Browsing by Author "Jovicic, Snezana (12243111800)"

Background: Symptom risk assessment in carotid artery stenosis (CAS) could be improved by parameters that reflect additional risk aspects such as chronic inflammation rate, and atherosclerotic activity on a systemic level. In light of that, we investigated the association of serum matrix metalloproteinases-2,7,9 (MMP-2,7,9), vascular cell adhesion molecule-1 (VCAM-1) and selectins-P and E with symptomatic status, stenosis degree and plaque morphology in CAS patients in order to select parameters that associate to important clinical determinants of the symptom development risk. Methods: The study included 119 CAS patients and 46 healthy subjects. Carotid arteries were examined by color flow Doppler and B-mode Duplex ultrasound. Serum parameters were assessed using commercially available enzyme-linked immunosorbent assays (ELISA). Difference was tested by Mann-Whitney U, Kruskal-Wallis and Chi-square tests, and Spearman’s correlation was tested. Results: MMP-7 and selectin-P levels were higher in CAS than in controls (p<0.001). Positive correlation with stenosis degree was found for MMP-7 (r=0.155, p=0.007), VCAM-1 (r=0.127, p=0.029) and selectin-P (r=0.269, p<0.001). MMP-7 and selectin-P were higher in subjects with Grey-Weale 2, comparing to subjects with Grey-Weale 3 plaques (p=0.036, p=0.009). Selectin-P was lower in the presence of Grey-Weale 4 than in Grey-Weale 2 (p=0.045). Conclusions: Concurrent association of MMP-7 and selectin-P with both stenosis degree and carotid plaque morphology shows the joint influence of these important determinants of symptom risk that is reflected in serum parameters. This indicates that they can supply additional information outside ultrasound CAS assessment only, and their integration in a future multiscale approach for CAS risk prediction could be beneficial. © 2025 Society of Medical Biochemists of Serbia. All rights reserved.

Objectives: Controversies regarding renal function impairment after open and endovascular aortic aneurysm repair still exist. The purpose of this study was to evaluate the renal function following open repair and endovascular aneurysm repair using Cystatin C. Methods: This prospective, observational case–control study was conducted in tertiary referral centre over 3 years, starting from 2012. In total, 60 patients operated due to infrarenal AAA either by means of open repair (30 patients) or endovascular aneurysm repair (30 patients) were included in the study. Biochemical markers of renal function (sCr, urea, potassium) were recorded pre-operatively and at these specific time points, immediately after the operation and at discharge, home (third postoperative day, endovascular aneurysm repair group) or from intensive care unit (third postoperative day, open repair group). Multivariate and propensity score adjustments were used to control for the baseline differences between the groups. Results: Creatinine levels in serum remained unchanged during the hospital stay in both groups without significant differences at any time point. Cystatin C levels in endovascular aneurysm repair patients significantly increased postoperatively and restored to values comparable to baseline at the discharge (0.865 ± 0.319 vs. *0.962 ± 0.353 vs. 0.921 ± 0.322, *p < 0.001). Cystatin C levels in patients treated with the open surgery was decreasing over time but not statistically significant comparing to Cystatin C values at the admission. However, decrease in Cystatin C serum levels in patients treated with conventional surgery resulted in statistically significant lower values compared to endovascular aneurysm repair patients both postoperatively and at the time of discharge (0.760 ± 0.225 vs. 0.962 ± 0.353, p < 0.05; 0.750 vs. 0.156, p < 0.05). Both multivariate linear regression models and propensity score adjustment confirm that, even after correction for previously observed intergroup differences, type of surgery, i.e. endovascular aneurysm repair is independently associated with the higher levels of Cystatin C both postoperatively and at the discharge. Conclusions: Dynamics of Cystatin C levels have been proven as a more vulnerable marker of renal dysfunction. Endovascular aneurysm repair is associated with higher levels of kidney injury markers. © 2017, © The Author(s) 2017.

Background: Galectin-3 is a protein widely distributed in the heart, brain and blood vessels, and has a regulatory role in inflammation, immunology and cancer. Many studies demonstrated that the increased level of galectin-3 is associated with progressive fibrosis and stiffening of the myocardium. The aim of this study was to investigate the role of galectin-3 in patients with type 2 diabetes (T2D) and/or arterial hypertension (HT). Methods: Study population included 189 patients, with no coronary artery disease, divided into three groups: group 1 (T2D), group 2 (T2D+HT), and group 3 (HT). All subjects underwent routine laboratory tests, as well as specific biomarkers assessment [galectin-3, glycosylated hemoglobin (HbA1c), N- terminal fragment B-type natriuretic peptide (NT-proBNP)]. Cardiological evaluation included physical examination, transthoracic tissue Doppler echocardiography and stress echocardiography. Results: The results of this study demonstrated significantly increased levels of galectin-3, blood glucose, and HbA1c in group 2. Also, echocardiographicaly, left ventricular (LV) diameters and IVS thickness were increased in this group of patients. Furthermore, in the same cohort a positive correlation between galectin-3 and NT-pro BNP, and galectin-3 and LV mass were demonstrated. In addition, a negative correlation between galectin-3 and LV end-diastolic diameter was revealed. Conclusions: This study revealed that levels of galectin-3 were higher in patients with both T2D and HT, and correlated with LV mass, indicating the potential role of this biomarker for early detection of myocardial structural and functional alterations.

