Jadranka Sertić

University of Zagreb, Zagrabia, Grad Zagreb, Croatia

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Publications (46)115.07 Total impact

  • Article: PP.05.05
    Journal of Hypertension 06/2015; 33:e170. DOI:10.1097/01.hjh.0000467846.16203.c3 · 4.72 Impact Factor
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    Karlo Golubic · Anton Smalcelj · Jadranka Sertic · Ljiljana Juricic
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    ABSTRACT: Aim To determine the association between the number of thymine-adenine (TA)n dinucleotide repeats in the promoter region of the gene coding for the estrogen receptor alpha (ESR1) and the prevalence of lone atrial fibrillation (AF) in men. Methods We conducted a case-control study involving 89 men with lone AF and 166 healthy male controls. The ESR1 genotype was established by polymerase chain reaction and capillary electrophoresis. To assess the association of ESR1 genotype with AF, logistic regression models were built with AF as outcome. Results Men with lone AF had significantly greater number of (TA)n repeats of single alleles than controls (mean ± standard deviation, 19.2 ± 4.2 vs 18 ± 4.3, P = 0.010). After adjustment for other factors, a unit-increase in (TA)n repeat number was associated with a significantly greater likelihood of AF (odds ratio 1.069; 95% confidence interval 1.024-1.116, P = 0.002). Conclusions Our results indicate that a greater number of (TA)n repeats in the promoter region of ESR1 is associated with a significantly increased likelihood of lone atrial fibrillation in men.
    Croatian Medical Journal 02/2014; 55(1):38-44. DOI:10.3325/cmj.2014.55.38 · 1.37 Impact Factor
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    ABSTRACT: Aim: The aim of the study was to estimate the influence of interactions between peroxisome proliferator-activated receptor γ (PPARγ) and target genes lipoprotein lipase (LPL), interleukin 6 (IL6), angiotensin converting enzyme (ACE), and angiotensin II type 1 receptor (AT1R) on metabolic syndrome (MetSy) and its traits. Methods: The study included 527 participants (263 with MetSy and 264 controls). Genotyping of PPARγ Pro12Ala, LPL PvuII (-/+), IL6 -174G>C, ACE I/D and AT1R 1166A>C was performed using polymerase chain reaction-restriction fragment length polymorphism-based methods. Results: Interaction between PPARγ Pro12Ala and LPL Pvu(-/+) improved prediction of MetSy over and above prediction based on a model containing no interactions (χ(2)=7.22; df=1; p=0.007). In the group of participants with PPARγ Pro12Ala or Ala12Ala genotypes, those with the LPL Pvu (-/+) or (+/+) genotype had greater odds for MetSy (odds ratio OR=5.98; 95% confidence interval CI: 1.46-24.47, p=0.013). Interaction between PPARγ Pro12Ala and IL6 -174G>C improved prediction of high fasting blood glucose (χ(2)=13.99; df=1; p<0.001). PPARγ Ala12 variant was found protective in patients with IL6 -174GG genotype (OR=0.10; 95% CI: 0.02-0.57, p=0.01), while in the case of IL6 -174C allele carriers, for PPARγ Ala12 carriers, larger odds for high glucose levels compared with Pro12 variant were observed (OR=2.39; 95% CI: 1.11-5.17, p=0.026). Interactions of PPARγ and ACE were significant for BMI. In the group with ACE DD genotype, those with PPARγ Pro12Ala or Ala12Ala genotype have greater odds for obesity (OR=9.98; 95% CI: 1.18-84.14, p=0.034). Conclusions: PPARγ gene variants can, in interaction with some of its target genes, modulate physiological processes leading to the development of MetSy.
