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Critical Care  2005 

Time course of endothelial damage in septic shock: prediction of outcome

DOI: 10.1186/cc3532

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Abstract:

We measured serum levels of IL-6, IL-8, sELAM-1 and sICAM-1 in 40 intensive care unit patients who developed septic shock. Measurements were performed until death or until resolution of septic shock. Clinical and laboratory data were also recorded.After 48 hours the levels of sELAM-1 and sICAM-1 increased in non-survivors and decreased in survivors. sELAM-1 was predictive for outcome on the third day (P = 0.02) and the fourth day (P = 0.02) after diagnosis of septic shock. This difference in the time course between survivors and non-survivors occurred 7 days before death of the patients (median, 10 days). sICAM-1 levels increased significantly in non-survivors over the study period (P < 0.001). sELAM-1 (P = 0.04), IL-6 (P = 0.04) and IL-8 (P = 0.008) were significantly higher in non-survivors over the whole study period. The age and norepinephrine dose >0.5 μg/kg/min were significantly different between the groups.sELAM-1 showed a markedly opposing course after 48 hours of septic shock. This adhesion molecule may be a useful early predictor of disease severity in the course of septic shock after early initial treatment of the patients, and might suggest considering endothelial-restoring therapy.Endothelial damage accounts for much of the pathology of sepsis, resulting in capillary leak, hypotension, microvascular thrombosis with consecutive tissue hypoxia and, finally, multiple organ failure (MOF) and lethal outcome [1-3]. Endothelial damage is worsened in septic shock [4]. The mortality of septic shock is higher than the mortality in sepsis (35–60% versus 20–40%) [4,5]. The release of cytokines (IL-6, IL-8) and adhesion molecules (soluble endothelial-linked adhesion molecule 1 [sELAM-1], soluble intercellular adhesion molecule 1 [sICAM-1]) has been shown to correlate well with endothelial damage in an experimental setting – especially for sELAM-I, which is specific for endothelial tissue [2,6,7]. Although the release of these mediators is not only sepsis related, t

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