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Update on the use of fibrates: focus on bezafibrate

Authors Goldenberg I, Benderly M, Goldbourt U

Published 8 February 2008 Volume 2008:4(1) Pages 131—141

DOI https://doi.org/10.2147/VHRM.S1434


Ilan Goldenberg1, Michal Benderly2, Uri Goldbourt2,3

1Heart Institute and 2Neufeld Cardiac Research Institute, Sheba Medical Center Tel Hashomer, Israel; 3Division of Epidemiology and Preventive Medicine, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel

Abstract: Low-density lipoprotein-cholesterol (LDL-C) is a well established coronary heart disease (CHD) risk factor. However, the ability of this metabolic risk factor alone to identify individuals at risk for future CHD events is limited. The raised triglycerides-low high-density lipoprotein-cholesterol (HDL-C) dyslipidemia was shown to be an important cardiovascular risk factor independently of LDL-C levels. Fibric acid derivatives (fibrates) have been used in clinical practice for more than 2 decades as a class of agents known to decrease triglyceride levels while substantially increasing HDL-C levels. Through peroxisome proliferator-activated α-receptors, fibrates have a significant impact on the synthesis of several apolipoproteins and enzymes of lipoprotein metabolism as well as on the expression of several genes involved in fibrinolysis and inflammation. Data from recent primary and secondary prevention clinical trials demonstrate the efficacy of fibrate therapy in patients with the raised triglycerides-low HDL-C dyslipidemia. This review summarizes current data regarding mechanism of action and the metbolic effects of fibrates, as well as results from major clinical trials on the efficacy of this mode of lipid lowering therapy. In addition, recent data from subgroup analyses of the Bezafibrate Infarction Prevention trial, demonstrating several important metabolic and long-term cardiovascular effects of bezafibrate therapy, are detailed.

Keywords: fibrates, high-density lipoprotein-cholsterol, metabolic syndrome, peroxisome proliferator-activated α-receptors, cardiac events

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