    Genetic Testing and Molecular Biomarkers 11/2013; DOI:10.1089/gtmb.2013.0344 · 1.15 Impact Factor
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    ABSTRACT: Peroxisome proliferator activated receptor-gamma (PPARG) and lipoprotein lipase (LPL) play important role in lipid homeostasis, insulin resistance and adipogenesis, and their gene variability could be considered as predictive genetic markers for metabolic syndrome (MetSy). The aim of the study was to estimate possible associations of PPARG (Pro12Ala) and LPL PvuII (+/-) polymorphisms with MetSy and its traits. Study included 527 subjects. According to the modified National Cholesterol Education Program Adult Treatment Panel III definitions, subjects were classified into the metabolic syndrome group and control group. Genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism methods. In the total sample, LPL variants were associated with waist circumference (chi2 = 7.263, d.f = 2, p = 0.026) and with BMI (chi2 = 6.549, d.f = 2, p = 0.038), where PvuII (+/+) genotype carriers had the highest risk for increased waist circumference (specific PvuII (+/+) vs. others analysis chi2 = 7.033, p = 0.008) and increased BMI (specific PvuII( +/+) vs. others analysis chi2 = 5.154, p = 0.023). LPL gene variants were also associated with HDL-C levels (chi2 = 6.901, d.f = 2, p = 0.032), where PvuII (-/-) genotype carriers had higher HDL-C values in comparison to others (specific Pvu (+/+) vs. others analysis chi2 = 6.504, p = 0.011). Furthermore, PvuII (-) allele carriers had significantly lower glucose (allele based analysis Add Value = -0.0878, chi2 = 5.878, d.f. = 1, p = 0.015). Significant interaction was detected between PPARG and LPL that affected HDL-C levels in male population (chi2 = 11.790, d.f = 1, p = 0.0006) in the manner that Ala/PvuII(+) contributed to the lowest HDL-C values (Specific Ala/ Pvu(+) vs. others analysis was chi2 = 11.750, p = 0.0006). According to obtained results LPL and PPARG gene variants could be susceptibility factors of obesity and lipid status, contributing to development of MetSy, particularly in males. Because of antiatherogenic function of HDL-C, the identification of genetic variants associated with HDL-C can provide useful information related to genotype-phenotype relationships. Since the interplay between PPARG and LPL gene and gender seems to be significant it could point to the personalized behavioural recommendations for prevention of metabolic and cardiovascular diseases.
    Collegium antropologicum 09/2013; 37(3):801-8. · 0.61 Impact Factor
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    ABSTRACT: The Romani, the largest European minority group with approximately 11 million people [1], constitute a mosaic of languages, religions, and lifestyles while sharing a distinct social heritage. Linguistic [2] and genetic [3-8] studies have located the Romani origins in the Indian subcontinent. However, a genome-wide perspective on Romani origins and population substructure, as well as a detailed reconstruction of their demographic history, has yet to be provided. Our analyses based on genome-wide data from 13 Romani groups collected across Europe suggest that the Romani diaspora constitutes a single initial founder population that originated in north/northwestern India ∼1.5 thousand years ago (kya). Our results further indicate that after a rapid migration with moderate gene flow from the Near or Middle East, the European spread of the Romani people was via the Balkans starting ∼0.9 kya. The strong population substructure and high levels of homozygosity we found in the European Romani are in line with genetic isolation as well as differential gene flow in time and space with non-Romani Europeans. Overall, our genome-wide study sheds new light on the origins and demographic history of European Romani.
    Current biology: CB 12/2012; 22(24). DOI:10.1016/j.cub.2012.10.039 · 9.92 Impact Factor
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    ABSTRACT: Familial hypercholesterolemia (FH) is caused by mutations in the genes for LDLR, APOB or PCSK9, and identification of the causative mutation provides definitive diagnosis so that the patient can be treated, their relatives tested and, therefore, premature heart disease prevented. DNA of eight unrelated individuals with clinically diagnosed FH were analyzed using a High-Resolution Melting method (HRM) for the LDLR gene (coding region, promoter and intron/exon boundaries), the APOB gene (part exon 26) and the PCSK9 gene (exon7). Variations found were sequenced and the effect on function of confirmed variants examined using predictive algorithms. Gross deletions and insertions were analysed using MLPA. Three novel LDLR variants were found, p.(S470C), p.(C698R) and c.2312-2A>C. All were predicted to be pathogenic using predictive algorithms. Three previously reported disease-causing mutations were identified (p.(G20R), p.(N272T) and p.(S286R); the latter was also carried by a hypercholesterolaemic relative. One patient carried the pathogenic APOB variant p.(R3527Q). No large LDLR deletions nor insertions were found, neither were any PCSK9 variants identified. HRM is a sensitive method for screening for mutations. While the causative mutation has been identified in 88% of these clinically defined FH patients, there appears to be a high degree of allelic heterogeneity in Croatian patients.
