Intestinal Fatty Acid Binding Protein Research Articles

Tranilast Reduces Intestinal Ischemia Reperfusion Injury in Rats Through the Upregulation of Heme-Oxygenase (HO)-1

Background: Intestinal ischemia reperfusion injury (IRI) is a harmful process that occurs during intestinal infarction and intestinal transplantation (ITx). It is characterized by severe inflammation which disrupts the mucosal barrier, causing bacterial translocation and sepsis. Tranilast (N-[3,4-dimethoxycinnamoyl]-anthranilic acid) (TL) is a synthetic compound with powerful anti-inflammatory properties. Objective: To investigate the effect of pretreatment with TL in a validated rat model of intestinal IRI (60 min of ischemia). Methods: TL (650 mg/kg) was administered by oral gavage 24 and 2 h before the onset of ischemia. Experiment 1 examined 7-day survival in 3 study groups (sham, vehicle+IRI and TL+IRI, n = 10/group). In Experiment 2, the effects on the intestinal wall integrity and inflammation were studied after 60 min of reperfusion using 3 groups (sham, IRI and TL+IRI, n = 6/group). The following end-points were studied: L-lactate, intestinal fatty acid-binding protein (I-FABP), histology, intestinal permeability, endotoxin translocation, pro- and anti-inflammatory cytokines and heme oxygenase-1 (HO-1) levels. Experiment 3 examined the role of HO-1 upregulation in TL pretreatment, by blocking its expression using Zinc protoporphyrin (ZnPP) at 20 mg/kg vs. placebo (n = 6/group). Results: Intestinal IRI resulted in severe damage of the intestinal wall and a 10% 7-day survival. These alterations led to endotoxin translocation and upregulation of pro-inflammatory cytokines. TL pretreatment improved survival up to 50%, significantly reduced inflammation and protected the intestinal barrier. The HO-1 inhibitor ZnPP, abolished the protective effect of TL. Conclusions: TL pretreatment improves survival by protecting the intestinal barrier function, decreasing inflammation and endotoxin translocation, through upregulation of HO-1.This rat study of severe intestinal ischemia reperfusion injury demonstrates a novel role for Tranilast as a potential therapy. Administration of Tranilast led to a marked reduction in mortality, inflammation and intestinal permeability and damage. The study proved that Tranilast functions through upregulation of heme oxygenase-1.

Characterization of gut dysbiosis and intestinal barrier dysfunction in patients with metabolic dysfunction-associated steatotic liver disease and chronic kidney disease: a comparative study

The mechanistic role of gut microbiota in metabolic dysfunction-associated steatotic liver disease (MASLD) and chronic kidney disease (CKD) is increasingly recognized. Despite their close association, comparative data regarding gut dysbiosis in these disorders are limited. This study included 22 healthy controls and 180 patients (90 MASLD, 60 CKD, and 30 both diseases with sex- and age-matched). Fecal bacterial 16 S ribosomal RNA sequencing and butyryl-CoA: acetate CoA transferase (BCoAT) gene expression were analyzed. Plasma intestinal fatty acid binding protein (I-FABP), representing intestinal barrier dysfunction, was assessed using the ELISA method. Our data showed that alpha and beta diversities of gut microbiota differed between MASLD and healthy controls. However, only beta diversities were different between CKD and healthy individuals. The MASLD and CKD groups displayed fewer SCFA-producing genera, particularly Bifidobacterium, than healthy controls. Fecal BCoAT levels were inversely correlated with eGFR and I-FABP levels. Patients with CKD had significantly enriched pathogenic bacteria, reduced BCoAT, and increased I-FABP levels versus MASLD. Combining significant bacterial genera discriminated MASLD from CKD with high diagnostic accuracy (AUC of 0.90). Among patients with both diseases, gut microbial alterations showed mixed characteristics of MASLD and CKD. These data highlighted the shared and distinct gut dysbiosis and related biomarkers, which could provide a better understanding of MASLD and CKD pathogenesis.

Ebastine in combination with low-dose antidepressants for refractory irritable bowel syndrome: A randomized controlled trial.

