Edston Erik, van Hage-Hamsten Marianne
Department of Forensic Medicine, University Hospital, S-581 85 Linköping, Sweden.
Forensic Sci Int. 2003 Jan 9;131(1):8-13. doi: 10.1016/s0379-0738(02)00383-3.
We have previously found increased mast cell tryptase in accidental deaths due to trauma, indicating that mast cell degranulation had occurred. The present study was designed to confirm the previous observation and to determine if tryptase release after trauma is acute or delayed. Furthermore, the importance of hemolysis and direct trauma to the mast cells was investigated.
Mast cell tryptase was measured in post-mortem blood from the femoral vein in 27 cases of death from trauma and in 27 control cases by means of a commercially available immunoassay. The trauma cases were further classified into groups with single versus multiple trauma, and groups with short survival time (i.e. death at the scene of the accident) versus longer survival time (death in hospital). In five multi-trauma deaths, blood was sampled locally from the sites of crush injury.
The mean value of tryptase in femoral vein blood was 35.6+/-34.6 microg/l in the entire trauma group and 14.7+/-6.5 microg/l in the controls (P<0.005). In bloody liquid sampled from crush injuries, tryptase was substantially elevated in all cases, with a mean of 227+/-146 microg/l. In cases with short survival time, tryptase was significantly higher than in those who died after several hours or days in hospital (P<0.001). No statistically significant difference was seen between multi- and single-trauma cases. A correlation between hemolysis in the samples and elevated tryptase was found only in the trauma cases (P<0.05), but experimentally induced hemolysis in vitro was not found to influence the measurements.
Mast cell tryptase becomes elevated in trauma deaths and this seems to be ascribable either to direct mechanical injury to tissue mast cells and/or to cell lysis. In patients initially surviving severe injuries, the effects of massive release of histamine and other mast cell mediators might be of importance for treatment strategies and prognosis.
我们之前发现,因创伤导致的意外死亡中肥大细胞类胰蛋白酶增加,这表明发生了肥大细胞脱颗粒。本研究旨在证实之前的观察结果,并确定创伤后类胰蛋白酶的释放是急性的还是延迟的。此外,还研究了溶血和对肥大细胞的直接创伤的重要性。
通过一种市售免疫测定法,对27例创伤死亡病例和27例对照病例股静脉的死后血液中的肥大细胞类胰蛋白酶进行了测量。创伤病例进一步分为单处创伤组和多处创伤组,以及生存时间短(即事故现场死亡)组和生存时间长(医院死亡)组。在5例多处创伤死亡病例中,从挤压伤部位局部采集血液。
整个创伤组股静脉血中类胰蛋白酶的平均值为35.6±34.6微克/升,对照组为14.7±6.5微克/升(P<0.005)。在从挤压伤部位采集的血性液体中,所有病例的类胰蛋白酶均显著升高,平均值为227±146微克/升。生存时间短的病例中,类胰蛋白酶显著高于在医院数小时或数天后死亡的病例(P<0.001)。多处创伤病例和单处创伤病例之间未发现统计学上的显著差异。仅在创伤病例中发现样本溶血与类胰蛋白酶升高之间存在相关性(P<0.05),但体外实验性诱导溶血未发现会影响测量结果。
肥大细胞类胰蛋白酶在创伤死亡中升高,这似乎归因于组织肥大细胞的直接机械损伤和/或细胞裂解。在最初从重伤中存活的患者中,组胺和其他肥大细胞介质的大量释放对治疗策略和预后可能具有重要意义。