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    Öğe
    Depresyon Hastalarında Endotel Fonksiyonları, Ekokardiyografik Parametreler ve Damar Sertliğine Antidepresan Tedavinin Etkisi
    (Kırıkkale Üniversitesi, 2013) Tulmaç, Murat; Özdemir, Hatice; Şahin, Ömer; Poyraz, Fatih; Şimşek, Vedat; Canlı, Derya
    Increasing evidence reveals that depression is emerging as an independent cardiovascular disease (CVD) risk factor. We investigated whether treating depression with seratonin reuptake inhibitors (SSRI) would effect echocardiographic systolic and diastolic functions, in addition endothelial function and arterial stiffnes indexes which are known CVD risk factors Fourtyone patients who were prescribed SSRI therapy for the first time due to major depression without known CVD and between 16-65 years of age were included. At the beginning of the study and after 8 weeks of SSRI therapy patients were underwent echocardiographic analysis of systolic and diastolic parameters, myocardial performance index (MPI) and aortic strain (Ao strain). Also by finger plethysmography with the aid of an auto-analyser pulse wave analysis were done and pulse propagation time (PPT), stiffness index (SI) and reflection index (RI) were measured. Endothelial functions were estimated with flow mediated dilatation method. Nineteen patients (46.3%) came to control visit after 8 weeks of therapy and the final analysis was done with their results. Compared to beginning, 8 weeks of therapy with SSRI resulted in an increase in systolic ejection fraction (%64,83±4,54 vs %66,80±3,3, p=0,020) and fractional shortening (%35,39±3,53 vs %37,11±2,49, p=0,013) and decrease in MPI (0,60±0,21 vs 0,45±0,15, p=0,004). The other parameters including left ventricular diastolic functions, aortic strain, endothelial function and aortic stiffness parameters were not significantly effected. Our results imply that short term therapy with SSRI in patients with newly diagnosed depression might favorably effect the left ventricular systolic functions whereas left ventricular diastolic functions, endothelial functions and aortic stifness parameters remain unchanged.
  • Küçük Resim
    Öğe
    The impact of CYP2C19 polymorphisms on citalopram metabolism in patients with major depressive disorder
    (Wiley, 2015) Uçkun, Zuhal; Başkak, Bora; Özel-Kızıl, Erguvan Tuğba; Özdemir, Hatice; Özgüven, Halise Devrimci; Süzen, Halit Sinan
    What is known and objective: Genetic variations in drug-metabolizing enzyme genes change drug pharmacokinetics and response. CYP2C19 is a clinically important enzyme that metabolizes citalopram (CIT). The objective of this study was to determine CYP2C19 genetic polymorphisms and to evaluate the impact of these polymorphisms on the metabolism of citalopram in a sample of the Turkish population. We also assessed *17 polymorphism in healthy subjects in this population. Methods: The CYP2C19 genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism method (209 healthy individuals and 50 patients for CIT metabolism), and the plasma concentrations of CIT and demethylcitalopram (DCIT) were quantified by high-performance liquid chromatography. Results and discussion: The CYP2C19*1 and *17 allele frequencies for the patient group and the healthy group were 71.0%, 18.0% and 81.1%, 18.9%, respectively. There was no significant difference between the two groups (P > 0 . 05). The mean plasma concentrations and the mean dose-corrected (C/D) plasma levels of DCIT were significantly higher in patients with the CYP2C19*1/*1 genotype compared to patients with CYP2C19*1/*2 and CYP2C19*2/*2 genotypes (P < 0 . 05). Furthermore, the mean metabolic ratio (MR, CIT/DCIT) was also significantly higher in the CYP2C19*1/*2 + CYP2C19*2/*2 genotypes (P < 0 . 05). On the other hand, plasma CIT, DCIT concentrations and M/R value in the CYP2C19*1/*1 genotypes were no different to those of the CYP2C19*1/*17 genotypes (P > 0 . 05). What is new and conclusion: Our data suggest that CYP2C19*17 polymorphism does not have a significant effect on CIT metabolism. In contrast CYP2C19*2 polymorphism has a prominent role and is likely to contribute to interindividual variability in CIT metabolism in vivo at therapeutic doses.