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机构地区:[1]广东省深圳市第二人民医院急诊科,广东深圳518035
出 处:《实用临床医药杂志》2004年第4期53-55,共3页Journal of Clinical Medicine in Practice
摘 要:目的 探讨创伤性休克患者血中脂多糖结合蛋白 (LBP)的变化规律及其临床意义。方法 动态监测 47例创伤性休克患者血LBP浓度 ,并对发生全身炎症反应综合征 (SIRS)或MODS的患者连续抽血 3次培养进行细菌学检查。比较创伤性休克和非休克 ,SIRS、MODS和非SIRS ,死亡组和存活组 ,血细菌培养阳和阴性患者之间LBP浓度的差异。描记所有创伤性休克患者LBP浓度的变化曲线。结果 创伤性休克患者血LBP浓度 [( 2 4 1± 11 3 ) μg/L]明显高于非休克患者 [( 8 9±6 4) μg /L] ,有显著性差异 ( P <0 0 1) ;SIRS、MODS组患者血LBP浓度 [( 3 8 7± 2 6 4)、( 4 2 6± 3 0 9) μg /L]明显高于非SIRS组患者 [( 19 1± 12 6) μg/L] ,有显著性差异 ( P <0 0 1) ;SIRS和MODS组之间 ,死 1 4亡组 [( 4 3 7± 2 9 1) μg/L]与存活组 [( 4 0 2± 3 1 2 ) μg/L]之间 ,14例血培养阳性 [( 3 8.7± 3 ) μg/L]与 3 3例阴性 [( 3 7 6± 2 7 8) μg/L]之间患者血LBP浓度差异均无统计学意义 (P >0 0 5 )。创伤性休克患者发病后 2 4~ 48h内 ,血LBP浓度开始升高 ,1周左右达高峰 ,此后逐渐下降 ,与患者的预后无明显相关。结论 LBP参与创伤性休克患者SIRS和MODS的发生 ,但并不与患者的预后密切相关 ;Objective: To explore the laws of changes and clinic significance of lipopolysaccharide binding protein (LBP) in traumatic shock patients. Methods: LBP in 47 traumatic shock patients was monitored dynamically. The patients with SIRS or MODS were taken blood bacteriology detection 3 times. The deferences of LBP were compared between groups of patients with traumatic shock and non、traumatic shock; patients with SIRS or MODS and non、SIRS; patients with SIRS and MODS; survivor and non、survivor; negative and positive in blood bacteriology culture respectively. The change curves of LBP concentration in all of the traumatic shock patients were painted. Results: There was significant deference in concentration of LBP between traumatic shock group [(24.1±11.3) μg /L] and non、traumatic shock [(8.9±6.4) μg/L] group; SIRS [(38.7±26.4) μg /L] or MODS [(42.6±30.9) μg/L] group and non、SIRS group [(19.1±12.6) μg/L] respectively (P<0.01). Concentration of LBP in traumatic shock group and SIRS or MODS group were higher than that of non、traumatic shock group and non、SIRS group respectively. There was no significant deference in concentration of LBP between SIRS group and MODS group; survivor group [(40.2±31.2) μg /L] and non、survivor group [(43.7±29.1) μg /L]; negative group [(37.6±27.8) μg /L] and positive group [(38.7±31.4) μg /L] in blood bacteriology culture respectively (P>0.05). LBP concentration in all of the traumatic shock patients were raised in 24 or 48 hours, and arrived at pinnacle after 1 week. Then it began falling. Con、clusions: LBP is a nonspecific marker of the acute phase response in causes of SIRS or MODS. There was no correlation between LBP and outcome of patients with traumatic shock. There would be negative feedback relationship between LBP and other inflammatory mediums in causes of SIRS or MODS in patients with traumatic shock.
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