目的 探讨脂多糖（LPS）、白细胞介素-6（IL-6）和血小板活化因子（PAF）与重症胸腹创伤后凝血功能紊乱发生的相关性及可能的致病机理。方法 收集2009年1月至2011年12月期间在中国人民解放军第二五三医院急诊科就诊、创伤指数≥17分且除外合并颅脑损伤及在急诊科内死亡的胸腹创伤患者62例，在予以抢救、治疗的同时抽血检查血小板计数（PLT）、血浆D-二聚体（D-D）、部分活化凝血酶原时间（APTT）、凝血酶原时间（PT）、LPS、IL-6和PAF，并对其结果进行相关性分析。结果 本组患者就诊时检测的PLT为（157.73±78.11）×109/L， D-D为（1 023.88±208.72） U/L，APTT为（46.95±17.85） s，PT为（19.44±6.95） s，TT为（58.27±12.44）s，除PLT降低外，其余4项指标均升高或延长； LPS为（322.85±104.54） U/L，IL-6为（285.51±81.46） ng/mL，PAF为 （14 714.70±4 427.95） ng/L， 三者均升高； PLT与LPS、IL-6和PAF之间呈负相关关系（P＜0.001），而D-D、APTT、PT和TT与LPS、IL-6和PAF之间均呈正相关关系（P＜0.001）。结论 LPS、IL-6及PAF可能参与了重症胸腹创伤后凝血功能障碍的发生；重症胸腹损伤后出现的微循环障碍及内毒素血症是凝血功能障碍发生的重要机理。针对LPS、IL-6和PAF进行早期干预，有可能改善重症胸腹创伤患者的凝血功能障碍。
ObjectiveTo 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. MethodsClinical 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±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 hospital were 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. ResultsPLT 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/L]. D-D[(1 823.89±608.02) U/L vs. (105.78±44.53) U/L], APTT [(68.24±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. ConclusionLPS, 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.
ObjectiveTo explore the relationship of platelet-activating factors and vascular endothelial activity markers to lacunar infarction (LI).MethodsA total of 100 inpatients diagnosed with LI in Shaanxi Provincial People’s Hospital between March 2018 and February 2019 were included, and 100 matched healthy controls were collected. Basic information, clinical baseline data, laboratory examinations, cerebral MRI and treatment data were collected after admission. The platelet-activating factors (platelet membrane glycoprotein Ⅱb/Ⅲa receptor and P-selectin) and vascular endothelial activity markers [von Willebrand factor (vWF), homocysteine (HCY), and high-sensitivity C-reactive protein (hsCRP)] levels of patients with LI were detected one month and three months after onset, and those of the control group were decteted when they were selected. SPSS 25.0 software was used for statistical analysis.ResultsAt one month after onset, there was no statistically significant difference in the levels of platelet activating factors between the LI group and the control group [platelet membrane glycoprotein Ⅱb/Ⅲa receptor: (2.84±1.00)% vs. (2.59±0.96)%, P=0.065; P-selectin: (3.05±0.63)% vs. (2.98±0.59)%, P=0.419], while the differences in the levels of vascular endothelial activity markers between the two groups were statistically significant [vWF: (141.80±17.60) vs. (124.63±10.65) ng/mL, P<0.001; hsCRP: (5.53±1.37) vs. (2.17±0.55) mg/L, P<0.001; HCY: (18.76±4.07) vs. (15.81±2.63) mmol/L, P<0.001]. At three months after onset, 94 LI patients were followed up. The levels of vWF and hsCRP between the 100 patients one month after onset and the 94 patients three months after onset were statistically different [(vWF: (141.80±17.60) vs. (134.86±13.35) ng/mL, P=0.002; hsCRP: (5.53±1.37) vs. (2.63±0.55) mg/L, P<0.001], but there was no statistically significant difference between the two time points in the levels of HCY or platelet-activating factors (P>0.05).ConclusionChronic platelet activation may not play a core role in LI pathophysiology, and endothelial dysfunction may be one of the pathological mechanisms of LI.