Association between injury pattern of patients with multiple injuries and circulating levels of soluble tumor necrosis factor receptors, interleukin-6 and interleukin-10, and polymorphonuclear neutrophil elastase.
BACKGROUND
Our knowledge about the bidirectional interactions between brain and whole organism after trauma is still limited. It was the purpose of this prospective clinical study to determine the influence of severe head trauma (SHT) as well as trauma in different anatomic injury regions on posttraumatic inflammatory mediator levels from patients with multiple injuries.


METHODS
Thirty-five healthy controls, 33 patients with an isolated SHT, 47 patients with multiple injuries without SHT, and 45 patients with both SHT and multiple injuries were studied. The posttraumatic plasma levels of soluble tumor necrosis factor receptors p55 and p75, interleukin (IL)-6, IL-10, and polymorphonuclear neutrophil (PMN) elastase were monitored using enzyme-linked immunosorbent assay technique. The influence of head injuries as well as thorax, abdomen, and extremity injuries on the mediator release from patients with multiple injuries was investigated by multivariate linear regression models.


RESULTS
The soluble tumor necrosis factor receptor p55/p75 ratio was significantly elevated within 3 hours of trauma in all three injury groups and returned to reference ratios after 12 hours. The lowest increase was found in patients suffering from an isolated SHT. Lowest mediator levels in this patient population were also found for IL-6, IL-10, and PMN elastase during the first 36 hours after trauma. Additional injuries to the head, thorax, abdomen, and extremity modulated mediator levels to a different degree. No specific effect was found for SHT when compared with other injury groups. Thorax injuries caused the quickest rise in mediator levels, whereas abdominal injuries significantly increased PMN elastase levels 12 to 24 hours after trauma.


CONCLUSIONS
Traumatic injuries cause the liberation of various mediators, without any specific association between anatomic injury pattern and the pattern of mediator release.
Hensler
Thorsten
T
Biochemical and Experimental Division, University of Cologne, Cologne, Germany.
Sauerland
Stefan
S
Bouillon
Bertil
B
Raum
Marcus
M
Rixen
Dieter
D
Helling
Hanns-J
HJ
Andermahr
Jonas
J
Neugebauer
Edmund A M
EA
D000328:Adult; D006259:Craniocerebral Trauma / Q000097:blood* / Q000276:immunology; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood*; D007155:Immunologic Factors / Q000097:blood*; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D019272:Leukocyte Elastase / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000097:blood* / Q000276:immunology; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood*; D015599:Trauma Severity Indices
D007074:Immunoglobulin G; D007155:Immunologic Factors; D018836:Inflammation Mediators; D015850:Interleukin-6; D018124:Receptors, Tumor Necrosis Factor; D016753:Interleukin-10; D019272:Leukocyte Elastase; D000068800:Etanercept