BackgroundDrug treatment of refractory irritable bowel syndrome (IBS) is not satisfactory at present. This study investigated the clinical effects of ebastine combined with low-dose antidepressants on refractory IBS.MethodsA total of 105 patients with refractory refractory IBS were randomly assigned to two different treatment groups after signing informed consent. And they didn't know about the treatment group they were in. They were administered with ebastine (Group A) or ebastine combined with flupentixol and melitracen (Group B) for 4 weeks. Drug efficacy was evaluated using scales before and after treatment. In addition, serum D-lactate (D-LAC) and human intestinal fatty acid binding protein (I-FABP) level were measured to assess intestinal permeability.ResultsSignificant improvements were observed in IBS Quality of Life (IBS-QOL) score, IBS Symptom Severity Scale (IBS-SSS) score, and total sleep quality score. Patients in Group A showed no improvements in anxiety (44.83 ± 9.62 vs. 43.92 ± 10.43, P = 0.415) and depression (39.08 ± 9.34 vs. 38.75 ± 9.35, P = 0.674) compared with the baseline level, while those in Group B improved significantly on anxiety (52.12 ± 8.19 vs. 39.28 ± 9.88) and depression (47.64 ± 9.53 vs. 38.24 ± 9.41) status. After treatment, the serum levels of D-LAC and I-FABP were significantly lower in Group B than in Group A.ConclusionRefractory IBS patients showed certain psychological abnormalities. Ebastine combined with antidepressants exhibited more obvious benefits on QOL, sleep quality, and SSS, with significant improvements in psychological status and intestinal permeability in refractory IBS patients.

Surrogate Markers of Intestinal Permeability, Bacterial Translocation and Gut-Vascular Barrier Damage Across Stages of Cirrhosis.

Portal hypertension, gut barrier dysfunction, and pathological bacterial translocation are hallmarks of cirrhosis driving complications. As measuring gut barrier function is demanding, surrogate markers have been proposed, but their intercorrelation and applicability across different stages of advanced liver disease, particularly in acute-on-chronic liver failure (ACLF), are largely unknown. Proposed markers of gut barrier dysfunction and bacterial translocation were quantified in sera from 160 patients with cirrhosis across different disease stages of compensated and decompensated cirrhosis as well as from 20 patients in hepatic and portal vein serum before and after the insertion of transjugular intrahepatic portosystemic stent (TIPS) using enzyme-linked immunosorbent assay (ELISA). Across all stages of liver disease, the gut-vascular barrier (GVB) marker plasmalemma vesicle protein-1 (PV-1) correlated with bacterial translocation markers endogenous endotoxin-core IgA antibodies (EndoCAb) and LPS-binding protein (LBP) but not with intestinal damage markers intestinal fatty acid binding protein (I-FABP) and zonulin-family peptides (ZFP). PV-1 and EndoCAb were higher in decompensated cirrhosis without further increase in ACLF. Among investigated markers, only I-FABP correlated with the portosystemic pressure gradient, and TIPS insertion significantly reduced portal concentrations within 24 h. Higher PV-1 levels indicated poor transplant-free survival in univariate and multivariable analysis. Surrogate markers of bacterial gut barrier dysfunction and bacterial translocation like ZFP, LBP and EndoCAb appear of limited use in advanced stages of cirrhosis and are confounded by hepatic synthesis capacity, portal congestion and acute phase responses. The prognostic implications of circulating PV-1 in decompensated cirrhosis levels demand further investigation.

Intestinal Fatty Acid-Binding Protein As a Marker of Prognosis and Non-Occlusive Mesenteric Ischemia in Refractory Cardiac Arrest Patients: a Pilot Study

Intestinal Fatty Acid-Binding Protein As a Marker of Prognosis and Non-Occlusive Mesenteric Ischemia in Refractory Cardiac Arrest Patients: a Pilot Study

An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers.

An exploratory study of cytokine and inflammatory profiles between young adult low-risk and at-risk drinkers.

The value of intestinal fatty acid binding protein as a biomarker for the diagnosis of necrotizing enterocolitis in preterm infants: a meta-analysis

BackgroundNecrotizing enterocolitis (NEC) is a serious condition mainly affecting newborns, especially preterm or low birth weight ones, with a poor prognosis. The present study aimed to comprehensively evaluate the diagnostic value of intestinal-type fatty acid-binding protein (I-FABP) in NEC through meta-analysis.MethodsRelevant documents on the diagnosis of I-FABP in neonatal NEC were retrieved from PubMed, ScienceDirect, Embase, Cochrane, Wanfang, and CNKI databases. Summary receiver operating characteristic curve (SROC), sensitivity, specificity, and likelihood ratio (LR) were constructed to evaluate the pooled diagnostic value. Meta-regression analysis was conducted to explore the sources of heterogeneity. Sensitivity analysis was performed to detect the robustness of current results.ResultsThe present study encompassed 15 studies. I-FABP had a high diagnostic value for NEC, with a sensitivity at 0.78 (0.70–0.85), a specificity of 0.85 (0.78–0.90), and the area under the curve (AUC) value was 0.89 (0.86–0.91). The combined diagnostic odds ratio (DOR) was 20.33 (10.90–37.90) indicating a high diagnostic potential with strong discriminatory power. Sample source, detection method, and critical value might be the source of heterogeneity. There was no significant publication bias.ConclusionI-FABP played a crucial role in diagnosing NEC in premature infants.

