Abstract

IntroductionEndothelial damage accounts greatly for the high mortality in septic shock. Higher expression of mediators (IL-6, IL-8, soluble intercellular adhesion molecule 1 [sICAM-1], soluble endothelial-linked adhesion molecule 1 [sELAM-1]) have been described for non-survivors in comparison with survivors. We investigated the predictive value of the mediators IL-6, IL-8, sELAM-1 and sICAM-1 and their time course in intensive care unit patients who developed septic shock with respect to outcome.Materials and methodsWe 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.ResultsAfter 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.ConclusionsELAM-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.

Highlights

  • Endothelial damage accounts greatly for the high mortality in septic shock

  • After 48 hours the levels of Sanodlunbolen-esnudrvoitvhoerlsiaol-vlienrketidmaedhesion molecule 1 (sELAM-1) and sbulerviinvtoerrscoelvluelratrimadehesion molecule 1 (sICAM-1) increased in non-survivors and decreased in survivors. sELAM

  • The release of cytokines (IL-6, IL-8) and adhesion molecules 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]

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Summary

Introduction

Endothelial damage accounts greatly for the high mortality in septic shock. Higher expression of mediators (IL-6, IL-8, soluble intercellular adhesion molecule 1 [sICAM-1], soluble endothelial-linked adhesion molecule 1 [sELAM-1]) have been described for non-survivors in comparison with survivors. The release of these mediators is sepsis related, the levels are significantly higher in sepsis and in septic shock than after trauma, postoperatively or after myocardial infarction [8,9,10,11,12]. These mediators have higher levels in non-survivors than in survivors, and the baseline levels have been correlated with outcome [2,3,8,10,11,12,13,14,15]

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