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Biomedical subjects

Y Erdem

Publications and source records attributed to Y Erdem.

52 records · Page 3Linked to original sources
PubMed1996

Coagulation, fibrinolysis and fibrinolysis inhibitors in haemodialysis patients: contribution of arteriovenous fistula.

BACKGROUND: End-stage renal disease (ESRD) patients, not uncommonly, might exhibit thrombotic complications, as well as they may present with a bleeding diathesis. Changes in vessel wall and/or blood flow in native arteriovenous fistula (AVF) might also augment these disarrangements, as vascular endothelium is predominantly involved in the regulation of haemostatic pathways. OBJECTIVE: This study was designed to evaluate the state of coagulation and fibrinolysis and the role of AVF on haemostatic defects, in ESRD patients on maintenance haemodialysis. METHODS: Plasma samples for prothrombin fragment 1+2, thrombin-antithrombin III complex, plasmin-alpha2 antiplasmin complex, tissue type plasminogen activator antigen, urokinase type plasminogen activator antigen, u-PA activity, plasminogen activity, alpha2-antiplasmin and alpha2-macroglobulin assays were obtained from AVF and contralateral large veins of ESRD patients and from peripheral veins of the control group. RESULTS: Our results indicate a predominant thrombotic state as evidenced by activated coagulation markers and enhanced fibrinolysis in systemic circulation of ESRD patients. However the most novel finding is the probable contribution of AVF on haemostatic activation, as proven by the statistically different and positively correlated concentrations of both coagulation, fibrinolysis, and fibrinolysis inhibitors in AVF when compared to the levels in peripheral venous circulation. CONCLUSION: In addition to systemic derangements of haemostasis in ESRD patients, AVF individually might have a substantial role in the modulation of coagulation and fibrinolytic cascade.

Adult↗
PubMed1995

Increased erythropoietin response to venesection in erythrocytosic renal transplant patients.

Anaemia of end-stage chronic renal failure improves following successful kidney transplantation. However, erythrocytosis occurs in 6.8-17.3% of transplanted patients. Mechanism of post-transplant erythrocytosis (PTE) and its erythropoietin (Epo) dependence are still controversial. Firstly, we compared basal serum Epo levels of 10 PTE patients, 14 non-erythrocytosic renal transplant (non-PTE) patients and 12 healthy blood donors. Then we performed venesection in PTE patients and healthy blood donors and compared their Epo response to venesection 5 hours later. The mean basal serum Epo of 24.3 mU/ml was significantly higher in the PTE group than the 10.8 mU/ml in the non-PTE and 8.6 mU/ml in the healthy blood donor group (p < 0.01). Epo levels in the non-PTE group did not differ significantly from those of healthy blood donors (p > 0.05). Following venesection the mean serum Epo levels increased significantly in both groups, from 24.3 mU/ml to 67.7 mU/ml (p < 0.001) in the PTE group and from 8.6 to 12.1 mU/ml (p < 0.01) in the healthy blood donor group, but the increment in the PTE group was more marked. We conclude that PTE patients have elevated basal serum Epo levels and there is a feedback regulation of Epo secretion in these patients like in healthy blood donors, but in an exaggerated way.

Adult↗
PubMed1995

Effects of ACE inhibition on left ventricular dimensions and haemodynamics in systemic hypertension: a radionuclide and echocardiographic study.

The aim of this study was to assess the effects of Angiotensin Converting Enzyme (ACE) inhibition on cardiac systolic and diastolic parameters and left ventricular muscle mass in hypertensive patients. For this purpose 30 patients (22 female and eight male) with mild to moderate essential hypertension, aged 47 +/- 2 years, were treated with enalapril maleate (MK 421, an ACE inhibitor) for six weeks. They underwent M-mode and Doppler echocardiography and radionuclide ventriculography at the beginning and after six weeks of enalapril treatment. In this study all patients treated with the ACE inhibitor enalapril responded with a significant decrease in mean arterial pressure (p < 0.001). A significant reduction in left ventricle and mass index were shown after six weeks of treatment with enalapril (p < 0.01). Total peripheral resistance and end-systolic stress decreased in the same time course (p < 0.001). Ejection fraction increased in both examinations after six weeks of therapy with enalapril, but this increase was not statistically significant. In radionuclide examinations, time to peak filling rate decreased significantly after six weeks of enalapril therapy (p < 0.02). Despite these improvements in cardiac systolic and diastolic parameters, cardiac output and stroke volume decreased slightly after enalapril treatment. We concluded that enalapril improves diastolic and systolic parameters in LV function but causes slight decreases in cardiac output and stroke volume in addition to lowering blood pressure.

Echocardiography, Doppler↗