Perng Diahn-Warng, Wu Cheng-Che, Su Kang-Cheng, Lee Yu-Chin, Perng Reury-Perng, Tao Chi-Wei
Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Lung. 2006 Jul-Aug;184(4):217-22. doi: 10.1007/s00408-005-2586-8.
The aim of this study was to determine whether combined inhaled corticosteroids and long-acting beta(2) agonists can suppress eosinophilic inflammation in chronic dostructive plumonary disease (COPD) and to investigate the association between the level of eosinophilia and the degree of bronchodilator reversibility. Sixty-two patients with stable COPD (forced expiratory volume in 1 [FEV(1)] of 30%-70% predicted before bronchodilation) were enrolled from our outpatient clinic. Patients received inhaled fluticasone (100 microg)/salmeterol (50 microg) twice daily for two months. Lung function measurements, bronchodilator tests, and sputum induction were performed. The number of inflammatory cells and mediators, including interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and eosinophilic cationic protein (ECP), were measured. Treatment with inhaled fluticasone and salmeterol significantly suppressed eosinophilic inflammation in COPD patients with sputum eosinophilia (mean 8.9% +/- 2.0% vs. 1.6% +/- 0.5%, p = 0.003), but insignificant differences in FEV(1) and FVC between patients with and without eosinophilia suggested that suppression of eosinophilic inflammation had no effect on FEV(1) or FVC. Reduction in the percentage of eosinophils was significantly correlated with decreased levels of ECP (r = 0.48, p < 0.001). Levels of neutrophils, IL-8, and TNF-alpha were not affected. Sputum eosinophilia was not related to the degree of bronchodilator reversibility. The degree of bronchodilator reversibility did not predict the increase in FEV(1) and FVC after treatment with inhaled corticosteroids/long-acting beta(2) agonists. Suppression of eosinophilic inflammation and bronchodilator responsiveness indices were not correlated with clinical outcomes in COPD patients treated with inhaled corticosteroids/long-acting beta(2) agonists.
本研究的目的是确定吸入性糖皮质激素与长效β₂受体激动剂联合使用是否能抑制慢性阻塞性肺疾病(COPD)中的嗜酸性粒细胞炎症,并研究嗜酸性粒细胞水平与支气管扩张剂可逆性程度之间的关联。从我们的门诊招募了62例稳定期COPD患者(支气管扩张前第1秒用力呼气容积[FEV₁]为预测值的30% - 70%)。患者每日两次吸入氟替卡松(100μg)/沙美特罗(50μg),持续两个月。进行肺功能测量、支气管扩张剂试验和痰液诱导。测量包括白细胞介素 - 8(IL - 8)、肿瘤坏死因子 - α(TNF - α)和嗜酸性粒细胞阳离子蛋白(ECP)在内的炎症细胞和介质数量。吸入氟替卡松和沙美特罗治疗显著抑制了痰嗜酸性粒细胞增多的COPD患者的嗜酸性粒细胞炎症(平均值8.9%±2.0%对1.6%±0.5%,p = 0.003),但有嗜酸性粒细胞增多和无嗜酸性粒细胞增多患者之间的FEV₁和FVC无显著差异,提示抑制嗜酸性粒细胞炎症对FEV₁或FVC无影响。嗜酸性粒细胞百分比的降低与ECP水平的降低显著相关(r = 0.48,p < 0.001)。中性粒细胞、IL - 8和TNF - α水平未受影响。痰嗜酸性粒细胞增多与支气管扩张剂可逆性程度无关。支气管扩张剂可逆性程度不能预测吸入性糖皮质激素/长效β₂受体激动剂治疗后FEV₁和FVC的增加。在接受吸入性糖皮质激素/长效β₂受体激动剂治疗的COPD患者中,嗜酸性粒细胞炎症的抑制和支气管扩张剂反应性指标与临床结局无关。