RELEASE OF SOLUBLE CD14 IN TRAUMATIZED PA TIENTS

Citation
M. Rosch et al., RELEASE OF SOLUBLE CD14 IN TRAUMATIZED PA TIENTS, Der Unfallchirurg, 100(10), 1997, pp. 805-810
Citations number
19
Categorie Soggetti
Surgery,"Emergency Medicine & Critical Care",Orthopedics
Journal title
ISSN journal
01775537
Volume
100
Issue
10
Year of publication
1997
Pages
805 - 810
Database
ISI
SICI code
0177-5537(1997)100:10<805:ROSCIT>2.0.ZU;2-L
Abstract
Membrane-fixed CD14 acts as a receptor for the protein-bound endotoxin (LPS) complex and mediates the cellular effects of endotoxin. Soluble CD14 (sCD14) is suggested to neutralize circulating LPS, i.e., acting as an endotoxin antagonist. The aim of this study was to elucidate th e release of both sCD14 and endotoxin in traumatized patients, startin g from the earliest phase after trauma. A total of 15 patients (phi IS S = 19, 9-75) suffering major trauma were enrolled in this prospective study. Blood samples were collected as early as immediately at the si te of accident, on hospital admission, and thereafter hourly, then dai ly. For patients (phi ISS = 47) died within 24 h because of their seve re injuries. Immediately after the accident as well as during the firs t 2 h after hospital admission, the mean sCD14 levels of surviving pat ients did not differ from those of healthy volunteers (n = 53). Therea fter, however, sCD14 increased continuously in the trauma group. The c oncentrations remained elevated throughout the entire observation peri od. There was, however, no relation between the sCD14 release and the pattern or the severity of injury. In contrast, endotoxin levels revea led a pattern-specific release. The highest plasma concentrations of L PS were observed in patients suffering from (additional) thoracic inju ry. On the basis of these results we conclude that the release of sCD1 4 after trauma does not reflect a strict principle such as action/reac tion caused by the appearance of endotoxin immediately after the injur y. Soluble CD14 is more likely release by an endotoxin-independent mec hanism.