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PubMed1980

[The effect of bezafibrate on biliary lipids (author's transl)].

The effect of bezafibrate (3 x 200 mg/day) on biliary lipids was studied in 12 healthy male subjects and in 13 patients with hyperlipidemias. In normal subjects, the lithogenic index, with bezafibrate and placebo administered in a double blind cross-over design, was 1.1 and 0.77 respectively. The difference was not significant. In patients, who have been treated with bezafibrate for 6 months to 3 years the index was 0.76, and 0.64 six weeks after discontinuation of the drug. This difference, too, was not significant. It appears, therefore, that contrary to findings with clofibrate, bezafibrate may not be associated with an increased risk of cholelithiasis. This question, however, can ultimately be answered with certainty only on the basis of long-time epidemiologic evidence.

Adult↗
PubMed1981

Improvement of hyperlipidaemia by bezafibrate treatment in RDT patients.

The pharmacokinetics and therapeutic effects of bezafibrate were studied in 15 RDT patients in a placebo controlled trial. Serum half life of bezafibrate was prolonged to 17--21.5 hours compared to 1.6--2.1 hours in normals. Adequate dosage in RDT patients was found to be 200mg every 3rd day. Bezafibrate treatment resulted in significant decrease in the serum concentrations of triglycerides, total cholesterol and LDL-cholesterol, whereas HDL-cholesterol serum levels increased. Under this dosage regimen no adverse side effects were observed. Bezafibrate offers the possibility of correcting disturbances of lipid metabolism of RDT patients, possibly involved in the pathogenesis of atherosclerosis of these patients.

Adult↗
PubMed1980

The effect of etofibrate retard, bezafibrate and procetofen.

The effects and side effects of 500 mg of etofibrate retard were comared with those of 100 mg t.i.d. of procetofene and of 200 mg t.i.d. of bezafibrate in two different studies in 60 and 63 outpatients respectively. In types IIa, IIb and IV hyperlipoproteinaemia cholesterol, triglycerides, LDL-cholesterol and HDL-cholesterol were affected markedly stronger by procetofene and bezafibrate than by etofibrate retard. This impact was not only superior in its quantity by also in its proportion of responding patients. Side effects were a flush under etofibrate retard and gastric discomfort, headache and nausea in about 5% under all three drugs. Etofibrate retard did not give significant changes in the laboratory parameters while procetofene and bezafibrate slightly increased transaminases and creatinine. Alcaline phosphatase and GT were significantly lowered. Uric acid decreased under procetofene and increased under bezafibrate.

Aged↗
PubMed1995

Design features of a five-year Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT).

Young survivors of myocardial infarction represent a poignant challenge to clinical research on atherogenic mechanisms and factors predisposing to and precipitating coronary thrombosis. Young male postinfarction patients are characterized by heavy smoking, dyslipoproteinaemias involving very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL), a family history of premature coronary artery disease, hyperinsulinaemic responses to oral and intravenous glucose challenges, an elevated plasma fibrinogen concentration and defective fibrinolytic function. Based on the multiplicity of metabolic and haemostatic disturbances present in these patients, a double-blind, randomized, placebo-controlled angiographic trial was initiated to determine whether bezafibrate, a clofibrate analogue, retards the progression or facilitates regression of premature coronary atherosclerosis. Men under the age of 45 years who survived a first myocardial infarction were screened for participation in the study. A fasting serum cholesterol value > or = 5.2 mmol/l and/or serum triglycerides > or = 1.6 mmol/l after three months of dietary treatment and angiographically demonstrable lesions in at least one coronary segment were required for inclusion. Treatment with diet and bezafibrate (200 mg t.i.d.) or matching placebo is continued for five years during which time re-angiography is performed after two years and at the end of the study. The primary aim of the trial is a comparison between the bezafibrate and placebo groups for change in mean minimum luminal diameter between the baseline and five-year coronary angiograms. This report presents the design features of the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) and a review of current knowledge of mechanisms underlying premature coronary atherosclerosis and myocardial infarction at a young age.

Adult↗
PubMed1994

Effect of bezafibrate on lipids, lipoproteins, apolipoproteins and platelet aggregation in hypertriglyceridemic patients.

