👤 Ana-Maria Simundic

Different models that include clinical variables and blood markers have been investigated to predict acute ischemic stroke treatment course and recovery. The aim of the study was to investigate associations between lipid levels, lifestyle factors, hemostatic (F5, F2, SERPINE1, F13A1, and FGB), and atherogenic (APOA5 and ACE) gene variants and acute ischemic stroke (AIS) severity. This study included 250 patients with AIS in which F5, F2, SERPINE1, F13A1, FGB, APOA5, and ACE genotypes were determined. Total cholesterol (TC), high-density cholesterol, low-density cholesterol, and triglycerides concentrations were measured within 24 h of the AIS onset. Examination of the neurological deficit was done using National Institutes of Health Stroke Scale/Score (NIHSS). APOA5 genotype [TC + CC] was more frequent (P = 0.026) in patients with the NIHSS score ≥ 21. Univariate regression analysis has shown that triglycerides (OR 0.55, 95% CI 0.34-0.91; P = 0.019), obesity (0.28, 95% CI 0.10-0.73; P = 0.010), age (OR 1.08, 95% CI 1.04-1.13; P < 0.001), and APOA5 genotype (TC + CC) (OR 2.40, 95% CI 1.10-5.25; P = 0.034) are significantly associated with a severe stroke. When all variables were included in model age (OR 1.06, 95% CI 1.01-1.11; P = 0.018), obesity (OR 0.25, 95% CI 0.08-0.77; P = 0.016) and APOA5 genotype (TC + CC) (OR 3.26, 95% CI 1.29-8.23; P = 0.012) remained significant for the risk of severe AIS. APOA5 genotype (TC + CC), age, and obesity could be used as prognostic risk factors for a very severe stroke (NIHSS ≥ 21). Show less

Significant abnormalities in lipid metabolism are frequently present in patients with type 2 diabetes mellitus (T2DM). Hypertriglyceridemia, a highly proatherogenic state, is associated with increased risk of coronary artery disease. Genetic polymorphism APOA5 -1131T>C has been recognized as a significant contributor to hypertriglyceridemia in both healthy and diabetic populations. The aim of the study was to investigate the association of APOA5 -1131T>C polymorphism with the serum levels of triglycerides, total cholesterol, high-density lipoprotein (HDL) cholesterol, and low-density lipoprotein (LDL) cholesterol in patients with T2DM. In total, 234 DNA samples from patients with T2DM were genotyped using the PCR-RFLP method. Serum lipid levels were measured using standard laboratory methods. Obtained APOA5 -1131T>C genotype frequencies were 89% (T/T) and 11% (T/C+C/C). There was no significant association between APOA5 -1131T>C genotypes and triglyceride levels (1.90 mM [1.32-2.74] vs. 1.78 mM [1.54-3.05] for T/T vs. T/C+C/C genotype; p=0.553), HDL cholesterol levels (1.30 mM [1.10-1.40] vs. 1.30 mM [1.05-1.40] for T/T vs. T/C+C/C; p=0.534), and LDL cholesterol levels (3.1 mM [2.3-3.8] vs. 3.0 mM [2.2-3.5] for T/T vs. T/C+C/C; p=0.313). Our results suggest that hypertriglyceridemia in patients with T2DM is not likely to be associated with the APOA5 -1131T>C polymorphism. Show less

Several authors have reported the association of postprandial hypertriglyceridemia with oxidative stress, systemic inflammation and endothelial dysfunction. Our aim was to investigate the effect of high-calorie meal on blood markers of oxidative stress and endothelial dysfunction and the association of APOA5 -1131T/C and -250G/A hepatic lipase (HL) polymorphisms with postprandial triglyceride response. This study included 102 healthy male volunteers. All participants consumed a high-calorie meal (823 calories, 50 g fat, 28 g protein, 60 g carbohydrates). Total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, hsCRP, TAS and ICAM-1 were measured at fasting state and postprandially. APOA5 -1131T/C and -250G/A HL polymorphisms were also determined. Postprandial triglycerides were significantly increased (1.4 (1.1-2.1) vs. 2.4 (1.9-3.3) mmol/l, P<0.001). Average triglyceride increase was 1.0+/-0.7 mmol/l (65 %). Concentration of triglycerides, HDL-cholesterol, LDL-cholesterol, TAS and ICAM-1 differed significantly between the fasting state and postprandial measurements (P<0.001). However, those differences were within the limits of analytical imprecision. Other parameters did not change 3 h after the meal. Triglycerides response did not differ respective to the APOA5 and HL polymorphisms. Family history of hypertension and acute myocardial infarction were associated with higher postprandial triglyceride concentrations. Postprandial hypertriglyceridemia is not associated with increased concentrations of hsCRP, TAS and ICAM-1. Furthermore, APOA5 -1131T/C and -250G/A HL polymorphisms are not associated with different postprandial triglyceride response. Show less