Background: Galectin-3 is a protein widely distributed in the heart, brain and blood vessels, and has a regulatory role in inflammation, immunology and cancer. Many studies demonstrated that the increased level of galectin-3 is associated with progressive fibrosis and stiffening of the myocardium. The aim of this study was to investigate the role of galectin-3 in patients with type 2 diabetes (T2D) and/or arterial hypertension (HT). Methods: Study population included 189 patients, with no coronary artery disease, divided into three groups: group 1 (T2D), group 2 (T2D+HT), and group 3 (HT). All subjects underwent routine laboratory tests, as well as specific biomarkers assessment [galectin-3, glycosylated hemoglobin (HbA1c), N- terminal fragment B-type natriuretic peptide (NT-proBNP)]. Cardiological evaluation included physical examination, transthoracic tissue Doppler echocardiography and stress echocardiography. Results: The results of this study demonstrated significantly increased levels of galectin-3, blood glucose, and HbA1c in group 2. Also, echocardiographicaly, left ventricular (LV) diameters and IVS thickness were increased in this group of patients. Furthermore, in the same cohort a positive correlation between galectin-3 and NT-pro BNP, and galectin-3 and LV mass were demonstrated. In addition, a negative correlation between galectin-3 and LV end-diastolic diameter was revealed. Conclusions: This study revealed that levels of galectin-3 were higher in patients with both T2D and HT, and correlated with LV mass, indicating the potential role of this biomarker for early detection of myocardial structural and functional alterations.

Introduction: Sphingolipids, essential to trophoblast and endothelial function, may impact inflammation in preeclampsia. However, their specific role in late-onset preeclampsia remains unclear. To address this research gap, we analyzed sphingolipid profiles in pregnancies at high risk for preeclampsia development to identify potential biomarkers and clarify their role in disease pathogenesis. Materials and methods: We monitored 90 pregnant women at high risk for preeclampsia development across four gestational points. These women were later categorized into the group of women with high risk who did not develop preeclampsia (HRG) (70 women) or the preeclampsia group (PG) (20 women). Sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate (S1P), ceramides C16:0/C24:0, and sphingomyelin C16:0) were quantified via liquid chromatography-tandem mass spectrometry. Results: Sphingolipid profiles revealed distinct patterns between groups. Concentrations of S1P in the HRG increased from the 1st trimester to delivery (P < 0.001). We did not notice significant changes in S1P during pregnancy in the PG but compared with the HRG we found significantly lower concentrations at each test point from the 2nd trimester until delivery (P = 0.020, P = 0.013, P = 0.011, respectively). Ceramides C16:0 and C24:0 demonstrated significant increases over time in HRG (P < 0.001, both). Sphingomyelin C16:0 increased significantly across pregnancy in both groups (P < 0.001 in HRG and P = 0.006 in PG), with no significant differences between groups. Conclusions: We identified S1P as a potential biomarker for late-onset preeclampsia, with lower concentrations observed in PG compared to HRG. Rising sphingomyelin concentrations in both cohorts might serve as a relevant cardiovascular risk indicator in pregnancies at high risk for preeclampsia. © by Croatian Society of Medical Biochemistry and Laboratory Medicine.

Introduction: Sphingolipids, essential to trophoblast and endothelial function, may impact inflammation in preeclampsia. However, their specific role in late-onset preeclampsia remains unclear. To address this research gap, we analyzed sphingolipid profiles in pregnancies at high risk for preeclampsia development to identify potential biomarkers and clarify their role in disease pathogenesis. Materials and methods: We monitored 90 pregnant women at high risk for preeclampsia development across four gestational points. These women were later categorized into the group of women with high risk who did not develop preeclampsia (HRG) (70 women) or the preeclampsia group (PG) (20 women). Sphingolipids (sphingosine, sphinganine, sphingosine-1-phosphate (S1P), ceramides C16:0/C24:0, and sphingomyelin C16:0) were quantified via liquid chromatography-tandem mass spectrometry. Results: Sphingolipid profiles revealed distinct patterns between groups. Concentrations of S1P in the HRG increased from the 1st trimester to delivery (P < 0.001). We did not notice significant changes in S1P during pregnancy in the PG but compared with the HRG we found significantly lower concentrations at each test point from the 2nd trimester until delivery (P = 0.020, P = 0.013, P = 0.011, respectively). Ceramides C16:0 and C24:0 demonstrated significant increases over time in HRG (P < 0.001, both). Sphingomyelin C16:0 increased significantly across pregnancy in both groups (P < 0.001 in HRG and P = 0.006 in PG), with no significant differences between groups. Conclusions: We identified S1P as a potential biomarker for late-onset preeclampsia, with lower concentrations observed in PG compared to HRG. Rising sphingomyelin concentrations in both cohorts might serve as a relevant cardiovascular risk indicator in pregnancies at high risk for preeclampsia. © by Croatian Society of Medical Biochemistry and Laboratory Medicine.