Twenty-seven hypertriglyceridemic patients were recruited for an open placebo-controlled, 7-month study of the effect of bezafibrate (CAS 41859-67-0, Bezalip, Cedur) on lipids, lipoproteins, apolipoproteins, and platelet aggregation. Patients received 3 placebo tablets a day for a stabilization period of 2 months, followed by a treatment period of 5 months during which one group received bezafibrate 200 mg 3 times a day, and a control group continued to receive placebo. Values measured at the end of the stabilization period were considered as the baseline values. Bezafibrate therapy significantly reduced triglycerides by 43%, and increased HDL-cholesterol by 22%. Apolipoprotein A-1 increased by 14%, and apolipoprotein A-2 by 42%. There was a small reduction of cholesterol (6%), and of apolipoprotein B (11%). A small increase occurred in LDL-cholesterol (2%), suggesting increased catabolism of high VLDL levels which were converted to LDL-cholesterol. Platelet aggregation was measured by the degree of light transmission through a platelet suspension. The improvement of the lipoprotein profile was associated with significant reduction of platelet aggregation in vitro, stimulated by adenosine diphosphate (ADP) at concentrations of 1.15 mumol/ml and 0.75 mumol/ml, and by collagen 2.0 micrograms/ml. Average decrease of platelet reactivity was 45%, 30% and 42%, respectively. The decrease of light transmission with ADP concentration of 2.3 mumol/ml was not significant, suggesting that the aggregatonic effect of the higher ADP concentration overcame the attenuating effect of bezafibrate. The control groups, displayed no significant changes in the blood constituents and platelet functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMedDate not supplied

Treatment of severe, resistant familial combined hyperlipidemia with a bezafibrate-lovastatin combination.

Familial combined hyperlipidemia (FCHL) is a common lipid disorder characterized by high levels of cholesterol, triglycerides, or both. The basic metabolic abnormality is overproduction of apolipoprotein B-100. High atherogenicity has been attributed to all forms of FCHL. We evaluated combined bezafibrate-lovastatin therapy in 10 patients (9 men and 1 woman) with FCHL and markedly high cholesterol and triglyceride levels who were at high risk of coronary artery disease and who had not responded to diet and bezafibrate treatment alone. Eight patients had coronary artery disease, 6 had hypertension, and 3 had noninsulin-dependent diabetes mellitus. Lovastatin 20 mg/day was added to the bezafibrate 600 mg/day regimen for 6 weeks; the lovastatin dosage was then doubled to 40 mg/day for an additional 6 weeks. The addition of 20 mg of lovastatin resulted in decreases of 15%, 20%, and 13% in total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride levels, respectively. Increasing the dose of lovastatin to 40 mg resulted in further moderate decreases of 4%, 3%, and 8% in total cholesterol, LDL cholesterol, and triglycerides, respectively, compared with the 20 mg/day dosage. Although previous reports have emphasized the potential side effects of combination treatment with lovastatin and fibric acid derivatives, our patients tolerated the regimen well, with no significant subjective complaints or laboratory abnormalities. The bezafibrate-lovastatin combination is a possible therapeutic option for severe, resistant FCHL, but close medical supervision is needed because of potential side effects.

Adult↗
PubMed2004

Prospective randomized crossover trial of combination therapy with bezafibrate and UDCA for primary biliary cirrhosis.

The aim of this study was to evaluate the effects of the combination therapy with bezafibrate and ursodeoxycholic acid (UDCA) for primary biliary cirrhosis (PBC), compared to UDCA monotherapy. Sixteen patients with compensated PBC were divided randomly into two groups. Group A received treatment with bezafibrate and UDCA for 6 months, while group B received UDCA alone, treatment protocols were then exchanged for another 6 months. The laboratory data was followed every month. The mean levels of alkaline phosphatase (ALP) decreased significantly more in group A than in group B in the first half of the study. Then serum ALP levels were elevated in group A after exchanged the therapy, but fell down in group B. Serum levels of gamma-glutamyl transferase (GGT), immunoglobulin M and triglycerides values were significantly lower in group B than in group A, after changing therapies from monotherapy to combination therapy with bezafibrate and UDCA. The mean levels of ALP, GGT and triglycerides were significantly lower at the end of the combination therapy than those at the end of the monotherapy. The combination therapy with bezafibrate and UDCA significantly improves the laboratory data that specific for PBC in comparison with UDCA monotherapy.

Journal Article↗
PubMed1978

[Lipid-lowering effect of bezafibrate in patients with diabetes mellitus and hyperlipidaemia (author's transl)].

600 mg of bezafibrate daily were administered to 13 well controlled diabetics with hyperlipidaemia for 12 weeks. Placebo was given before and after the treatment period. Compared with pretreatment placebo, bezafibrate reduced triglycerides (between 37 and 47%) and cholesterol (between 12 and 19%) significantly. Blood glucose levels during treatment were significantly lower at 8 and 12 weeks compared with post-treatment placebo values. Urinary glucose excretion did not change. Hypoglycaemia was not observed. No change in antidiabetic medication was necessary. Bezafibrate was well tolerated. It lowered blood lipids effectively in diabetics with hyperlipidaemia. No additional precautions have to be taken to control carbohydrate metabolism during bezafibrate treatment.

