Gut barrier protein levels in serial blood samples from critically ill trauma patients during and after intensive care unit stay.

PURPOSE: In an effort to better manage critically ill patients hospitalised in the intensive care unit (ICU) after experiencing multiple traumas, the present study aimed to assess whether plasma levels of intestinal epithelial cell barrier proteins, including occludin, claudin-1, junctional adhesion molecule (JAM-1), tricellulin and zonulin, could be used as novel biomarkers. Additional potential markers such as intestinal fatty acid-binding protein (I-FABP), D-lactate, lipopolysaccharide (LPS) and citrulline were also evaluated. We also aimed to determine the possible relationships between the clinical, laboratory, and nutritional status of patients and the measured marker levels. METHODS: Plasma samples from 29 patients (first, second, fifth and tenth days in the ICU and on days 7, 30 and 60 after hospital discharge) and 23 controls were subjected to commercial enzyme-linked immunosorbent assay (ELISA) testing. RESULTS: On first day (admission) and on the second day, plasma I-FABP, D-lactate, citrulline, occludin, claudin-1, tricellulin and zonulin levels were high in trauma patients and positively correlated with lactate, C-reactive protein (CRP), number of days of ICU hospitalisation, Acute Physiology and Chronic Health Evaluation II (APACHE II) score and daily Sequential Organ Failure Assessment (SOFA) scores (P < 0.05-P < 0.01). CONCLUSION: The results of the present study showed that occludin, claudin-1, tricellulin and zonulin proteins, as well as I-FABP, D-lactate and citrulline, may be used as promising biomarkers for the evaluation of disease severity in critically ill trauma patients, despite the complexity of the analysis of various barrier markers. However, our results should be supported by future studies.

Increased oxidative and chromosomal DNA damage in patients with ankylosing spondylitis: its role in pathogenesis.

Increased DNA damage has been suggested to contribute to the pathogenesis of chronic inflammatory diseases, but controlled studies are lacking in ankylosing spondylitis (AS). Therefore, we assessed oxidative stress, oxidative DNA damage, chromosomal DNA damage, cell proliferation and cell death in the peripheral blood lymphocytes of patients with AS as well as the possible role of DNA damage in the development of the disease. In total, 25 newly diagnosed AS patients who had not received anti-inflammatory agents and 25 healthy controls were recruited. Oxidative DNA damage was assessed by plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, and chromosomal DNA damage was assessed by the cytokinesis-block micronucleus cytome (CBMN-cyt) method. Compared to controls, the micronucleus (MN) frequencies, nucleoplasmic bridge (NPB) frequencies, nuclear bud (NBUD) frequencies, apoptotic cell frequencies, necrotic cell frequencies and plasma 8-OHdG levels were significantly higher in patients with AS (p < 0.001, p < 0.05, p < 0.01, p < 0.001, p < 0.001, and p < 0.001, respectively), and the metaphase cell numbers, binucleated (BN) cell frequencies and nuclear division index (NDI) values were significantly lower in patients with AS (p < 0.01, p < 0.001 and p < 0.001, respectively). Thus, the present findings suggested that oxidative stress, oxidative DNA damage, and chromosomal DNA damage may be involved in the pathogenesis of AS similar to other chronic inflammatory diseases. In addition, the increased plasma 8-OHdG levels, MN frequencies, NPB frequencies and NBUD frequencies in AS patients may reflect an increased cancer risk.

Oxidative and chromosomal DNA damage in patients with type I Gaucher disease and carriers.

BACKGROUND AND AIMS: Gaucher disease (GD) is caused by a genetic deficiency of the beta-glucocerebrosidase enzyme which results in the accumulation of glucosylceramide in macrophages. This accumulation may induce oxidative stress, resulting in DNA damage in patients with GD. The aim of this study was to assess plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels and cytokinesis-block micronucleus cytome (CBMN-cyt) assay parameters in the peripheral blood lymphocytes of patients with GD and carriers, evaluate the possible associations of these values with GD, and determine whether they can be used as potential biomarkers in GD. METHODS: This study included 20 patients with type 1 GD, six carriers, and 27 age- and sex-matched healthy controls. CBMN-cyt assay parameters in peripheral blood lymphocytes of the patients with GD, carriers, and controls were evaluated and 8-OHdG levels in their plasma samples were measured. RESULTS: CBMN-cyt assay parameters in patients with GD and carriers were not significantly different when compared with controls (p > 0.05). However, plasma 8-OHdG levels were found to be higher in both patients with GD and carriers than in control subjects (p < 0.01). CONCLUSIONS: Oxidative DNA damage may be a useful prognostic tool, whereas the CBMN-cyt assay cannot be used as a predictive biomarker of GD.