Hyperbaric oxygen therapy alleviates intestinal and brain damage in experimental necrotizing enterocolitis.

Necrotizing enterocolitis is the most common gastrointestinal emergency in newborns. Its etiology involves bacterial colonization, enteral formula feeding, and hypoxic-ischemic injury. The pathology of necrotizing enterocolitis is characterized by coagulation necrosis and bacterial overgrowth, with limited preventative methods available. In addition to affecting the intestine, this disease has long-term neurological consequences for survivors. Hyperbaric oxygen therapy, a well-established treatment for soft tissue infections and injuries caused by hypoperfusion, may serve as an alternative approach for necrotizing enterocolitis. In this study, a necrotizing enterocolitis model was developed in newborn Sprague-Dawley rat pups through the administration of a hyperosmolar formula, combined with exposure to hypothermia and hypoxia. The rat pups received hyperbaric oxygen therapy sessions at 3 absolute atmospheres for 2 hours each, which were administered over 1 or 2 days. The results demonstrated that hyperbaric oxygen therapy significantly reduced mortality in rats with necrotizing enterocolitis and preserved the number of brain cells in the hippocampus. Additionally, hyperbaric oxygen therapy increased the expression of nitric oxide synthase, intestinal fatty acid-binding protein, and superoxide dismutase 3 in the intestine, and elevated superoxide dismutase 3 levels in the hippocampus. These findings suggest that hyperbaric oxygen therapy not only reduces mortality but also mitigates the severity of intestinal and brain lesions in experimental necrotizing enterocolitis, preserving intestinal cell integrity and enhancing antioxidant mechanisms.

Impact of moderate environmental heat stress during running exercise on circulating markers of gastrointestinal integrity in endurance athletes.

In the present study, we aimed to determine the effect of moderate ambient heat stress on exercise-provoked patterns of "leaky gut" biomarkers and stress markers in well-trained athletes. Eleven triathletes performed a strenuous 1-h treadmill run, both under normal ambient conditions (N, 18-21°C) as well as under moderate heat environmental conditions (H, 28-30°C). Core body temperature (Tc), heart rate (HR), and rating of perceived exertion (RPE) significantly increased under both conditions, with significantly higher values during and after the H run. We observed a significant main effect of acute exercise on circulating leukocyte numbers, release of cell-free human DNA (cfDNA) but not bacterial DNA (bacDNA), and on plasma levels of intestinal fatty-acid binding protein (I-FABP), lipopolysaccharide-binding protein (LBP), endotoxin (LPS), and D-lactate. Exercising under H conditions accelerated the mobilization of circulating neutrophils and lymphocytes, and significantly affected the release of cfDNA, D-lactate, I-FABP, creatinine, and blood potassium levels. Multiple correlation analysis revealed a significant association between Tc, max and exercise-provoked release of cfDNA (r = 0.583, p = 0.012) as well as with I-FABP (r = 0.554, p = 0.026). Our data indicate that acute exercising and heat stress may not only affect paracellular but also transcellular intestinal permeability.

Longitudinal analysis of serum intestinal fatty acid-binding protein in a patient with non-occlusive mesenteric ischemia following brachial plexus block-induced hypotension: a case study.

Intestinal fatty acid-binding protein (I-FABP) is a promising biomarker for small-bowel ischemia including non-occlusive mesenteric ischemia (NOMI). A 75-year-old woman with diabetic nephropathy sustained a distal radius fracture. Two days later, she underwent a brachial plexus block to facilitate orthopedic surgery, which resulted in hypotension. Despite prompt fluid resuscitation and ephedrine administration, the patient developed abdominal pain. Contrast-enhanced computed tomography revealed hepatic portal venous gas, but no direct evidence of small-bowel ischemia. The gastrointestinal surgery team opted for cautious in-hospital observation overnight. Unfortunately, the patient's condition significantly worsened the following day, prompting an urgent laparotomy. Surgery confirmed ileal segment necrosis, macroscopically characterized by a distinctive geographic pattern. Retrospective analysis of stored serum samples using a human enzyme-linked immunosorbent assay demonstrated that I-FABP levels were moderately elevated (7.2ng/mL) at the initial outpatient visit for the fracture, peaked (17.9ng/mL) at the clinical onset of NOMI, and returned to normal (0.7ng/mL) by postoperative day 2. Serum I-FABP levels correlated with the progression of NOMI, showing potential as an early detection marker. However, the longitudinal analysis of serum I-FABP also highlighted significant challenges of this biomarker, including the influence of renal function and the importance of sampling timing.

