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机构地区:[1]长治医学院附属和平医院呼吸科,山西长治150040 [2]中南大学湘雅医院二院呼吸科,长沙410001
出 处:《中外医疗》2011年第30期4-7,共4页China & Foreign Medical Treatment
基 金:湖南省科技厅科技计划重点项目;编号2010FJ2004
摘 要:目的 探讨急性发作期及缓解期的COPD患者全身炎症反应和气道炎症反应的变化及其相互关系。方法 选取符合COPD诊断标准的患者45例、采用ELISA法分析COPD急性发作期(AECOPD)、缓解期患者诱导痰上清液和外周血清中白介素8(IL-8)和肿瘤坏死因子α(TNF-α)的水平,散射比浊法分析诱导痰上清液和外周血清中C反应蛋白(CRP)水平,并同时测定患者FEV1.0占预计值百分数(FEV1.0pre)。采用SPSS12.0软件进行统计分析。结果 (1)COPD急性发作时外周血清及诱导痰上清液中IL-8、TNF-α和CRP均明显高于缓解期水平(均P<0.01)。(2)痰液及外周血清IL-8、TNF-α、CRP水平与FEV1.0pre呈负相关(均P<0.05)。(3)痰上清液中IL-8和TNF-α与血清中IL-8和TNF-α水平无明显相关(分别为r=0.492,P>0.05;r=0.412,P>0.05),痰上清液中CRP与血清CRP水平明显相关(r=0.864,P<0.01)。结论 (1)COPD急性加重期较缓解期气道局部炎症和全身炎症反应增强,并可能加重了COPD患者的气流阻塞;(2)COPD的全身及气道炎症反应可能存在不同的炎症反应途径。Objective To investigate the changes and correlations between airway inflammation and systemic inflammation during acute exacerbations of chronic obstructive pulmonary disease(AECOPD)and clinical stable state.Methods Blood serum levels and induced sputum supernate fluid contents of IL-8, TNF-α were measured with ELISA and CRP by nephelometry method in 45 patients with COPD both during exacerbation and remission.As well as lung function FEV1.0% Pred was examined in patients with COPD during acute exacerbation and remission.SPSS 12.0 was used to perform statistics.Results (1)After treatment,both the blood serum levels and induced sputum supernate fluid contents of IL-8, TNF α,CRP during remission were significantly lower than those in patients with COPD during exacerbation(all P〈0.01).(2)Both the blood serum levels and induced sputum supernate fluid contents of respectively IL-8,TNF-α,CRP were negatively correlated with the FEV1.0% Pred in patients with COPD(all P〈0.05).(3)The levels of IL-8,TNF-α were not correlated between in blood serum and in induced sputum supernate fluid(r=0.492,P〈0.05;r=0.412,P〈0.05), but CRP were closely correlated(r=0.864,P〈0.01).Conclusion (1)Airway inflammation and systemic inflammation during exacerbation were obviously reinforced than during remission, and possibly aggravated air current obstruct of COPD.(2)There were possibly different inflammatory pathways between airway inflammation and systemic inflammation.
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