Abstract
Sepsis is a leading cause of death in critically ill patients and is characterized by a marked increase of the host proinflammatory cytokine release that is precipitated by infectious agents. The sepsis response to therapy has not appreciably improved. The procalcitonin (PCT) concentration is increased in the serum samples of septic patients and correlates with severity of the illness. LPS is a pivotal bacterial product involved in pathogenesis of sepsis and septic shock. Preventing the beginning of inflammatory systemic cascade by means of LPS modulating agents might have a valuable effect in the control of such deadly illness. The aim of the present study was to evaluate the potential effect of procalcitonin on in vitro LPS-induced release of cytokines from human PBMC.
Highlights
In 2002, the Surviving Sepsis Campaign defined a strategy that aimed to reduce the high mortality due to sepsis
For example at 5 μg/ml LPS, the expression of GIPR was reduced to 86% and INSR 72% of control in U937: while in HUH7 cells at 1 μg/ml LPS, the GIPR expression was decreased to 63%, GLP-1R 95% and INSR 89% compared with control (P
As a result of this study we have developed a standardized sepsis protocol to integrate into the AE triage pro forma, as well as a pathway to help instigate treatment earlier to those patients identified as septic on the wards
Summary
In 2002, the Surviving Sepsis Campaign defined a strategy that aimed to reduce the high mortality due to sepsis. Patients admitted to ICUs with severe sepsis have a 39.8% risk of death [2], and for each hour delay in antibiotic administration, a 7.6% increase in mortality [3]. The objective of the present study was to evaluate the impact of early fluid resuscitation on serial TNFα and IL-6 levels and its association with mortality in severe sepsis. Our laboratory has demonstrated in preliminary clinical studies among the various biomarkers of endothelial dysfunction that blood levels of endocan (ESM-1), a pulmonary vascular endothelial cell-specific molecule participating in the control of endothelial–leukocyte interactions, are associated with the severity and evolution of septic states. The objective, of our study was to predict the development of organ failure at 24 hours using only the data available from the first 4 hours post inoculation Methods This pneumonia-sepsis model included 19 sheep with ALI. The sera were analyzed through serological (IgM and IgG specific ELISA) and molecular (gel-based and real-time RT-PCR) testing
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