血必净对危重病患者可溶性髓系细胞表达触发受体1及炎症因子表达的影响

目的 探讨血必净注射液对危重病患者可溶性髓系细胞表达的触发受体1(sTREM-1)及炎症因子表达的影响.方法　将入住我院重症加强治疗病房(ICU)的危重病患者92例随机分为常规治疗组44例和与血必净治疗组48例,在相同的常规治疗基础上,血必净治疗组给予血必净注射液100 ml静脉滴注,每日2次,连续使用7天.两组患者治疗前及治疗后7天,分别抽血检测sTREM-1、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素10(IL-10)的水平,记录全身炎症反应综合征(SIRS)、多器官功能障碍综合征(MODS)发生的情况及预后.结果 血必净治疗组能明显降低危重病患者体内sTREM-1、TNF-α、IL-6、IL-6/IL-10水平,治疗后sTREM-1和IL-6明显低于常规治疗组(49.17±30.42)ng/L vs(70.24±36.17)ng/L;(20.41±21.72)ng/L vs (54.91±21.02) ng/L( P＜0.01),MODS发生率、28天病死率明显下降(P＜0.05).结论 血必净注射液能有效改善患者预后,降低脏器功能不全的发生率,其机制可能与降低体内sTREM-1的水平、减轻全身炎症反应有关.

Effects of Xuebijing injection on soluble triggering receptor expressed on myeloid cells-1 and cytokine expression in critical patients

Objective To investigate the effects of Xuebijing injection on soluble triggering receptor expressed on myeloid cells-1 （sTREM-1） and cytokine expression in critical patients. Methods Ninety-two patients,admitted to intensive care unit （ICU） were randomly divided into the routine therapy group （ n =44） and Xuebijing therapy group （ n =48）,the latter group was given with Xuebijing injection 100 ml twice daily for 7 days besides routine therapies. Serum sTREM-1, tumor necrosis factor-α （TNF-α）, interleukim6 （IL-6）, IL-10, IL-6/IL-10 concentrations were determined before and 3 days and 7 days after administration. The ratio of （systemic inflammatory response syndrome, SIRS） and（multiple organ distress syndrome, MODS）were observed and the mortality was calculated at day 28. Results The concentrations of serum sTREM-1 ,TNF-α,IL 6 ,IL 6/IL-10 were significantly lower in Xuebijing therapy group after the treatment,compared with the routine therapy group, sTREM-1 and IL -6 in Xuebijing therapy group showed significant decrease,（49.17±30.42） ng/L vs （70.24±36.17） ng/L;（20. 41±21. 72） ng/L vs （54.91±21.02） ng/L （ P 〈0.05）. The ratio of MODS and the 28--day mortality decreased significantly in Xuebijing therapy group （ P 〈0.05）. Conclusion Xuebijing injection administration can improve clinical outcome,decrease the ratio of organ dysfunction by the mechanism of decreasing serum sTREM-1 and alleviating inflammatory response possibly in critical patients.