Abstract
Cholesterol ester transfer protein (CETP) is principally associated with HDL in plasma and it plays the role of a key modulator not only of the intravascular metabolism of HDL and apoA-I but also triglyceride(TG)-rich lipoproteins and low-density lipoprotein, it mediates the transfer of cholesteryl esters from HDL to proatherogenic apoB-lipoproteins, with heterotransfer of TG mainly from VLDL to HDL. The studies were performed in 42 post-renal transplant patients (Tx) (women, n=20 and men, n=22) at the age between 21–60 years. The post-renal transplant patients received cyclosporine A + prednisone (n=28), tacrolimus + prednisone (n=11) and sirolimus + prednisone (n=3). Hypertensive patients with hypercholesterolemia and hypertriglyceridemia treated with fibrate and athorvastatin or simvastatin used anti-hypertensive medications. Forty five healthy patients were the reference group (22 women and 23 men, aged 22 to 60 years). Tx patients were divided into 2 groups: triglyceride (TG)>150mg/dl and TG<150 mg/dl using TG concentration of 150mg/dl as a cut-point. The aim of this study was to investigate serum lipid and lipoprotein profiles and lipid and lipoprotein ratios, CETP levels and BMI index in post-renal transplant patients with TG>150mg/dl and TG<150mg/dl. Tx patients with TG>150 mg/dl had TG, TC, nonHDL-C, and lipid ratios (TC/HDL-C, TG/HDL-C) significantly higher but lipoprotein ratios (apoAI/apoB, HDL-C/apoAI) were significantly lower as a comparison to patients with TG<150mg/dl. However, lipids (TG, TC, LDL-C, nonHDL-C, HDL-C) and lipid ratios (TC/HDL-C, LDL-C/HDL-C, TG/HDL-C) and lipoproteins (apoAI, apoB) and lipoprotein ratios (apoAI/apoB, HDL-C/apoAI) in both groups were significantly disturbed as compared to healthy subjects. Moreover, both studied groups of Tx patients had no change in CETP levels and were non-statistically different as compared to the reference group. We conclude that Tx patients with hypertriglyceridemia received statins and immunosuppressive therapy tend to exclude dysregulation of CETP in the pathogenesis of dyslipidemia but future studies are required.
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