摘要：

Cigarette smoking induces neutrophilic airway inflammation and relative resistance to inhaled corticosteroids (ICS).We evaluated the influence of cigarette smoking on airway inflammation in patients with asthma and also compared the effect of ICS between smoking and nonsmoking in patients with asthma.Smokers with asthma (n = 81) and nonsmokers with asthma (n = 52) were recruited for the study. We examined lung function, fractional exhaled nitric oxide (FeNO) concentration, induced sputum, and acetylcholine inhalation before and 6 months after inhaling budesonide at 800 μg/day. Thirty-four healthy volunteers were included as controls.Smokers with asthma showed a lower forced expiratory volume in 1 second (FEV1) to forced volume capacity (FVC) ratio (p < 0.05), a lower FeNO (p < 0.01), a lower eosinophil proportion (p < 0.05), and a higher neutrophil proportion (p < 0.05) in induced sputum than nonsmokers with asthma. Bronchial hyperresponsiveness (the provocative concentration of acetylcholine [Ach] that produced a 20% fall in FEV1 [PC20-Ach]) was increased in smokers with asthma compared with nonsmokers with asthma (p < 0.05). Both smokers with asthma and nonsmokers with asthma exhibited more prominent airway obstruction, a higher FeNO, and a higher percentage of sputum eosinophils than the controls (p < 0.05 to p < 0.001, each). After 6 months of treatment with inhaled budesonide at 800 μg/day, the improvement in lung function (FEV1 to FVC ratio, flow at 50% forced vital capacity [V50% predicted] and flow at 25% forced vital capacity [V25% predicted]), the eosinophil proportion in induced sputum and PC20-Ach were lower in smokers with asthma than nonsmokers with asthma (p < 0.05).Smokers with asthma showed neutrophilic airway inflammation in addition to eosinophilic inflammation, and cigarette smoking impaired the efficacy of ICS treatment in mild-to-moderate asthma. These findings have important implications for the management of patients with asthma and who smoke.

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