连续性血液净化对多脏器功能障碍综合征患者炎症介质的影响

目的探讨连续性血液净化（CBP）在多器官功能障碍综合征（MODS）中的应用及对血浆TNFα-、IL-1β和高迁移率族蛋白1（HMGB-1）浓度的影响。方法 MODS患者39例,在基础治疗上给予CBP治疗,于CBP前、CBP开始后4 h、12 h、24 h、48 h、72 h留取血标本,用ELISA法测定血浆TNF-,αIL-1β和HMGB-1;治疗前、治疗后24 h、48 h、72 h行急性生理功能和慢性健康状况（APACHEⅡ）评分,同时以未行CBP治疗的MODS患者25例作为对照。结果与CBP前比较,TNFα-、IL-1,βHMGB-1明显下降（P〈0.05）;CBP治疗48 h、72 h后APACHEⅡ评分明显下降（P〈0.05）。与对照组相比,在各时间点TNFα-、IL-1β、HMGB-1均下降,差异有统计学意义（P〈0.05）;APACHEⅡ评分明显降低（P〈0.05）。两组患者28 d病死率差异无统计学意义（P〉0.05）。结论过度的炎症反应是MODS发生的本质原因之一,CBP能够削弱血循环中炎症介质的峰值浓度,有效遏制过度的炎症反应,从而起到防治MODS的作用。

Effects of Continuous Blood Purification on the Levels of Plasma Inflammatory Mediators in Patients with Multiple Organ Dysfunction Syndrome

Objective To investigate the application and the effect of TNF-α,IL-1βand high mobility group-1 protein（HMGB-1）in plasm of continuous blood purification in patients with multiple organ disorder syndrome（MODS）.Methods Thirty-nine patients with MODS received CBP besides regular treatment,plasma levels of TNF-α,IL-1β and HMGB-1 were detected by enzyme-linked immunosorbent assay（ELISA）before（baseline）and 4 hours,12 hours,24 hours,48 hours and 72 hours after CBP,respectively.acute physiological and chronic health evaluation Ⅱ（APACHEⅡ）score were recorded before CBP and 24 hours,48 hours and 72 hours after CBP.Twenty-five patients with MODS who treated with conventional regular treatment without CBP served as control group.Results TNF-α,IL-1β,HMGB-1 were significantly decreased compared with the baseline values before CBP（P0.05）,APACHEⅡ score were significantly decreased after CBP（P0.05）.The levels of TNF-α,IL-1β and HMGB-1 at 4 hours,12 hours,24 hours,48 hours and 72 hours after CBP in CBP group were lower than those in control group at according time（P0.05）.There were no significant difference in 28 day mortality between the treatment group and the control group（P0.05）.Conclusion Excessive inflammatory response may be the essential pathogenesis of MODS.CBP can cut down the peak value of inflammatory cytokines which can prevent and treat MODS through restraining excessive inflammatory response.