Contribution of genes polymorphism to susceptibility and outcome of sepsis

Abstract

Sepsis and its sequelae are still a major cause of morbidity and mortality in intensive care units (ICU). The evidence that endogenous mediators actually mediate the individual’s response to infection has led to various approaches to assess the individual’s contribution to the course of the
disease. The role of an individual’s genetic background and predisposition for the extent of inflammatory responses is determined by variability of genes encoding endogenous mediators that constitute the pathways of inflammation. Pro- and anti-inflammatory responses contribute to the
susceptibility and outcome of patients with systemic inflammation and sepsis. Therefore, all genes encoding proteins involved in the transduction of inflammatory processes are candidate genes to determine the human genetic background that is responsible for interindividual differences in systemic inflammatory responses. Polymorphism of TNA a, TNFB, IL-10, IL-6, IL-1b, IL-1RN, HMGB1, TLR, PAI-1, DEFB1, HSP and MMP-9 has contribution to susceptibility and outcome of sepsis in some research. Examination of the association between genetic polymorphisms and sepsis
promises to provide clinicians with new tools to evaluate prognosis, to intervene early and aggressively in treating high risk persons, and to avoid the use of therapies with adverse effects in treating low risk persons. Genomic information may be useful to use to identify groups of
patients with a high risk of developing severe sepsis and multiple organ dysfunctions.