Intestinal Fatty Acid Binding Protein (I-FABP) in Patients with Inflammatory Bowel Diseases with and without MAFLD

Intestinal Fatty Acid Binding Protein (I-FABP) in Patients with Inflammatory Bowel Diseases with and without MAFLD

Intestinal epithelial injury and inflammation after physical work in temperate and hot environments in older men with hypertension or type 2 diabetes.

We tested whether older adults with well-controlled type 2 diabetes or hypertension, compared with age-matched adults without chronic disease, exhibit greater intestinal damage, microbial translocation and inflammation during exertional heat stress. Twelve healthy men (age 59 years, SD 4 years), nine with type 2 diabetes (age 60 years, SD 5 years) and nine with hypertension (age 60 years, SD 4 years) walked for 180min at 200W/m2 in temperate conditions (wet-bulb globe temperature 16°C) and high-heat stress conditions (wet-bulb globe temperature 32°C). Serum intestinal fatty acid binding protein (IFABP), plasma soluble cluster of differentiation 14, lipopolysaccharide-binding protein (LBP), interleukin-6 and tumour necrosis factor-alpha were measured pre- and postexercise and after 60min recovery. Total exercise duration was lower in men with hypertension and diabetes (p≤0.049), but core temperature did not differ. All markers increased more in heat versus temperate conditions (p<0.002). In the heat, individuals with type 2 diabetes had greater postexercise increases in IFABP [+545pg/mL (95% confidence interval: 222, 869)] and LBP [+3.64µg/mL (1.73, 5.56)] relative to healthy control subjects (p<0.048), but these resolved after recovery. Despite reduced exercise duration, hypertensive individuals showed similar increases in IFABP and LBP to control subjects. Our findings suggest that older workers with well-controlled type 2 diabetes or hypertension might have greater vulnerability to heat-induced gastrointestinal barrier disturbance and downstream inflammatory responses when compared with otherwise healthy, age-matched adults during prolonged exercise in the heat.

Helminth driven gut inflammation and microbial translocation associate with altered vaccine responses in rural Uganda

Vaccine responses are sometimes impaired in rural, low-income settings. Helminth-associated gut barrier dysfunction and microbial translocation (MT) may be implicated. We used samples from a trial of praziquantel treatment-effects on vaccine responses in Schistosoma mansoni (Sm)-endemic Ugandan islands, measuring intestinal fatty acid-binding protein 2 (I-FABP2), lipopolysaccharide-binding protein, anti-endotoxin core antibodies (EndoCab), soluble CD14 (sCD14) in plasma, and faecal lipocalin-2, occult blood (FOB), and calprotectin (fCAL), and evaluating their associations with baseline helminth infection, praziquantel treatment, and responses to BCG, yellow fever, typhoid, HPV, and tetanus-diphtheria vaccines. Sm associated positively with fCAL and FOB, hookworm with I-FABP2, and any helminth with EndoCab IgM, fCAL and FOB. Sm associated inversely with sCD14. Praziquantel treatment reduced all marker concentrations, significantly fCAL and FOB, implying that Sm-associated gut inflammation and MT is reversible. Associations of assessed markers with vaccine-specific responses were predominantly inverse. Interventions to improve gut barrier function may enhance vaccine responsiveness.

Fecal Microbiota and Associated Metabolites Are Minimally Affected by Ten Weeks of Resistance Training in Younger and Older Adults.

