| Background:Bronchial asthma is a chronic inflammatory disorder of airway which involves multicellular and a variety of cytokines. The pathophysiological changes of asthma include inflitration of eosinophil and other inflammatory cells, airway hypersensitivity and airway remodeling. Cysteinyl leukotrienes (CysLTs) stimulates the accumulation of eosinophil, overdevelopment of mucus glands, excessive production of mucus and bronchoconstriction. The leukotriene receptor antagonists (LTRAs) block the leukotriene-related inflammatory reaction in the airways, and subsequently reduce symptoms, frequency of asthma attack, and improve the pulmonary function. The guidelines of the global initiative of asthma (GINA, 2006 revision) and our national guidelines for diagnosis and prevention of childhood asthma (2008 revision) have recommended the low-dose inhaled steroids (ICS) and oral LTRAs respectively as the first-line monotherapy for mild persistent asthma in children. The ICS are well-accepted anti-inflammatory treatments for asthma which inhibit the initial processes of airway inflammation as well as subsequent reactions involving airway inflammatory cellular and airway structural cells. However, the LTRAs only work by blockade of leukotriene-related inflammatory reaction in airways. Currently, there is no consensus that the LTRA can achieve the equivalent treatment effects as that of ICS. Objective:To compare the efficacy of ICS and LTRAs management of mild persistent asthma in children.Methods:Sixty subjects with mild persistent asthma were randomized to inhaled budesonide (BUD) or oral montelukast (LTRA) groups. In BUD group, the subjects (16 male and 14 femal, mean aged (8.37±2.04) years) inhaled budesonide 200μg twice daily for 8 weeks. In LTRA group, the subjects (15 male and 15 femal) received montelukast 5mg quaque nocte for 8 weeks. Before and after 8-week treatment, the FEV1, PD20, EOS% and concentration of LTs in sputum, and asthma symptom score were measured.Results1. At baseline, there is no significantly difference in all characteristics between the subjects in two treatment arms.2. Both daytime symptoms and nighttime symptoms were significantly reduced after treatments of either BUD (asthma symptom score: daytime (1.26±0.51) vs. (0.13±0.18), p<0.01; nighttime (0.13±0.18) vs. (0.093±0.28), p<0.05) or LTRA (asthma symptom score: daytime (1.17±0.27) vs. (0.19±0.26), p<0.01; nighttime (0.48±0.38) vs. (0.12±0.22), p<0.05)..3. Pulmonary ventilation function: The pulmonary function was significantly improved after treatment of BUD. The mean FEV1 measured after BUD treatment was (1.61±0.35)L compared with (1.42±0.46)L at baseline (p<0.01). However, no significant improvement of pulmonary function was observed in LTRA group.4. Bronchial hyperactivity: Significant reduction of the airway hypersensitivity was observed in both treatment groups. The PD20 increased from (1.68±1.74)μmol to (3.19±2.17)μmol in BUD group, and from (1.90±1.79)μmol to (2.87±1.75)μmol in LTRA group (both p<0.01).5. Sputum EOS cell counts: The EOS% in sputum was significantly decreased from (22.2±23.6)% to (6.39±6.63)% in BUD group (p<0.01), although there was no significant change in concentration of LTs in sputum after BUD treatment.6. Sputum serum LTs: The concentration of LTs in sputum was reduced by LTRA from (1263.29±680.78)pg/ml to (569.45±577.89)pg/ml (p<0.01), whilst no statistically significant change of sputum EOS% was observed in this groupConclusions:The present study showed that both the inhaled budesonide and oral montelukast significantly reduced symptoms of persistent asthma and airway hypersensitivity. The inhaled budesonide is more effective in improving pulmonary function and decreasing eosinophil accumulation. The montelukast is better in reducing cysteinyl leukotrienes. |
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