    Annals of Human Genetics 11/2012; 77(1). DOI:10.1111/j.1469-1809.2012.00735.x · 1.93 Impact Factor
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    ABSTRACT: The aim of this study was to identify KRAS and BRAF gene mutations in colorectal cancer patients and to assess whether they are linked with clinicopathological features. The results of KRAS and BRAF mutation analysis could be used in the selection of patients for anti-EGFR therapy. All specimens were obtained during routine surgery of patients with colorectal carcinoma. The diagnoses were established by standard procedures and confirmed histopathologically. After DNA extraction, KRAS mutations were analyzed using quantitative real-time PCR and BRAF mutations were analyzed using real-time PCR by fluorescence melting curve analysis. Our results show that KRAS gene mutations were detected in 35.6% samples and the most frequent mutation was Gly12Val. BRAF gene mutation Val600Glu was detected in 8.5% samples. Statistical analysis revealed a significant association between the KRAS mutation and Dukes' stage (p=0.034), with the lowest frequency in Dukes'A, and between the KRAS mutation and histological grade (p=0.044), with no KRAS mutation found in poor differentiated tumors. The first data about KRAS and BRAF mutational status in the sample of Croatian population with colorectal cancer shows that the incidence of KRAS and BRAF mutations is within generally valid limits. Prospective studies are to be continued in order to determine whether these mutations contribute to progression of colorectal cancer.
    Neoplasma 04/2012; 59(4):376-83. DOI:10.4149/neo_2012_049 · 1.64 Impact Factor
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    ABSTRACT: Human obesity is accepted as an important risk factor for development of MetS. Adiponectin is linked to central obesity and ADIPOQ variants are promising markers for understanding the genetic base of obesity-related disorders. We performed analyses of adiponectin concentrations and ADIPOQ variants and tested their associations with obesity and MetS in young subjects of Croatian origin. Biochemical and anthropometric parameters of MetS were obtained for 149 unrelated subjects. Adiponectin levels were measured by ELISA assay. ADIPOQ -11391G>A and -11377C>G were genotyped by real-time PCR. BMI and WC, TG and GLUC showed inverse correlation, whereas HDL-C showed a positive correlation with adiponectin concentrations. For central obesity, we found association with -11377C>G and with -11391G>A polymorphisms. ADIPOQ -11377GG and -11391GA significantly increased the risk for the development of central obesity (OR 5.57 and OR 3.37, respectively). Significant association was found between -11391A, -11377G allele and haplotype and increased TG. -11377C>G and -11391G>A variant were significantly associated with the incidence of MetS. C>G mutation at position -11377 significantly increased the risk of MetS development (OR = 2.93). Compared with the -11391G homozygotes, carriers of the A allele had a significantly increased risk for the development of MetS (OR = 3.15). The test of overall association showed a statistically significant correlation of MetS with -11377C>G and -11391G>A haplotypes (p = 0.008). Analysis of adiponectin concentration and ADIPOQ -11391G>A and -11377C>G gene variants may be clinically meaningful for estimation of MetS risk in a young population.
    Archives of medical research 02/2012; 43(2):145-53. DOI:10.1016/j.arcmed.2012.02.004 · 2.41 Impact Factor
  • Kidney and Blood Pressure Research 01/2012; 35(2):95-95. · 1.82 Impact Factor
  • European Journal of Cancer 09/2011; 47. DOI:10.1016/S0959-8049(11)71686-0 · 4.82 Impact Factor
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    ABSTRACT: There is accumulating evidence for an increased prevalence of metabolic syndrome (MetS) in bipolar patients, which is comparable to the prevalence of MetS in patients with schizophrenia. Hyperhomocysteinaemia has emerged as an independent and graded risk factor for the development of cardiovascular disease (CVD), which is, at the same time, the primary clinical outcome of MetS. The aim of this study was to ascertain if the presence of MetS was associated with hyperhomocysteinaemia in patients with bipolar disorder (N=36) and schizophrenia (N=46) treated with second-generation antipsychotics (SGA). MetS was defined according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP-III) criteria and the cut-off point for hyperhomocysteinaemia was set up at 15 μmoll(-1). Results of the study indicated that the presence of the MetS is statistically significantly associated with the elevated serum homocysteine in all participants. As hyperhomocysteinaemia has emerged as an independent risk factor for psychiatric disorder and CVD, it could be useful to include fasting homocysteine serum determination in the diagnostic panels of psychiatric patients to obtain a better assessment of their metabolic risk profile.