Preclinical evidence suggests that short chain fatty acids (SCFAs) produced by gut microbiota may impact body composition and muscle growth. While aging is implicated in negative alterations to the gut microbiome, exercise may mitigate these changes. Limited human evidence indicates that resistance training (RT) does not appreciably alter the gut microbiome in older adults, and no human study has examined whether resistance training differentially alters the gut microbiome and associated SCFAs between younger and older individuals. Therefore, we examined whether 10 weeks of RT differentially altered fecal microbiota composition, fecal and circulating SCFAs, and serum markers associated with gastrointestinal integrity in two cohorts of adults. Fecal and serum samples were obtained from untrained younger (22 ± 2 years, n = 12) and older (58 ± 8 years, n = 12) participants prior to and following 10 weeks of supervised twice-weekly full-body RT. Outcome measures immediately before (PRE) and after the intervention (POST) included dual X-ray absorptiometry for body composition, ultrasound for vastus lateralis (VL) thickness, 16S rRNA gene sequencing fecal microbiome data, serum and fecal SCFAs measured by gas chromatography, and serum intestinal fatty acid-binding protein 2 (FABP2), lipopolysaccharide-binding protein (LBP), and leucine-rich alpha-2 glycoprotein (LRG-1) quantified by enzyme-linked immunosorbent assays. Main effects and interactions were measured by repeated measures analysis of variance (group × time; G × T) for all dependent variables, and Spearman correlations were used to explore relationships among changes in relevant outcomes. The intervention significantly increased VL thickness and lean body mass (p < 0.05) equally in both groups. Although group differences in microbiome beta diversity were identified, no effects of age, time, or their interaction were observed for the alpha diversity measures. Seven SCFAs were detected in the fecal samples, albeit no significant age, time, or interaction effects were evident. In serum, acetic acid was the only SCFA detected, with no significant age, time, or interaction effects. Serum LRG1 decreased for all participants (p = 0.007) with higher levels in younger adults (p = 0.015), but no G × T interactions were observed for this marker, serum FABP2, or LBP. No significant correlations were observed among RT-induced changes in muscle mass-related outcomes and changes in fecal microbiome diversity, total or individual SCFAs, or serum FABP2/LBP/LRG-1. These results highlight that 10 weeks of RT largely does not affect fecal microbiota, associated SCFAs, or select markers of gastrointestinal integrity in untrained younger or older adults.

Microbial translocation and gut damage is associated with hepatic fibrosis but not steatosis in women with and without HIV.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent in people living with HIV. Gut microbial translocation and gut damage may play a role in MASLD pathogenesis. We determined associations of circulating biomarkers of translocation and gut damage with hepatic steatosis and fibrosis in a large US cohort of women with HIV (WWH) and without HIV. Vibration controlled transient elastography (VCTE) was conducted from 2013-2018 among 854 WWH and 349 women without HIV. Serum biomarkers were measured within 6 months of the VCTE: kynurenine to tryptophan (KT) ratio, intestinal fatty acid binding protein (I-FABP), and immune activation markers soluble CD14 (sCD14) and soluble CD163 (sCD163). We used multivariable linear regression to evaluate independent associations of each biomarker, HIV serostatus, and demographic, metabolic, and HIV-specific covariates with hepatic steatosis (controlled attenuation parameter [CAP]) and fibrosis (liver stiffness [LS]). In multivariable analysis, increasing in KT ratio was associated with a 6 dB/m lower CAP and 6% higher LS, and sCD14 with a 5 dB/m lower CAP and 8% higher LS. sCD163 was not associated with CAP but was associated with a 12.5% higher LS value. I-FABP was not associated with either CAP or LS values. Higher KT ratio, sCD14, and sCD163 were associated with increased hepatic fibrosis but not steatosis. In fact, higher KT ratio and sCD14 were associated with decreased steatosis. This suggests that microbial translocation and gut damage may contribute to the pathogenesis of fibrosis in WWH in a mechanism unrelated to increased steatosis.

Intestinal fatty-acid binding protein as a diagnosis marker in younger with celiac diseases.

Celiac disease (CD) is an autoimmune disorder known to be highly associated with autoimmune manifestations and genetic factors. The aim of this paper was to assess the diagnostic accuracy of serum I-FABP in CD patients. Fifty patients with CD were classified into two groups: (30) exhibiting positive titers of tTG-IgA test and tTG-IgG test value more than 18 AU/mL and (20) patients with a potential diagnosis of CD (equivocal titers of IgG and IgA tTG 12-18 AU/mL) for comparison, as well as 50 healthy individuals were included as a control. The ELISA Kit was used to measure serum I-FABP where serum iron and serum ferritin were measured through the standard methods on the Smart-150 autoanalyzer biochemistry, instead of IgG and IgA tTG that was determined using an immunoenzymatically technique. The concentration of serum I-FABP in the CD group was significantly higher than that of the healthy subjects (p < 0.05). There was a significant difference in the serum I-FABP concentrations between two patients. There were substantial positive connections between serum 1-FAPB concentration and IgG, as well as strong positivity correlations between serum 1-FAPB and serum IgA Ttg in CD patients. The concentration of serum 1-FAPB, on the other hand, had no significant association with the anti Ttg IgG and serum IgA Ttg. The area under the curve was excellent (AUC = 1, p = 0.0001), with high diagnostic accuracy (96.2) in differentiating CD from the healthy subject group. I-FABP levels in the sera of were shown to be higher and I-FABP levels were shown to be significantly linked between activated immune response (IgA-tTG) and enterocyte damage (I-FABP) in CD patients.

