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Publications (7)14.35 Total impact

  • Article: Thrombopoietin and Mean Platelet Volume in Patients With Ischemic Stroke.
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    ABSTRACT: Objective: The aim of this study was to evaluate mean platelet volume (MPV), thrombopoietin (TPO), and platelet levels in patients with ischemic stroke and compare this with healthy controls. Methods: We prospectively studied 50 patients with ischemic stroke and compared them with 37 control participants who have evaluated in internal medicine polyclinic and had no history of cerebrovascular events. All patients were within 24 hours after stroke; MPV and TPO were measured on admission. Results: Both TPO and MPV values were significantly higher in patients with stroke (P = .00; P = .001). Conclusion: Increased TPO levels may increase both platelet count and platelet size, resulting in more hemostatic tendency, which may contribute to the progression of ischemic stroke.
    Clinical and Applied Thrombosis/Hemostasis 02/2012; · 1.33 Impact Factor
  • Article: Serum thrombopoietin levels in patients with non-alcoholic fatty liver disease.
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    ABSTRACT: To observe thrombopoietin (TPO) levels in patients with non-alcoholic fatty liver disease (NAFLD). The study was performed between November 2010 and March 2011 at the Department of Internal Medicine, Faculty of Medicine, Fatih University, Ankara, Turkey. A total of 60 consecutive patients with ultrasound proven NAFLD (study group), and 28 healthy volunteers (control study) were included in the study. The patient group was divided into 3 subgroups according to the ultrasonographic images as follows: minimal, intermediate, and marked hepatosteatosis. The TPO levels of the patient subgroups were compared with the healthy controls. All the data were collected prospectively, and recorded in FUHIS data collecting system, which is produced by our data-knowledge team. Quantitative measurements of thrombopoietin level were carried out by using the Human Thrombopoietin Quantikine ELISA Kit (R&D Systems, Minneapolis, Minnesota, USA). Thrombopoietin levels were significantly increased in the patient subgroups compared with the controls. The TPO levels were also higher in the patient subgroup of grade 1-nonalcoholic fatty liver disease (grade 1- NAFLD) compared with the control group. The TPO increased in patients with NAFLD possibly as an acute phase reactant to decreased inflammation. In clinical practice, physicians should be alerted to increased TPO levels in patients.
    Saudi medical journal 01/2012; 33(1):30-3. · 0.52 Impact Factor
  • Article: Some inflammatory cytokine levels, iron metabolism and oxidan stress markers in subjects with nonalcoholic steatohepatitis.
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    ABSTRACT: The relation between nonalcoholic steatohepatitis and iron metabolism is still controversial. Free fatty acids, iron, and other sources of oxidative stress probably result in cell damage, and necroinflammation mediated by various cytokines. Sixty patients were diagnosed with NASH were included in the study, and the patient group was divided into three subgroups. Iron metabolism markers, inflammatory cytokines, including TNF-α, IL-6 and IL-8, MDA and nitric oxide levels were measured. Serum ferritin, inflammatory cytokines, and oxidative stress markers were significantly higher in the patient group. Among three patient groups, divided according to the results of ultrasonic examination, there were significant changes with regard to these parameters. The study results suggest that liver iron and fat accumulation, oxidant stres, and inflammatory cytokines are closely related. Therefore, levels of serum ferritin, MDA, IL-6, TNF-α and IL-8 could represent the indices of activity and progression of NASH.
    Clinical biochemistry 12/2011; 44(17-18):1375-9. · 2.02 Impact Factor
  • Article: Association of serum calcitonin with coronary artery disease in individuals with and without chronic kidney disease.
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    ABSTRACT: Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Recent data implicate disordered bone and mineral metabolism, including changes in serum levels of calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and fetuin A, as novel risk factors for arterial calcification. The potential role of calcitonin, another hormonal regulator of mineral and bone metabolism, has not been studied in detail. We investigated the link between serum calcitonin and the total burden of coronary artery disease (CAD) using the validated Gensini score, in a cross-sectional study of 88 patients with estimated GFR (eGFR) between 46 and 87 ml/min/1.73 m² who underwent coronary angiography. We evaluated the associations between serum calcitonin, minerals (calcium, phosphate), calcium × phosphate product, and other factors that regulate mineral metabolism (intact PTH, 25-OH-vitamin D, FGF-23, and fetuin A) and the severity of CAD. The mean serum calcitonin was 11.5 ± 7.8 pg/ml. In univariate analysis, the Gensini CAD severity score correlated significantly with male gender, eGFR, and serum levels of 25-OH-vitamin D, iPTH, FGF-23, fetuin A, and calcitonin (R = 0.474, P = 0.001 for the latter). In multivariate analysis adjusted for calcium, phosphate, 25-OH-vitamin D, iPTH, FGF 23, fetuin A, and calcitonin, only calcitonin (β = 0.20; P = 0.03), FGF-23, fetuin A, and 25-OH-vitamin D emerged as independent predictors of Gensini score. In the second step, we adjusted for the presence of traditional risk factors, proteinuria, and GFR. After these adjustments, the FGF-23 and fetuin A remained statistically significant predictors of the Gensini score, while calcitonin did not. Our study suggests that, in addition to other well-known components of mineral metabolism, increased calcitonin levels are associated with greater severity of CAD. However, this relation was not independent of traditional and nontraditional cardiovascular risk factors. Longitudinal studies in larger populations including patients with more advanced CKD are needed.