    Psychiatry Research 08/2011; 189(1):21-5. DOI:10.1016/j.psychres.2010.11.021 · 2.68 Impact Factor
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    ABSTRACT: Tubular proteinuria and enzymuria are hallmarks of endemic nephropathy (EN). The role of I/D angiotensin convertase (ACE) gene polymorphism has not yet been elucidated in this peculiar chronic tubulointerstitial nephritis, and our aim was to investigate the role of this polymorphism in EN focusing on the urinary N-acetyl-β-D-glucosaminidase (NAG) excretion, a biomarker of proximal tubular damage. ACE genotype and allele frequencies were determined in 229 farmers (147 women and 82 men) from an endemic Croatian village. The farmers were stratified according to the WHO criteria into the following subgroups: those 'at risk' for EN (n = 37), 'suspected of having EN' (n = 57), and 'others' (n = 135). There were 74 (32.3%) subjects homozygous for the D allele, 99 (43.2%) heterozygous (ID genotype) and 56 (24.4%) homozygous for the I allele. No differences in allele frequency were found between the established WHO subgroups (p > 0.05). In the whole group, DD subjects had significantly higher values of diastolic blood pressure (p = 0.003) and urinary NAG than subjects with ID and II genotype (5.5 ± 1.2 vs. 4.0 ± 3.0 vs. 3.8 ± 4.2, respectively; p = 0.023). The highest values of serum creatinine (p = 0.02), proteinuria (p = 0.03) and urinary NAG (6.0 ± 3.7 vs. 3.7 ± 2.1 vs. 3.0 ± 1.6, respectively; p = 0.008) were observed in those suspected of having EN group with the DD genotype. ACE gene polymorphism is not a risk factor for EN. However, it might influence the clinical course of EN, and increased excretion of NAG might be a prognostic marker of this chronic tubulointerstitial nephritis.
    Nephron Clinical Practice 07/2011; 119(2):c105-12. DOI:10.1159/000327528 · 1.65 Impact Factor
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    ABSTRACT: Thorough control of risk factors is pivotal for cardiocerebrovascular diseases. As classic risk assessment accounts for only 50% of risk variability and due to the role of inflammatory processes in endothelial dysfunction and atherosclerotic plaque rupture, it is necessary to identify new biomarkers for risk prediction. In addition to the inflammatory marker high sensibility C-reactive protein (hs-CRP), lipoprotein associated phospholipase A2 (Lp-PLA2) is gaining increasing significance, since it is directly involved in the pathogenesis of atherosclerotic plaque progression. Lp-PLA2 is highly specific for vascular inflammation, has low biological variability, and plays a causative role in atherosclerotic plaque inflammation. It belongs to the group of intracellular and secretory phospholipase enzymes that can hydrolyze sn-2 phospholipid ester bond of cellular membranes and lipoproteins. Lp-PLA2 enzyme is formed by macrophages and foam cells in atherosclerotic plaque, and is associated primarily with LDL particles in blood. Lp-PLA2 that is bound to LDL is the sole enzyme responsible for hydrolysis of oxidized phospholipids (oxPL) on LDL particles. Lp-PLA2 hydrolyzes oxPL at the surface of lipoproteins, but has weak activity against non-oxPL. Lp-PLA2 is also the enzyme that hydrolyzes oxPL on HDL particles, where it may have a role in the antioxidative function of HDL. The distribution of Lp-PLA2 between LDL and HDL particles depends on the extent of Lp-PLA2 glycosylation, which may affect the activity of Lp-PLA2 in plasma. Stable atherosclerotic plaques contain few inflammatory cells and a small amount of Lp-PLA2. In contrast, unstable plaques most often do not have significant impact on arterial lumen but may be detected by its thin connective tissue cap, low collagen and high lipid content. A distinguishing factor between stable and unstable atherosclerotic plaque may also be the presence of activated inflammatory cells and increased Lp-PLA2 concentration in unstable plaque. These new insights indicate that Lp-PLA2 may be a risk factor, which is important for the formation of atherosclerotic plaque but also for its rupture. The purpose of applying markers of inflammation is to improve stratification