摘要目的 测定慢性阻塞性肺疾病急性加重期(AECOPD)和COPD稳定期患者血清、诱导痰中脂连素(Adiponectin,APN)水平,以探讨APN在COPD发病机制中的作用.方法 采用前瞻性观察研究,收集2008年10月至2009年10月上海市第五人民医院急诊科30例男性AECOPD患者(A组)、呼吸科门诊30例男性COPD稳定期患者(B)组及30例男性非吸烟健康体检者(C组)的血清和诱导痰.所有入选对象均为正常体质量的男性(BMI范围为18.5～24.9 kg/m2),并排除严重支气管哮喘、支气管扩张及自身免疫系统等疾病.计数诱导痰中细胞总数并分类,采用ELISA法测定血清和诱导痰中APN与白介素-8(IL-8)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的水平,并测定三组人群的肺功能.组间资料比较用成组t检验、方差分析或非参数检验,相关性分析用Pearson相关或Spearmn秩相关.结果 A组血清、诱导痰中APN水平显著高于B组和C组(P＜0.01),B组血清、诱导痰中APN水平显著高于C组(P＜0.01).A组血清、诱导痰中APN与IL-8,TNF-α呈正相关(r值分别0.739,0.734,0.852,0.857,P＜0.05).B组血清、诱导痰中APN与IL-8,TNF-2呈正相关(r值分别为0.751,0.659,0.707,0.867,P＜0.05).A组诱导痰中APN与气道中性粒细胞呈正相关(r=0.439,P＜0.05).结论 APN参与了COPD的全身和气道炎症过程,此过程与气道中性粒细胞和IL-8,TNF-α等炎症因子有关,可作为一种新的炎症标志物.

abstractsObjective To determine the level of adiponectin (APN) in serum and induced sputum of patients with chronic obstructive pulmonary disease both during acute exacerbation (AECOPD) and silent stage, and investigate APN' s role as a marker of inflammation in the pathogenesis of COPD. Method From October 2008 to October 2009,30 male AECOPD patients in the emergency department, 30 male silent COPD patients in the department of respiratory diseases and 30 healthy nonsmoking male volunteers were included. All subjects' serum and induced sputum were collected, and they were all of normal weight(BMI range of 18.5～ 24.9 kg/m2). Patients were excluded if they suffered from severe bronchial asthma, bronchiectasis or autoimmune disease. The number of cells in induced sputum was counted and the cell type was classified. The concentrations of APN, IL-8, IL-6 and TNF-α in both serum and sputum were measured by using ELISA, and their pulmonary function was tested. The different groups were compared among them by using the t -tests, ANOVA analysis or nonparametric analysis, the relation between variables was assessed by using the Pearson or Spearman correlation test. Results The concentrations of APN in both serum and induced sputum of AECOPD patients were significantly higher than those in the silent COPD patients and the control subjects ( P ＜ 0.01 ). The concentrations of APN in the silent COPD patients were significantly higher than those in the control subjects ( P ＜ 0. 01 ). There were significant relationships between the concentrations of APN in serum and induced sputum and the levels of IL-8 and TNF-α in AECOPD patients ( r = 0.739, 0. 734,0.852 and 0. 857, respectively, P ＜ 0. 05) and in silent COPD patients ( r = 0.751,0.659, 0.707 and 0.867, respectively, P ＜0.05). There was significant relation betweenship between APN and neutrophil in induced sputum of AECOPD patients (r = 0.439, P ＜ 0.05). Conclusions APN was involved in the process of systemic and airway inflammation of COPD, and it was related with IL-8 and TNF-α. APN can be used as a new inflammation marker for COPD.