The Role of I-FABP, REG3α, sCD14-ST, and LBP as Indicators of GI Tract Injury in MODS Patients

<b>Background/Objectives</b>: The aim of this study was to evaluate potential biomarkers of bacterial translocation (lipopolysaccharide-binding protein (LBP) and soluble CD14 subtype (sCD14-ST)) and intestinal wall damage (intestinal fatty acid binding protein (I-FABP), Zonulin, and regenerating islet-derived protein-3α (REG3α)) in patients with multiple organ dysfunction syndrome (MODS). <b>Methods</b>: The study involved 327 patients divided into two groups: Group 1 comprised 227 patients with MODS (main group), while Group 2 comprised 100 patients with identical pathologies but without MODS (control group). To examine these biomarkers in the blood, venous blood was taken in the control group on the day of admission to the hospital, in patients with MODS on the first day of MODS staging, and later on Days 3 and 7 of its development. Levels of these markers in blood serum were determined by enzyme-linked immunosorbent assays according to the manufacturers' instructions. <b>Results:</b> In the control group, values of all the investigated markers were lower than in the group of MODS patients (<i>p</i> < 0.0001). In the main group, the mortality rate was 44.9% (<i>n</i> = 102). The values of sCD14-ST on Day 1 and of I-FABP and REG3α on Days 1 and 3 were higher in deceased MODS patients (<i>p</i> < 0.05), while LBP levels on Day 7 were conversely lower in the deceased patients (<i>p</i> = 0.006). SOFA and APACHE II scores were higher in the deceased patients (<i>p</i> < 0.0001). <b>Conclusions:</b> In MODS patients, the increased I-FABP, REG3α, and sCD14-ST but decreased LBP levels may indicate increased intestinal wall permeability and bacterial translocation, which may exacerbate the course of multiple organ dysfunction and increase the risk of mortality. Despite the limitations of this study, the studied potential biomarkers can be considered noteworthy candidates for identifying MODS patients at high risk of mortality.