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      Etofibrate but not controlled-release niacin decreases LDL cholesterol and lipoprotein (a) in type IIb dyslipidemic subjects

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          Abstract

          Etofibrate is a hybrid drug which combines niacin with clofibrate. After contact with plasma hydrolases, both constituents are gradually released in a controlled-release manner. In this study, we compared the effects of etofibrate and controlled-release niacin on lipid profile and plasma lipoprotein (a) (Lp(a)) levels of patients with triglyceride levels of 200 to 400 mg/dl, total cholesterol above 240 mg/dl and Lp(a) above 40 mg/dl. These patients were randomly assigned to a double-blind 16-week treatment period with etofibrate (500 mg twice daily, N = 14) or niacin (500 mg twice daily, N = 11). In both treatment groups total cholesterol, VLDL cholesterol and triglycerides were equally reduced and high-density lipoprotein cholesterol was increased. Etofibrate, but not niacin, reduced Lp(a) by 26% and low-density lipoprotein (LDL) cholesterol by 23%. The hybrid compound etofibrate produced a more effective reduction in plasma LDL cholesterol and Lp(a) levels than controlled-release niacin in type IIb dyslipidemic subjects.

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          Pronounced lowering of serum levels of lipoprotein Lp(a) in hyperlipidaemic subjects treated with nicotinic acid.

          A Hamsten, Brett L. Carlson, A. Asplund (1989)
          Thirty-one consecutive unselected hyperlipidaemic patients were treated daily with 4 g of nicotinic acid for 6 weeks. The concentrations in serum of lipoprotein Lp(a), and the major lipoprotein classes, were determined before and after the treatment. Nicotinic acid significantly reduced the serum levels of Lp(a) in the whole patient group. Linear regression analysis showed a strong negative relationship between the percentage reduction of Lp(a) and the serum triglyceride level before treatment (r = -0.78), which implied that for patients with a serum triglyceride concentration above 7.5 mmol l-1 there was a rise of Lp(a). The average individual percentage decrease of the concentration of Lp(a) was calculated after the exclusion of four patients who had serum triglyceride levels above 10 mmol l-1. The decrease was 38% with a 95% confidence interval of 28-47%. The absolute decrease of Lp(a) was correlated with the pretreatment levels of Lp(a) (r = 0.91). Within the whole group of patients there was a linear relationship between the percentage decrease of Lp(a) and that of LDL cholesterol (r = 0.88). This latter strong relationship might be due to an inhibition of the synthesis of the protein common to the two lipoproteins, apolipoprotein B.
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            Reduction of Mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by Combined Treatment with Clofibrate and Nicotinic Acid

            GUNNAR ROSENHAMER, Lars Carlson (1988)
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              HMG CoA reductase inhibitors lower LDL cholesterol without reducing Lp(a) levels.

              K Bolzano, Marc J Breslow, M. Weintraub … (1989)
              Lp(a) is a plasma lipoprotein particle consisting of a plasminogenlike protein [apo(a)] disulfide bonded to the apo B moiety of low-density lipoprotein (LDL). Increased plasma levels of Lp(a), either independently or interactively with LDL levels, have been shown to be a risk factor for atherosclerosis. Recently, a new class of lipid-lowering drugs, HMG CoA reductase inhibitors, have been introduced. These drugs act by decreasing liver cholesterol synthesis resulting in up-regulation of LDL receptors, increased clearance of LDL from plasma, and diminution of plasma LDL levels. In this study, we examined the effect of HMG CoA reductase inhibitors on Lp(a) levels in three groups of subjects, five volunteers and two groups of five and 14 patients. In all 24 subjects, mean decreases were observed in total cholesterol (43 +/- 5%), total triglyceride (35 +/- 8%), very low-density lipoprotein (45 +/- 9%), and LDL cholesterol (43 +/- 5%). The mean change in high-density lipoprotein cholesterol was an increase of 7 +/- 8%. Despite the very significant decrease in LDL cholesterol levels (p less than 0.001), Lp(a) levels increased by 33 +/- 12% (p less than 0.005). This was not associated with a measurable change in the chemical composition or size of the Lp(a) particle. This emphatically suggests that Lp(a) particles, despite consisting principally of LDL, are cleared from plasma differently than LDL. The surprising finding of an increase in Lp(a) levels suggests this class of drugs may have a direct effect on Lp(a) synthesis or clearance independent of its effect on LDL receptors.
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                Author and article information

                Journal
                Journal ID (publisher-id): bjmbr
                Title: Brazilian Journal of Medical and Biological Research
                Abbreviated Title: Braz J Med Biol Res
                Publisher: Associação Brasileira de Divulgação Científica (Ribeirão Preto, SP, Brazil )
                ISSN (Print): 0100-879X
                ISSN (Electronic): 1414-431X
                Publication date (Print and electronic): February 2001
                Volume: 34
                Issue: 2
                Pages: 177-182
                Affiliations
                [01] São Paulo SP orgnameUniversidade de São Paulo orgdiv1Faculdade de Medicina orgdiv2Instituto do Coração Brasil
                Article
                Publisher ID: S0100-879X2001000200004 Publisher ID: S0100-879X(01)03400204
                DOI: 10.1590/S0100-879X2001000200004
                PubMed ID: 11175492
                SO-VID: 6e605126-081a-4982-bffd-d62d3e367e55
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date accepted : 17 November 2000
                Date received : 02 February 2000
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 44, Pages: 6
                Product

                SciELO Brazil

                Categories
                Subject: Clinical investigation

                Keywords: etofibrate,lipoprotein (a),triglycerides,cholesterol,niacin
                Data availability:
                Keywords: etofibrate, lipoprotein (a), triglycerides, cholesterol, niacin

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