The receiver operating characteristic curve analysis for diagnosis of severe sepsis showed higher discriminative value for CRP and IL-6 (AUC = 0.909, 95% CI: 0.829-0.99 and AUC = 0.854, 95% CI: 0.728-0.980, respectively) than sTREM-1 (AUC = 0.733, 95% CI: 0.596-0.870).
The aim of this study was to evaluate whether Interleukin-6 (IL-6) could be a faster indicator of treatment success in adults with severe sepsis and septic shock compared to procalcitonin (PCT) and C-reactive protein (CRP).
In predicting the development of severe sepsis, the highest AUCs were found for PCT (0.744, 95% CI 0.638-0.85) and sTREM-1 (0.664, 95% CI 0.55-0.778); and in septic shock prediction, for PCT (0.766, 95% CI 0.665-0.867) and IL-6 (0.707, 95% CI 0.595-0.819). sTREM-1 positively correlated with APACHE II, SAPS II and SOFA scores.
Patients with severe sepsis had log-fold higher median concentrations of IL-6, hs-CRP, D-dimer, E-selectin, sICAM-1, and sVCAM-1 compared with non-hospitalized volunteers (P <0.05).
The genotype results demonstrated that carriers of the TNF-α rs1800629 A allele had a 4.28-fold higher risk for septic shock (adjusted odds ratio [OR], 4.28; 95% confidence interval [CI], 2.24-8.18; P < .01) compared with severe sepsis, and carriers of the IL-6rs1800795 C allele had a 2.42-fold higher risk for septic shock (OR, 2.42; 95% CI, 1.08-5.45; P < .01) compared with severe sepsis.
Baseline lHSP72 was higher in SS (p < 0.03), and mHSP72 in SIRS (p < 0.02), compared to H. Only HS induced l/mHSP72/mRNA HSP72; LPS induced IL-6, IL-8, IL-10, and MCP-1.
Protein C -1641 AA genotype is associated with decreased survival, more organ dysfunction, and more systemic inflammation in patients having severe sepsis and with increased interleukin-6 levels after cardiopulmonary bypass surgery.
Candidate single nucleotide polymorphisms (SNPs) within bacterial recognition (TLR4 +896, CD14 -159) and inflammatory response (TNF-alpha -308, IL-1beta -31, IL-6 -174) loci were evaluated for association with increased risk for severe sepsis (sepsis plus organ dysfunction or septic shock) and mortality.
There was no association between the IL-6 -174 genotypes and the ex vivo, stimulated IL-6 response: 25% of the patients developed severe sepsis later in the clinical course.