Snezana Jovicić

Klinički centar Srbije, Belgrade, SE, Serbia

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Publications (3)3.96 Total impact

  • Article: Association of lipid and inflammatory markers with C-reactive protein in cardiovascular risk assessment for primary prevention.
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    ABSTRACT: High-sensitivity C-reactive protein (hsCRP) has been recognized as an independent marker of cardiovascular risk. Since atherosclerosis is a multifactorial disease, the aim of this study was to determine association between hsCRP and other markers of inflammation and dyslipidemia. In 242 healthy volunteers, total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), nonHDL-C, triglycerides (TG) and hsCRP were measured using Olympus AU2700. Apolipoprotein A-I (apoAI), apolipoprotein B (apo B), lipoprotein (a) (Lp(a)), haptoglobin, alpha1-acid glycoprotein (A1AGP), C3 and C4 complement components were determined on Architect c8000, and serum amyloid A (SAA) and fibrinogen on BN II nephelometer and ACL 7000, respectively. Significant (P < 0.05) partial Pearson's correlation coefficients were found between hsCRP and TC (r = 0.172), nonHDL-C (r = 0.182), LDL-C (r = 0.154), apoB (r = 0.167), fibrinogen (r = 0.411), SAA (r = 0.493), A1AGP (r = 0.462), haptoglobin (r = 0.310), C3 (r = 0.349) and C4 (r = 0.371). In multiple regression analysis, BMI, SAA, A1AGP, fibrinogen and nonHDL-C showed independent correlation with hsCRP. Multinomial logistic regression analysis demonstrated that BMI, nonHDL, fibrinogen and SAA were strong predictors of hsCRP concentration. Odds ratios for intermediate and high risk categories compared with the low risk category were 1.177 (1.033-1.341) and 1.289 (1.091-1.523), 1.515 (1.021-2.249) and 2.062 (1.246-3.411), 2.241 (1.268-3.959) and 7.123 (3.259-15.568), and 1.387 (1.179-1.632) and 1.691 (1.397-2.047), for BMI, nonHDL-C, fibrinogen and SAA, respectively. The prediction of risk for future cardiac events based on hsCRP concentration, which is the recommended parameter for improving cardiovascular risk stratification, might be complemented with the information about BMI, nonHDL-C, fibrinogen and SAA.
    Clinical laboratory 01/2009; 55(11-12):411-9. · 0.90 Impact Factor
  • Article: The values of estimated glomerular filtration rate calculated with creatinine and cystatin C based equations in healthy adults.
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    ABSTRACT: The glomerular filtration rate (GFR) is widely accepted as the best overall index of kidney function. GFR can be measured as the clearance of exogenous or endogenous filtration markers or clinically estimated from serum concentrations of creatinine or cystatin C. Recently, it has been recommended that an estimated GFR (eGFR) should be reported in addition to the value of filtration markers. In this study, we determined the values of eGFR, based on creatinine and cystatin C equations, in 125 healthy volunteers aged 20-75 years. Creatinine was measured by a kinetic alkaline picrate method on an ARCHITECT ci8200 analyzer (Abbott Diagnostics, Wiesbaden, Germany). Cystatin C was determined by a latex particle-enhanced immunonephelometric assay (BNII, Dade Behring, Marburg, Germany). The eGFR values were calculated for creatinine using the Modification of Diet in Renal Disease (MDRD) study equation and Rule's quadratic equation and for cystatin C according to the equation published by Hoek et al. The reference intervals for eGFRs with MDRD, Rule's quadratic and Hoek's equations were calculated nonparametrically and were determined to be 63.5-124.6 mL/min/1.73 m2, 78.3-139.2 mL/min/1.73 m2 and 72.2-115.6 mL/min/1.73 m2, respectively. According to the US National Kidney Foundation, chronic kidney disease (CKD) can be defined as a GFR < 60 mL/min/1.73 m2. Our results showed that healthy adults had eGFR values > 63.5 mL/min/1.73 m2. However, it is important to note that these normal values overlap with values in stages 1 and 2 of CKD, thus an eGFR greater than 60 mL/min/1.73 m2 does not exclude kidney disease.
    Clinical laboratory 01/2008; 54(5-6):153-9. · 0.90 Impact Factor
  • Article: Analytical performance and clinical efficacy for cardiovascular risk estimation of an Olympus immunoturbidimetric high-sensitivity C-reactive protein assay.
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    ABSTRACT: Increased C-reactive protein (CRP) concentration within the reference interval (<10.0 mg/L) is a strong predictor of cardiovascular disease (CVD) in apparently healthy adults. Cutoff points for use of CRP in estimating CVD risk are <1, 1-3 and >3 mg/L for low, average and high relative risk, respectively. For measuring CRP concentrations to assess cardiovascular risk, high-sensitivity CRP (hsCRP) assays have been developed. The aim of this study was to evaluate the analytical performance and clinical efficacy for cardiovascular risk estimation of the Olympus immunoturbidimetric latex CRP assay (sensitive application). The comparative method used was the CardioPhase* hsCRP assay, approved by the Food and Drug Administration for use in CVD risk assessment. The imprecision of the Olympus hsCRP assay in the concentration range 0.2-10.0 mg/L was 0.38-8.16% within runs and 3.75-9.63% between runs. For method comparison studies, 194 fresh serum samples were selected to cover the interval 0.15-10.0 mg/L CRP. Comparison of the Dade Behring and Olympus methods was performed using weighted Deming regression analysis (slope 0.99 mg/L, intercept 0.002 mg/L, S(y,x)=0.02 mg/L, r=0.992) and a Bland-Altman relative difference plot (mean difference -0.002%, SD=0.040%). The agreement between the Dade Behring and Olympus methods for relative risk class assignments was 95.4%. Statistical analysis of the agreement between the two methods for each relative risk class showed that the differences between the methods were not statistically significant (p>0.10). Although previous reports found poor performance of the Olympus CRP tests for use in cardiovascular and peripheral vascular risk estimation, our study proved good analytical performance and clinical efficacy of the Olympus hsCRP assay for this use.
    Clinical Chemistry and Laboratory Medicine 01/2006; 44(2):228-31. · 2.15 Impact Factor

Institutions

  • 2006–2009
    • Klinički centar Srbije
      Belgrade, SE, Serbia