Arch Surg Chicago
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The proteolytic enzyme elastase released by granulocytes (polymorphonuclear leukocytes [PMN]) in high concentrations during sepsis causes degradation of essential plasma proteins, endothelial damage, and tissue edema. This may result in organ dysfunction and organ failure during sepsis, since increased elastase plasma levels correlate with the mortality rate of patients with sepsis. In vitro studies demonstrated a regulatory role of inflammatory cytokines (tumor necrosis factor-alpha [TNF-alpha], interleukin 1 beta [IL-1 beta], IL-8]) upregulating protease release by PMN. In this light, the interactions between cytokine release by macrophages and altered elastase secretion during sepsis remain to be determined. ⋯ These data indicate an increased release of elastase by PMN despite a reduced secretion of PMN-activating cytokines. Although priming effects of TNF-alpha, IL-1 beta, and IL-8 on protease secretion in vivo cannot be excluded completely, other mediators or mechanisms may be involved in the upregulation of detrimental protease release during sepsis.
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To find a predictive model for postinjury multiple organ failure (MOF). ⋯ Age greater than 55 years, ISS greater than or equal to 25, and greater than 6 U RBC/12 hours are early independent predictors of MOF. Subgroup analyses indicate that BD and lactate levels may add substantial predictive value. Moreover, these results emphasize the predominant role of the initial insult in the pathogenesis of postinjury MOF.