Synergistic effects of multi-enzyme supplementation on nutrient digestion and absorption in the foregut and hindgut.

This study was conducted to investigate the effect of dietary multi-enzyme (MCPC) supplementation on synergistically enhancing the functions of both the foregut and hindgut, ultimately improving the nutrient digestion and utilization throughout the gastrointestinal tract. In vitro results demonstrated that MCPC increased the phosphorus and reducing sugar levels in the supernatant during enzymatic hydrolysis. Furthermore, during the fermentation of the enzymatic hydrolysis products, MCPC significantly increased the FRD0 value of the enzymatic hydrolysis products from both the positive control (PC) and negative control 1 (NC1) diets (p < 0.05). MCPC reduced the T1/2 value of in vitro fermentation products from the PC diet (p < 0.01), and decreased the VF (p = 0.082) and K (p < 0.05) values for the NC1 diet. Additionally, 72 crossbred barrows [Duroc × (Landrace × Yorkshire)], weighing 25 kg, were fed one of six diets until their live weight approached 50 kg. The basal diets consisted of PC, NC1 and negative control 2 (NC2), while the remaining three diets were prepared by adding 100 mg/kg MCPC to the respective basal diets. The results showed that MCPC supplementation significantly upregulated the expression of solute carrier family 17 member 4 (SLC17A4) and vitamin D receptor (VDR) genes in the duodenum (p < 0.05), while downregulating the expression of Calbindin-D28k (CaBP-D28K) and solute carrier family 1 member 4 (SLC1A4) genes (p < 0.05) in growing pigs. Moreover, MCPC supplementation significantly upregulated the expression of VDR, glucose transporter 2 (GLUT2) and intestinal fatty acid binding protein (FABP2) genes in the jejunum of growing pigs. Furthermore, MCPC supplementation significantly increased the relative abundances of Bacteroidota, Prevotella and Phascolarctobacterium (p < 0.05), while reducing the relative abundances of Verrucomicrobiota and Clostridium_sensu_stricto_1 (p < 0.05) in the colon of growing pigs. In conclusion, MCPC enhances nutrient digestion and absorption in the foregut, provides fermentable substrates for hindgut microbial fermentation, and improves gut microbiota composition. This improves hindgut fermentation and supports the synergistic interaction between the foregut and hindgut, ultimately improving nutrient utilization and benefiting animal health.

Potential of intestinal fatty acid-binding protein in assessing enteral tolerance in neonates of different gestational ages: A cross-sectional cohort study

Potential of intestinal fatty acid-binding protein in assessing enteral tolerance in neonates of different gestational ages: A cross-sectional cohort study

Acute gastrointestinal injury in the intensive care unit: diagnosis, severity assessment, and general approaches to correction

Introduction. Acute gastrointestinal injury is a polymorphic syndrome with many causes.The objective was to consider modern aspects of diagnosis and assessment of severity of acute gastrointestinal injury.Materials and methods. The literature search and analysis was performed in the medical information systems PubMed and eLibrary, using following keywords: acute gastrointestinal injury, intestinal fatty acid-binding protein (iFABP), D-lactate.Results. In this review, we present the scores for assessment of the severity of acute gastrointestinal tract injury, clinical symptoms, as well as new laboratory and instrumental diagnostic approaches.Conclusion. Early detection of this category of patients is vital to provide a personalized intensive therapy aimed at restoration of adequate function of the gastrointestinal tract.

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

Background/Objectives: 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). Methods: 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. Results: In the control group, values of all the investigated markers were lower than in the group of MODS patients (p < 0.0001). In the main group, the mortality rate was 44.9% (n = 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 (p < 0.05), while LBP levels on Day 7 were conversely lower in the deceased patients (p = 0.006). SOFA and APACHE II scores were higher in the deceased patients (p < 0.0001). Conclusions: 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.