Articles: sepsis.
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Extracorporeal blood purification (EBP) therapies have shown promise as potential rescue treatments for patients with septic shock. However, precise evidence regarding their effectiveness is lacking. This case-control study aimed to evaluate the 28-day survival benefit of a resin cartridge-based EBP therapy compared to conventional therapies in patients with septic shock. ⋯ The findings suggest that administering resin cartridge-based EBP therapy to patients with septic shock may improve their survival compared to conventional therapies.
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The aim of the study was to compare the Quick Sequential Organ Failure Assessment tools (qSOFA), and Quick Sequential Organ Failure Assessment-Lactate (LqSOFA) to detect pre-hospital sepsis among patients with or without suspicion of infection. ⋯ An appropriate strategy for reducing the morbidity and mortality from sepsis must necessarily include the prompt identification of this time-dependent pathology by using all the tools at our disposal. The qSOFA and LqSOFA can be used in the prehospital environment and help the diagnosis of suspected sepsis in patients with medical pathology, highlighting the predictive capacity of LqSOFA in the group of patients with suspected infection.
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Background: Sepsis-induced liver injury (SILI) is an independent risk factor for organ dysfunction and mortality in critical care units. Methods: In this study, the roles of lipocalin 2 (LCN2) in SILI were investigated because LCN2 expression was increased in liver tissues of the septic mice induced by caecal ligation and puncture (CLP), as well as in hepatocytes treated with lipopolysaccharide (LPS). To evaluate liver injury in mice, the levels of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) were measured in both serum and liver tissues. ⋯ Results: The results demonstrated that LCN2 depletion significantly exacerbated SILI, oxidative stress, and ferroptosis. Moreover, in in vitro sepsis model, LCN2 overexpression notably ameliorated LPS-induced cell injury, oxidative stress, and ferroptosis by inhibiting PTGS2 expression. Conclusion: In conclusion, our study provides evidence that LCN2 depletion aggravates SILI by regulating PTGS2-mediated ferroptosis.