Biomarkers of early sepsis may be correlated with outcome

Abstract

BackgroundSepsis causes high mortality, and the mortality due to secondary infections is even higher. No studies to date have investigated the time from the primary infection to death due to a secondary infection; similarly, the factors that are significantly different in sepsis survivors relative to non-survivors or in severe sepsis patients who suffered a late death relative to those who recover have not been explored. We hypothesized that patients who survive sepsis have a weaker pro-inflammatory response than those who do not and that the mid-term survivors (which acquire secondary infections) would have a pronounced anti-inflammatory response (making them susceptible to infection); this hypothesis was verified in this study.MethodsWe examined 24 patients with severe sepsis; the patients were subdivided by outcome into early death (n = 5), mid-term survival (survival through severe sepsis but death within six months or continued hospitalization for six months, n = 6), and long-term survival (recovery and survival for more than six months, n = 13) groups. The levels of CD3+, CD4+, CD8+, and CD19+ lymphocytes were analyzed by flow cytometry, and the plasma levels of carbonic anhydrase IX (CA IX), MCP-1, IL-6, IL-7, IL-8, and IL-10 were measured by ELISA on days 0, 1, 2, and 3. A statistical comparison of the variables in the groups was conducted using a mixed model.ResultsThe plasma levels of MCP-1, IL-6, and IL-8 in early death and survivors were significantly different, and all had p values <0.01. The plasma levels of MCP-1, IL-6, and IL-8 were also significantly different in mid-term survivors and long-term survivors, with p values of <0.01, 0.04, and <0.01, respectively.ConclusionsOur data support the hypothesis that survivors have a weaker pro-inflammatory response than non-survivors, but the mid-term survivors did not have a more pronounced anti-inflammatory response. The levels of pro-inflammatory cytokines in the mid-term and long-term survivors were significantly different.

Sepsis‐induced activation of endogenous GLP‐1 system is enhanced in type 2 diabetes

“…This was associated with significantly lower pH levels as well as a significant increase of CRP inflammatory marker in the nonsurvivors compared with surviving patients underscoring the dominant effect of the inflammatory response in upregulating GLP‐1 during sepsis and indicating that a sharp rise in total and active GLP‐1 during sepsis may serve as a prognostic marker of poor outcome. These findings are supported by a previous demonstration of a weaker pro‐inflammatory response in sepsis survivors as compared with nonsurvivors . Indeed, active GLP‐1 levels were positively correlated with pH in our surviving patients but negatively correlated with Ph levels in the nonsurviving patients.…”

“…The hallmark of sepsis is an acute inflammatory state with excessive response resulting in activation and/or depression of numerous systems including immune and metabolic pathways . Various metabolic, immune, and inflammation markers are considered prominent prognostic markers indicating higher morbidity and mortality in sepsis . Hyperglycaemia during sepsis is associated with more severe disease and poorer prognosis .…”

“…1,2 Various metabolic, immune, and inflammation markers are considered prominent prognostic markers indicating higher morbidity and mortality in sepsis. [3][4][5][6] Hyperglycaemia during sepsis is associated with more severe disease and poorer prognosis. 4 However, mortality in hyperglycaemic critically ill patients has been reported to be significantly higher in patients without a history of diabetes mellitus compared to patients with known diabetes.…”

Differential Immune Phenotypes in Human Monocytes Induced by Non-Host-Adapted Salmonella enterica Serovar Choleraesuis and Host-AdaptedS. Typhimurium

“…activator of transcription (JAK/STAT) pathway include gamma interferon receptor 1 (IFN-␥R1), interleukin 6 receptor (IL-6R), and IL-10R (4), and the cytokines which signal via these receptors (IFN-␣, IL-6, and IL-10) have been studied as prognostic markers during the systemic inflammatory response syndrome (SIRS) and compensatory antiinflammatory response syndrome (CARS) phases of sepsis (5)(6)(7). The JAK/STAT pathway is not only activated by a range of different cytokines but is also responsible for the transcription of many different cytokine genes (4).…”

Protein from Hevea brasiliensis “Hev b 13” latex attenuates systemic inflammatory response and lung lesions in rats with sepsis

“…In addition to negatively modulating Th1, it deactivates the synthesis of pro-inflammatory cytokines from monocytes/macrophages and inhibits cell migration (Hong et al, 2014). The protective effects of IL-10 in experimental sepsis may be associated with the sepsis induction model (CLP or LPS-lipopolysaccharide) and intervention time (Kalechman et al, 2002), but in general, treating septic rats with IL-10 delays lethality, increases survival, and extends the therapeutic window (Remick et al, 2000).…”