of patients at risk, so that treatment intensity may be adjusted to the risk level. Lp-PLA2 inhibition is associated with decreased cytokines. Lipid-affecting drugs stabilize atherosclerotic plaque by reducing the central lipid core, decreasing macrophage infiltration, and thickening of the connective tissue cap. These drugs reduce Lp-PLA2 concentration and the frequency of cardiocerebrovascular events as well. Besides acting as a specific marker of atherosclerotic plaque inflammation, Lp-PLA2 has a significant prognostic value because of its direct role in the formation of rupture-prone atherosclerotic plaque, unlike classic risk factors, for example lipid measurement or vascular imaging, which do not directly estimate acute ischemic potential in the arterial wall. Studies have demonstrated correlation between increased Lp-PLA2 concentrations and enhanced risk of cardiocerebrovascular events, even after multivariate adjustment to classic risk factors. In addition to its high specificity for vascular inflammation, Lp-PLA2 concentration is stable in terms of time, unlike, for instance, CRP levels. Lp-PLA2 has been confirmed as an independent risk predictor, which is complementary to hsCRP. It could be used in clinical practice for improved risk assessment in patients with transient cardiocerebrovascular risk, particularly in those with metabolic syndrome (obese patients with mixed dyslipidemia, hyperglycemia, insulin resistance, and arterial hypertension). Lp-PLA2 levels allow for further risk stratification of high-risk patients into a very high risk group where more aggressive therapy is recommended, as well as the achievement of LDL-cholesterol levels < 2.5 or, even better, < 2.0 mmol/L as a feasible therapeutic target. Similar to hsCRP, the levels of Lp-PLA2 are reduced by lipid-affecting drugs, while its low concentrations are associated with a very low risk of cardiocerebrovascular events both in low- and high-risk population. According to recent American guidelines for assessing the risk of cardiovascular disease, Lp-PLA2 determination is recommended as an additional marker to the classic risk assessment in patients with moderate and high risk.
    Acta medica Croatica: c̆asopis Hravatske akademije medicinskih znanosti 10/2010; 64(4):237-45.
  • Journal of Hypertension 06/2010; 28. DOI:10.1097/01.hjh.0000379926.39435.59 · 4.72 Impact Factor
  • Atherosclerosis Supplements 06/2010; 11(2):131-131. DOI:10.1016/S1567-5688(10)70605-X · 9.67 Impact Factor
  • Atherosclerosis Supplements 06/2010; 11(2):210-210. DOI:10.1016/S1567-5688(10)71001-1 · 9.67 Impact Factor
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    ABSTRACT: Interactions of MinK and e-NOS Gene Polymorphisms Appear to Be Inconsistent Predictors of Atrial Fibrillation Propensity, but Long Alleles of ESR1 Promoter TA Repeat May Be a Promising Marker. We analyzed minK, e-NOS and ESR1 gene polymorphisms in 40 patients with atrial fibrillation (AF) without major structural heart disease compared to 35 healthy controls. A missense polymorphism in the minK gene with A/G substitution at nucleotide 112 causing serine (S) to glycine (G) change, 786 T/C polymorphism in the 5' flanking region of e-NOS gene and TA polymorphism in the regulatory region of estrogen receptor ESR1 gene with long (> or = 19 TA repeats) and short alleles were examined. Only a slight increase in minK G allele frequency, but with marked excess in AG/TT combination of minK and e-NOS polymorphisms was found in the AF group. The interpretation remains tentative due to small groups precluding statistical significance of differences, possible lab flaws and inconsistencies with earlier data. However, ESR1 long allele homozygotes were strikingly more frequent in the AF than in control group, reaching statistical significance surprisingly in males (p < 0.02). Functional activity of estrogen receptors may be more critical in males than in females with abundance of circulating estrogen. Contrasting the intricate complexity of genetic polymorphisms influencing cardiac rhythm with our modest research, we would limit the conclusion to the plea for further research of ESR1 role in AF.
