title: Mast cell tryptase and hemolysis after trauma.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Forensic Medicine, University Hospital, S-581 85 Linköping, Sweden. eried@ihm.liu.se
authors.forename: Erik
authors.initials: E
authors.lastname: Edston
authors.forename: Marianne
authors.initials: M
authors.lastname: van Hage-Hamsten
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000097:blood; D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D005260:Female; D005268:Femoral Vein; D005554:Forensic Medicine / Q000379:methods; D006461:Hemolysis / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008407:Mast Cells / Q000201:enzymology*; D008875:Middle Aged; D015203:Reproducibility of Results; D012697:Serine Endopeptidases / Q000097:blood*; D013997:Time Factors; D053802:Tryptases; D014947:Wounds and Injuries / Q000097:blood* / Q000145:classification
chemical_list: D043925:Angiogenesis Inducing Agents; D015415:Biomarkers; D018836:Inflammation Mediators; D012697:Serine Endopeptidases; D053802:Tryptases