Scopus İndeksli Yayınlar Koleksiyonu
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Browsing Scopus İndeksli Yayınlar Koleksiyonu by Author "Akdeniz, C.S."
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Article CYP3A4 *1b Gene Polymorphism in Coronary Artery Disease Patients with Obesity Undergoing Statin Treatment(Bentham Science Publishers, 2021) Gezer, E.; Cevik, M.; Akdeniz, C.S.; Canbolat, I.P.; Yurdakul, S.; Sünbül, M.; Çaǧatay, P.Objective: Coronary artery disease (CAD) is one of the leading causes of morbidity and mortality worldwide and statins are frequently prescribed in the treatment of CAD to help lower blood cholesterol levels. Since the main enzyme involved in the metabolism of statins is CYP3A4, we aimed to investigate the effect of CYP3A4 * 1B genotypes on plasma lipid profile in Turkish cardiovascular disease subjects with and without obesity taking statin. Materials and Methods: The study group consisted of 85 cardiovascular disease patients who were prescribed statins and had routine biochemical analysis data. Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) assay was performed for genotyping of CYP3A4 *1B (rs2740574) polymorphism. Results: Genotype distribution of CYP3A4 *1B polymorphism was found for homozygous wild (AA) and homozygous polymorphic (GG) genotypes as 94.1% and 5.9%, respectively. We did not detect patients with heterozygous genotype in our study group. We found that the mean LDL-c, TG and TC levels were higher in patients with CYP3A4 *1B GG compared to the AA genotype. The frequency of CYP3A4 *1B GG genotype frequency (9.5%) was detected higher in the obese patients compared to the non-obese patients (7.7%) (χ2=0.037, p=0.85). Conclusion: Our results demonstrate that CYP3A4 *1B homozygous polymorphic genotype distribution tends to be higher in obese patients compared to non-obese patients with cardiovascular disease which may point to *1B allele having a slight effect on serum lipids during statin therapy. Ad-ditional studies with higher samples are needed for evaluating the role of CYP3A4 *1B on lipids in patients under statin therapy. © 2021 Bentham Science Publishers.Article Prevalence of CYP2C19 Polymorphisms in Clopidogrel Treated Turkish Patients: Preliminary Results, 2017(Bentham Science Publishers, 2021) Süsleyici, B.; Çiftçi, C.; Yurdakul, S.; Cevik, M.; Akdeniz, C.S.; Canbolat, I.P.; Deliorman, G.Background: Clopidogrel is one of the most frequently prescribed antiplatelet agents to reduce the risk of atherosclerotic symptoms. CYP2C19 enzyme is involved in clopidogrel metabolism, and several genetic variations of CYP2C19gene are able to affect the clinical response of clopidogrel. Despite the lack of a fully accepted guideline for CYP2C19 pharmacogenetic testing before clopidogrel treatment by relevant communities, we believe that determination of the variant frequencies is important to predict the efficiency and possible clopidogrel related risks before the initiation of treatment on the basis of populations. Our aim was to determine the distribution of gene polymor-phisms affecting the enzyme activity in Turkish cardiac patients prescribed clopidogrel. Methods: 54 clopidogrel prescribed patients were included in the study. The presence of CYP2C19*2, *3, *4, *5, *6, *7, *8, *9, *10 and *17 polymorphisms were investigated using a microarray platform. Results: No variant allele was detected for *4, *5, *6, *7, *8, *9 and *10 polymorphisms. The geno-type frequencies were detected as 38.89% for *1/*1, 16.67% for *1/*2, 11.11% for *2/*17, 1.85% for *1/*3, 1.85% for *2/*3, 27.78% for *1/*17 and 1.85% for *17/*17. According to genotype analysis, 1.85% of the patients were recorded as poor and 29.63% intermediate; whereas 27.78% as rapid and 1.85% ultra-rapid metabolizers. Conclusion: Although our study population does not consist of a high number of patients, since the high frequency of intermediate, rapid and ultra-rapid metabolizer patients were detected in relatively high frequencies, CYP2C19 polymorphisms should be taken into account for efficiency and possible clopidogrel related risks in Turkish cardiac patients. © 2021 Bentham Science Publishers.

