Browsing by Author "Saric-Matutinovic, Marija (57211507979)"

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.

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.