    International Urology and Nephrology 12/2011; 44(4):1169-75. · 1.47 Impact Factor
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    Article: Uric acid and pentraxin-3 levels are independently associated with coronary artery disease risk in patients with stage 2 and 3 kidney disease.
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    ABSTRACT: Cardiovascular disease is prevalent in chronic kidney disease (CKD). Uric acid is increased in subjects with CKD and has been linked with cardiovascular mortality in this population. However, no study has evaluated the relationship of uric acid with angiographically proven coronary artery disease (CAD) in this population. We therefore investigated the link between serum uric acid (SUA) levels and (i) extent of CAD assessed by the Gensini score and (ii) inflammatory parameters, including C-reactive protein (CRP) and pentraxin-3, in patients with mild-to-moderate CKD. In an unselected population of 130 patients with estimated glomerular filtration rate (eGFR) between 90 and 30 ml/min/1.73 m(2), we measured SUA, serum pentraxin-3, CRP, urinary protein-to-creatinine ratio, lipid parameters and the severity of CAD as assessed by coronary angiography and quantified by the Gensini lesion severity score. The mean serum values for SUA, pentraxin-3 and CRP in the entire study population were 5.5 ± 1.5 mg/dl, 6.4 ± 3.4 ng/ml and 3.5 ± 2.6 mg/dl, respectively. The Gensini scores significantly correlated in univariate analysis with gender (R = -0.379, p = 0.02), uric acid (R = 0.42, p = 0.001), pentraxin-3 (R = 0.54, p = 0.001), CRP (R = 0.29, p = 0.006) levels, eGFR (R = -0.33, p = 0.02), proteinuria (R = 0.21, p = 0.01), and presence of hypertension (R = 0.37, p = 0.001), but not with smoking status, diabetes mellitus, and lipid parameters. After adjustments for traditional cardiovascular risk factors, only uric acid (R = 0.21, p = 0.02) and pentraxin-3 (R = 0.28, p = 0.01) remained significant predictors of the Gensini score. SUA and pentraxin-3 levels are independent determinants of severity of CAD in patients with mild-to-moderate CKD. We recommend a clinical trial to determine whether lowering uric acid could prevent progression of CAD in patients with CKD.
    American Journal of Nephrology 03/2011; 33(4):325-31. · 2.54 Impact Factor
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    Article: Fibroblast growth factor 23 and fetuin A are independent predictors for the coronary artery disease extent in mild chronic kidney disease.
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    ABSTRACT: Cardiovascular disease in chronic kidney disease (CKD) is explained in part by traditional cardiovascular risk factors; by uremia-specific factors; and by abnormalities of mineral metabolism, factors involved in its regulation, and in the vascular calcification process. In an unselected population of 177 patients with calculated GFR (eGFR) between 90 and 30 ml/min per 1.73 m(2), the link between the mineral metabolism abnormalities (calcium, phosphorus, calcium-phosphorus product), regulatory factors (parathyroid hormone [PTH], intact PTH [iPTH], vitamin D, fibroblast growth factor 23 [FGF 23], and fetuin A), and the severity of coronary artery disease (CAD) assessed by coronary angiography were evaluated in three subgroups defined by tertiles of Gensini lesion severity score. The mean serum values for FGF 23 in the entire study population was 28.1 ± 17.3 RU/ml and for fetuin A was 473.1 ± 156.2 μg/ml. Patients with eGFR < 60 ml/min per 1.73 m(2) had significantly higher values of FGF 23 compared with patients with eGFR > 60 ml/min per 1.73 m(2). The Gensini score values significantly correlated with gender; arterial hypertension; and HDL cholesterol, eGFR, iPTH, FGF 23, and fetuin A levels. After the adjustments for traditional and uremia-related cardiovascular risk factors, the FGF 23 and fetuin A remained significant predictors of the Gensini score. This study suggests that in a relatively young population with mild-to-moderate alteration of kidney function and with less traditional cardiovascular risk factors, anomalies of the serum FGF 23 and fetuin A levels appear early in the course of disease and are independent major predictors for extent of CAD.
    Clinical Journal of the American Society of Nephrology 10/2010; 5(10):1780-6. · 5.23 Impact Factor
  • Article: Hemostatic alterations in fatty liver disease.
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver failure. Whatever its cause, the liver failure is accompanied by multiple changes in the hemostatic system. The objective of the current report was to study several homeostasis parameters such as protein C, protein S, factor 7, factor 8 levels, platelet counts, prothrombin time and activated partial thromboplastin time, and plasminogen activator inhibitor in patients with fatty liver. A total of 28 consecutive patients with ultrasound proven NAFLD and 33 healthy volunteers were included in the study. Plasma prothrombin time and activated partial thromboplastin time were within normal ranges in both NAFLD and control groups. Plasma factor 7, factor 8, protein S, and protein C levels were decreased in NAFLD patients but the difference was not statistically significant, whereas plasminogen activator inhibitor 1 levels were significantly increased in patients with NAFLD compared to controls. In conclusion, in all types of liver disease, some alterations in hemostatic parameters are awaited. As fatty liver disease is very common in clinical practice, clinicians should be aware of this kind of alterations.
    Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 06/2010; 21(4):325-7. · 1.25 Impact Factor