内毒素、磷脂酶A2、血小板活化因子与重症胸腹创伤后凝血功能障碍的相关性及机制

目的探讨内毒素（LPS）、磷脂酶A2（PLA2）和血小板活化因子（PAF）与重症胸腹创伤后凝血功能障碍的相关性和机制。方法回顾性分析2009年1月至2012年6月解放军第二五,医院82例创伤指数（TI）≥17分、排除颅脑损伤及在急诊科死亡的重症胸腹创伤患者（重症胸腹创伤组）的临床资料，男58例，女24例；年龄16～76（43．59±16．33）岁。开放性损伤17例，闭合性损伤65例；坠落伤23例，交通伤47例，钝性打击伤8例，锐器剌伤4例。选取本院门诊部42例体检的正常健康志愿者为对照组，其中男27例，女15例；年龄24～47（37．32±10．45）岁。检测两组患者的血小板计数（PLT）、血浆D-二聚体（D．D）、部分活化凝血酶原时间（APTT）、内毒素（1ipopolysaccha—ride，LPS）、磷脂酶A2（phospholipaseA2，PLA2）和血小板活化因子（platelet．activatingfactor，PAF），对检验结果进行比较并进行线性相关性分析。结果重症胸腹创伤组PLT低于对照组（83．44±38．52）×109/Lvs．（191．52±23-31）×109／L]，D．Dl（1823．89±608．02）U／LVS．（105．78±44．53）U／L]、APTTl（68．24±24．12）SVS．（22．47±9．41）S]、LPS（438．66±106．02）U／LVS．（87．384-46．51）U／L]、PLA2（41．35-14．26）ng／mlVS．（7．474-5．27）ng／m1]和PAF（15765-3l4-4431．65）ng／LVS．（3823．45±529．72）ng／L]均较对照组增高，差异有统计学意义（P〈0．001）。PLT与损伤因子LPS、PLA：、PAF之间相关系数（r）值均小于一O．9335，呈显著负相关。D．D、APTT与损伤因子LPS、PLA：、PAF之间的r值均大于0．9216，呈显著正相关。结论LPS、PLA2、PAF参与了重症胸腹创伤后凝血功能障碍的发生过程。对LPS、PLA2、PAF进行早期干预，或有可能改善重症胸腹创伤患者的凝血功能障碍，提高患者的生存率。

Correlations between Lipopolysaccharide,Phospholipase A2 and Platelet-activating Factor with Coagulopathy afterSevere Chest and Abdominal Injuries and Their Mechanisms

Objective To investigate the correlations between lipopolysaccharide （LPS）, phospholipase A2 （PLA2） and platelet-activating factor （PAF） with coagulopathy after severe chest and abdominal injuries and their mechanisms. Methods Clinical data of 82 patients with severe chest and abdominal injuries whose trauma index （TI） was greater than or equal to 17 points in No. 253 Hospital of People＇s Liberation Army from January 2009 to June 2012 were retrospectively analyzed （ severe chest and abdominal injury group）. Those patients who had concomitant traumatic brain injuries or died in the Emergency Department were excluded from this study. There were 58 male and 24 female patients with their age of 16-76 （43.59 4± 16.33 ）years. There were 17 patients with open injuries and 65 patients with closed injuries. There were 23 patients with fall injuries, 47 patients with traffic injuries, 8 patients with blunt force injuries, and 4 patients with penetrating injuries. Forty-two healthy volunteers who received routine medical examinations in the outpatient department of our hospitalwere chosen as the control group, including 27 males and 15 females with their age of 24-47 （37.32 ±10.45 ）years. Blood platelet （PLT）count, D-dimer （D-D）, activated partial thromboplastin time （APTT）, LPS, PLA2 and PAF were compared between the 2 groups, and linear correlation analysis was performed. Results PLT of the severe chest and abdominal injury group patients were significantly lower than that of the control group （ 83.44 ±38.52 ） × 109/L vs. （ 191.52 ±23.31 ） 109/El. D=D （ 1 823.89±608.02） U/L vs. （105.78±44.53） U/L], APTT （68.244-24.12） s vs. （22.47±9.41） s], LPS （438.66± 106.02） U/L vs. （87.38±46.51） U/L ], PLA2 （41.35 ±14.26） ng/ml vs. （7.47＋_5.27） ng/ml ] and PAF （ 15 765.31 ± 4 431.65 ）ng/L vs. （3 823.45 -＋ 529.72 ）ng/L ] of the severe chest and abdominal injury group patients were significantly higher than those of the control group （P 〈 0.001 ）. PLT was significantly negatively correlated with LPS, PLA2 and PAF with all the respective correlation coefficient （r）less than -0.933 5. D-D and APTT were significantly positively correlated with LPS, PLA2 and PAF with all the respective r larger than 0.921 6. Conclusion LPS, PLA2 and PAF participate in the pathogenesis of coagulopathy in patients with severe chest and abdominal injuries. Early intervention against LPS, PLA2 and PAF may improve coagulopathy and survival rate of patients with severe chest and abdominal injuries.