function and a clinically relevant decrease in asthma exacerbation days.

Lung function in infants with chronic pulmonary disease after severe adenoviral illness.

OBJECTIVE: To evaluate pulmonary function and bronchodilator responses in young children with chronic pulmonary disease (CPD) after a severe adenoviral lower respiratory tract infection. METHODS: Pulmonary function tests were performed in 13 patients (mean age, 1.32 +/- 0.8 years) with CPD and were compared with a control group of 13 healthy infants (mean age, 1.16 +/- 0.4 years). RESULTS: Respiratory rate, peak tidal expiratory flow (PTEF), PTEF/tidal volume, absolute time up to PTEF, time percentage to PTEF, volume percentage for PTEF, and compliance and resistance of the respiratory system were significantly affected in the CPD group. Similarly, maximal flow at functional residual capacity (V'maxFRC) was 56.0 +/- 42 mL/s and 373 +/- 107 mL/s in the CPD and control groups, respectively (P =.001). No within-group differences with baseline values or between-group differences were noted in response to treatment with ipratropium bromide or albuterol. CONCLUSION: Young children with CPD caused by adenovirus have pulmonary function changes characterized by severe obstruction and diminished lung distensibility not responsive to the administration of inhaled ipratropium bromide or albuterol.