Background. This study is aimed at investigating whether albumin-to-fibrinogen ratio (AFR) could independently predict the prognosis in patients with peritonitis-induced sepsis. Methods. A total of 246 eligible patients who were scheduled to undergo surgical treatment for peritonitis-induced sepsis were enrolled in this study. The primary observational endpoint was 28-day hospital mortality. Cox proportional hazards regression analysis with the Wald test was performed to identify prognostic factors for 28-day mortality in septic patients. Receiver operating characteristic (ROC) and Kaplan-Meier curve analyses were carried out to evaluate the association of baseline AFR and prognosis in septic patients. Results. Of all the cohort study participants, there were 59 nonsurvivors with a 28-day mortality of 24.0% (59/246). Baseline AFR (hazard ratio (HR): 0.67, 95% confidence interval (CI): 0.42–0.93, P=0.018) and the presence of septic shock (HR: 2.43, 95% CI: 1.42–3.91, P=0.021) were two independent prognostic factors for 28-day mortality in patients with peritonitis-induced sepsis by multivariate Cox analysis. Baseline AFR was a significant predictor for 28-day mortality with an area under the curve (AUC) of 0.751, a cut-off value of 8.85, a sensitivity of 66.10%, and a specificity of 70.05%, respectively (95% CI: 0.688–0.813, P<0.001). A low baseline AFR level (≤8.85) was significantly associated with a lower overall survival rate in septic patients by Kaplan-Meier curve analysis with log-rank test (P=0.004). Conclusions. This study indicates that AFR independently predicts 28-day mortality in patients with peritonitis-induced sepsis.

Sepsis is a life-threatening condition in which an uncontrolled inflammatory host response is triggered. The exact pathogenesis of sepsis remains unclear. The aim of the present study was to identify key genes that may aid in the diagnosis and treatment of sepsis. mRNA expression data from blood samples taken from patients with sepsis and healthy individuals was downloaded from the Gene Expression Omnibus database and differentially expressed genes (DEGs) between the two groups were identified. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and protein-protein interaction (PPI) network construction, was performed to investigate the function of the identified DEGs. Furthermore, for validation of these results, the expression levels of several DEGs were analyzed by reverse transcription quantitative-polymerase chain reaction (RT-qPCR) in three patients with sepsis and three healthy blood samples to support the results obtained from the bioinformatics analysis. Receiver operating characteristic analyses were also used to analyze the diagnostic ability of the identified DEGs for sepsis. The results demonstrated that a total of 4,402 DEGs, including 1,960 upregulated and 2,442 downregulated genes, were identified between patients with sepsis and healthy individuals. KEGG pathway analysis revealed that 39 DEGs were significantly enriched in toll-like receptor signaling pathways. The top 20 upregulated and downregulated DEGs were used to construct the PPI network. Hub genes with high degrees, including interleukin 1 receptor-associated kinase 3 (IRAK3), S100 calcium-binding protein (S100)A8, angiotensin II receptor-associated protein (AGTRAP) and S100A9, were demonstrated to be associated sepsis. Furthermore, RT-qPCR results demonstrated that IRAK3, adrenomedullin (ADM), arachidonate 5-lipoxygenase (ALOX5), matrix metallopeptidase 9 (MMP9) and S100A8 were significantly upregulated, while ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1) was upregulated but not significantly, in blood samples from patients with sepsis compared with healthy individuals, which was consistent with bioinformatics analysis results. Therefore, AGTRAP, IRAK3, ADM, ALOX5, MMP9, S100A8 and ENTPD1 were identified to have potential diagnostic value in sepsis. In conclusion, dysregulated levels of the AGTRAP, IRAK3, ADM, ALOX5, MMP9, S100A8 and ENTPD1 genes may be involved in sepsis pathophysiology and may be utilized as potential diagnostic biomarkers or therapeutic targets.

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