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目的 探讨重症急性呼吸综合征 (SARS)患者肺部严重炎症反应的发生机制。方法 选择 2 4例本院确诊的SARS患者 ,于发病第 1、第 2、第 3～ 4周及康复出院后 1个月 (发病 8～ 9周 )收集抗凝静脉血 ,以定量ELISA法检测其血浆白细胞介素 (IL) 1β、IL 2、IL 4、IL 8、IL 10、IL 12 p70、干扰素γ(IFNγ)及肿瘤坏死因子α(TNFα)水平在病程中的改变。并选择 12例正常人作为对照。结果 数据以中位数 (四分位数间距 )表示 ,与正常对照组 [IL 8:6 2 8ng/L( 3 4 3ng/L) ;TNFα :3 77ng/L( 3 4 0ng/L) ]相比 ,所有SARS病人在发病第 1周血浆IL 8浓度明显升高 [31 2 3ng/L( 78 5 1ng/L) ],P <0 0 1,75 % ( 18/2 4 )的病人在发病 3～ 4周达到最高峰 14 9 6 5ng/L( 2 4 5 97ng/L) ,P <0 0 1,至出院后 1个月 (发病 8～ 9周 )平均血浆IL 8浓度降至 8 2 3ng/L( 8 0 7ng/L)。血浆TNFα浓度也有异常升高 ,在发病第 2周为 2 3 12ng/L( 2 6 7 33ng/L) ,P <0 0 1,发病 3～ 4周达到高峰136 35ng/L( 4 76 83ng/L) ,P <0 0 5 ,出院后 1个月下降至 94 88ng/L( 2 77 18ng/L) ,仍高于正常水平 (P <0 0 1)。其他 6种细胞因子与对照组比较 ,差异无显著性。结论 SARS病人体内发生着复杂的细胞因子网络性连锁反应 ,由此产?
Objective To investigate the pathogenesis of severe pulmonary inflammatory response in patients with severe acute respiratory syndrome (SARS). Methods Twenty-four patients with SARS diagnosed in our hospital were enrolled in this study. Anticoagulation venous blood was collected on the 1st, 2nd, 3rd to 4th weeks of illness and 1 month after the discharge (8 to 9 weeks) The changes of plasma interleukin (IL) 1β, IL 2, IL 4, IL 8, IL 10, IL 12 p70, IFN γ and tumor necrosis factor α (TNFα) 12 normal subjects were chosen as control. Results The data are presented as median (interquartile range) versus normal control [IL 8: 62 8 ng / L (34 3 ng / L); TNFa: 77 77 ng / L Compared with all patients with SARS, the plasma IL-8 levels were significantly increased in the first week of illness [31 2 3 ng / L (78 5 1 ng / L)], P <0.01 1 1% (18/2 4) The peak value reached 14 9 6 5ng / L (2 457ng / L) at 3 ~ 4 weeks after the onset of disease, P <0.01, and the average plasma IL 8 concentration decreased to 8 after 1 month (8-9 weeks of onset) 2 3ng / L (8 0 7ng / L). There was also an abnormal increase of plasma TNFα concentration in the second week of the disease, which was 2 3 12 ng / L (267 33 ng / L), P 0 01, peaked at 35 weeks 4 ~ 83 ng / L, P <0.05, and dropped to 94 88 ng / L (2 77 18 ng / L) one month after discharge, still higher than the normal level (P <0.01). The other 6 kinds of cytokines compared with the control group, the difference was not significant. Conclusion SARS patients occur in complex cytokine network chain reaction, thus producing?