Abstract

The focus of sepsis has shifted from inflammation to organ dysfunction on the basis of a recent definition based on the sequential organ failure score (SOFA). A diagnostic and prognostic marker is necessary under this definition but is currently unknown. We enrolled 80 sepsis patients consecutively admitted to an intensive care unit through the emergency department and 80 healthy control patients who received routine health check-ups from August 2018 to January 2019. SEPSIS-3 criteria were used for the diagnosis of patients based on SOFA score ≥ 2 from the baseline along with evidence of infection. Concentrations of 28 cytokines, eight chemokines, and nine growth factors were measured on the day of diagnosis. Hierarchical cluster analysis was performed for molecules. The majority of infections were pneumonia (45% of patients) and urinary tract infections (40% of patients). Most of the measured molecules were increased in patients with sepsis. Area under receiver operating characteristic curve (AUROC) values were found to be as follows: hepatic growth factor (HGF), 0.899; interleukin-1 receptor antagonist (IL-1RA), 0.893; C-C motif ligand 5 (CCL5) 5, 0.887; C-X-C motif chemokine 10 (CXCL10), 0.851; CCL2, 0.840; and IL-6, 0.830. IL-1RA, IL-6, IL-8, IL-15, and CCL11 concentrations correlated with SOFA score with statistical significance. Prognosis multivariate analysis revealed an odds ratio of 0.968 for epidermal growth factor (EGF). Three clusters were formed, of which Clusters 2 and 3 were associated with nonsurvivors. Diagnosis of sepsis was performed using cytokines, chemokines, and growth factors. HGF revealed the highest diagnostic capability, and EGF predicted favorable prognosis among the tested molecules.

Highlights

  • Sepsis is an organ dysfunction caused by a dysregulated host response to infection [1, 2]

  • We evaluated the levels of 45 molecules that are typically examined in sepsis patients, which included cytokines, chemokines, and growth factors

  • 53 (66.2%) had infection confirmed by bacterial growth and 27 (33.8%) had evidence of suspected bacterial infection

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Summary

Introduction

Sepsis is an organ dysfunction caused by a dysregulated host response to infection [1, 2]. The global population incidence rates of sepsis and severe sepsis were 288 and 148 per 100,000 person years, respectively, from 1979 to 2015 and have increased to 437 and 270 per 100,100 person years, respectively, during the last decade [3]. Hospital mortality rates of 17% and 26% for sepsis and severe sepsis, respectively, were reported. Immune dysregulation represents an imbalance of proinflammatory and anti-inflammatory aspects of immune function or of innate immunity- and adaptive immunityrelated functions [4,5,6,7]. Anti-inflammatory cytokines include IL-4, IL-10, and transforming growth factor-beta (TGF-β) [5, 8]. A proinflammatory state followed by an anti-inflammatory state was implicated

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