Biomarkers of sepsis

Abstract

Sepsis remains a leading cause of death in critically ill patients, despite efforts to improve patient outcome. Thus far, no magic drugs exist for severe sepsis and septic shock. Instead, early diagnosis and prompt initial management such as early goal-directed therapy are key to improve sepsis outcome. For early detection of sepsis, biological markers (biomarkers) can help clinicians to distinguish infection from host response to inflammation. Ideally, biomarkers can be used for risk stratification, diagnosis, monitoring of treatment responses, and outcome prediction. More than 170 biomarkers have been identified as useful for evaluating sepsis, including C-reactive protein, procalcitonin, various cytokines, and cell surface markers. Recently, studies have reported on the usefulness of biomarker-guided antibiotic stewardships. However, the other side of these numerous biomarkers is that no novel single laboratory marker can diagnose, predict, and track the treatment of sepsis. The purpose of this review is to summarize several key biomarkers from recent sepsis studies.

Keywords: Biomarkers; Cytokines; Diagnosis; Outcome; Prognosis; Sepsis.

Figure 1

Systemic responses to sepsis and possible biomarkers. Systemic response to sepsis results from multiple changes to the inflammatory, coagulatory, and vascular systems. Candidate biomarkers include proteins such as cytokines, soluble receptors, and acute phase reactants. DAMP, damage-associated molecular pattern; PAMP, pathogen-associated molecular pattern; SIRS, systemic inflammatory response syndrome.

Figure 2

Inflammatory response to sepsis. Immune response to sepsis is both proinflammatory and anti-inflammatory. An initial hyper-inflammatory phase is followed by a hypo-inflammatory (immunosuppressive) phase. Immunosuppression in sepsis contributes to increased mortality in elderly patients. Ideally, good biomarkers can reflect the hyper- (A) or hypo-inflammatory (B) status and the direction of inflammatory response (A or C).