    Collegium antropologicum 09/2009; 33(3):933-7. · 0.61 Impact Factor
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    ABSTRACT: The aim of this study was to determine if insertion-deletion polymorphism of angiotensin-converting enzyme is a risk factor for the development of preeclampsia. Sixty women with preeclampsia and 50 normotensive pregnant women were included in this study. Preeclampsia was defined as blood pressure >140/90 mmHg in a previously normotensive women with proteinuria >300 mg/L in a 24-hours. Twelve women also had preeclampsia in previous pregnancy. The genotyping of polymorphism in the intron 16 of the angiotensin-converting enzyme was performed by the polymerase chain reaction followed by the agarose electrophoresis. The patients were divided into three groups according to the presence (I) or absence (D) of insertional polymorphism (II, ID, and DD). Genotype distribution and allele frequencies were compared by Mantel-Haenszel chi2 testing. The frequency of DD genotype was not significantly higher in women with preeclampsia (26/60) than in the control group (14/50, p=0.096). The D allele frequency was significantly higher in 17 women with preeclampsias who required delivery before 34 weeks of pregnancy (0.735), than in 43 women in whom obstetric complications took place after 34 weeks of pregnancy (0.56, p=0.036). The D allele frequency was 0.83 in women having recurrent preeclampsia, i.e. significantly higher compared with women, who were for the first time, experienced preeclampsia (0.57, p=0.013). This study showed a significantly positive association between D allele frequency and risk of recurrent preeclampsia and preterm delivery before 34 weeks of pregnancy. The deletion genotype could be an important contributing factor for an early onset and recurrent preeclampsia.
    Collegium antropologicum 07/2008; 32(2):339-43. · 0.61 Impact Factor
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    ABSTRACT: A 40-year-old man was admitted to the emergency department after a suicide attempt. The patient was found at home unconscious, with an open bottle of antifreeze near him. The patient was in a coma on admission, but neurological examination excluded intracranial changes. Results of initial urine and serum toxicological screening tests were negative. Laboratory values indicated metabolic acidosis, leukocytosis, urinalysis revealed hematuria and unrecognized crystals. Osmolality and osmol gap were not determined on patient admission. Treatment with ethanol as an antidote and hemodialysis were started because of metabolic acidosis, anamnestic data and clinical status of the patient, and subsequently led to improvement of his condition. Further toxicological analyses of glycolic and oxalic acids in serum and urine samples were performed by ion-chromatography (IC) method and showed high values in spot urine and serum ultrafiltrate at admission, but during therapy the values progressively decreased. Treatment of poisoned patient for 3 weeks resulted in complete recovery.
    Forensic science international 09/2007; 170(2-3):213-5. DOI:10.1016/j.forsciint.2007.03.025 · 2.12 Impact Factor
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    ABSTRACT: Controversy exists as to whether the deletion/deletion (DD) genotype of angiotensin l-converting enzyme (ACE) gene polymorphism is associated with coronary heart disease (CHD). There are only a few studies dealing with this issue in the elderly, also with controversial results. The aim of this study was the assessment of correlation between genetic markers and the risk of CHD in the elderly. The results indicated DD genotype importance for CHD in the elderly as proven by discriminant analysis (chi2 = 25.77; df = 16; p = 0.0620). However, the use of univariate method demonstrated no correlation between DD genotype of ACE gene polymorphism and coronary artery disease. D allele of ACE gene was associated with higher activities of ACE plasma. A weak, but increased risk of MI is associated with high frequency of DD genotype in the elderly. Strong correlation between ACE polymorphism and ACE plasma activities was demonstrated.
    Collegium antropologicum 04/2007; 31(1):179-83. · 0.61 Impact Factor

Publication Stats

149 Citations
115.07 Total Impact Points

Institutions

  • 2004–2014
    • University of Zagreb
      • Department of Medical Chemistry, Biochemistry and Clinical Chemistry
      Zagrabia, Grad Zagreb, Croatia
  • 1999–2012
    • University Hospital Centre Zagreb
      • Department of Laboratory Diagnostics
      Zagrabia, Grad Zagreb, Croatia