Blood Glucose↗
PubMed2003

Effects of bezafibrate and simvastatin on endothelial activation and lipid peroxidation in hypercholesterolemia: evidence of different vascular protection by different lipid-lowering treatments.

Hypercholesterolemia is combined with enhanced lipid peroxidation, which can promote atherogenesis by inducing endothelial adhesion molecule expression. Statins may protect vascular endothelium in hypercholesterolemia by reducing enhanced plasma levels of low-density lipoprotein and decreasing oxidative stress. Herein, we describe increased circulating levels of soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin and total 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)) concentrations, as indexes of endothelial activation and lipid peroxidation, respectively, in 67 hypercholesterolemic patients compared with 32 normocholesterolemic subjects. Significant cholesterol reductions were achieved in hypercholesterolemic patients after 6 months under either simvastatin (40 mg/d) or bezafibrate (800 mg/d) treatment, given according to a randomized double-blind trial. Simvastatin but not bezafibrate simultaneously reduced soluble adhesin and total 8-iso-PGF(2 alpha) concentrations also. Vitamin E supplementation (400 IU/d) further reduced indexes of endothelial activation and lipid peroxidation in simvastatin-treated patients and significantly reduced the above indexes in bezafibrate-treated patients. Changes in circulating soluble adhesion molecule levels were directly correlated with changes in total 8-iso-PGF(2 alpha) concentrations in simvastatin-treated patients also receiving vitamin E supplementation. All together, our data demonstrated that hypercholesterolemia was combined with endothelial activation and lipid peroxidation, which were efficaciously counteracted by simvastatin but not bezafibrate treatment. Thus, a different vascular protection can be achieved by different lipid-lowering treatments.

Adult↗
PubMed2002

Bioavailability study of tablet Bezafibrate 200 mg (Lipocor).

In order to determine the ultimate quality of any formulated dosage form and rationalize the therapeutic plan as well as to individualize the prescription, in vivo measurement of drug is the modem and specialized expertise of the clinical/research area of pharmacy practice, which provides effectiveness and assures the safety of drugs. All pharmacological, therapeutic or toxic responses are subject to reaching of drug at the site of action through connective tissue. Other than physico chemical properties of drug, there are numerous factors from manufacturing process to biochemical behaviour of the individual which resist in the absorption, distribution, metabolism and elimination of drugs in the biological system. Bezafibrate Tablet 200 mg (Lipocor) an oral conventional formulation manufactured by Efroze Chemical Industries (Pvt.) Ltd. was investigated for bioavailability followed by pharmacokinetic studies on adult, male, healthy, human local population. For this purpose, a sensitive, specific and validated method was used for the estimation of bezafibrate in blood. HPLC was performed on a reversed phase C18 column (flow rate 1.5 ml/min, UV = 230 nm) with 0.02 M buffer of KH2PO4 (Adjusted pH 3.5 with Phosphoric Acid) and Methanol (40: 60) whereas extraction of the drug from the plasma was carried out by deproteinization of plasma according to classical method described in previous studies (Obaid A. et al., 1999). Peak level (Tmax) of Bezafibrate Tablet 200 mg (Lipocor) was observed at about 1.42 +/- 0.53 hours after the dose and practically free Bezafibrate Tablet 200 mg (Lipocor) could be detected in blood after 9 hours. Cmax of the investigated formulation of Lipocor register mark or target was 1732 +/- 374.2 ng/ml. Area under curve (AUC) was 5198.65 +/- 1231.8 ng. hr/ml.

Journal Article↗
PubMed1999

Uncoupling protein-3 mRNA levels are increased in white adipose tissue and skeletal muscle of bezafibrate-treated rats.

Fibrates are hypolipidemic drugs that are also able to improve glucose tolerance in animals and diabetic patients through an unknown mechanism. Since uncoupling proteins (UCP) seem to play an important role in the pathogenesis of non-insulin-dependent diabetes mellitus (NIDDM), we examined whether treatment of rats with bezafibrate for 3, 7, or 15 days modified UCP mRNA levels. Using RT-PCR, we observed a weak ectopic expression of UCP-1 and a 2-fold increase in UCP-3 mRNA levels in white adipose tissue after 7 and 15 days of treatment. Moreover, bezafibrate administration caused a 1. 7-fold induction in UCP-3 mRNA levels in skeletal muscle on day 7. Since UCP-3 mRNA levels are reduced in skeletal muscle of diabetic patients, this effect may be involved in the improvement of insulin sensitivity caused by bezafibrate in NIDDM.

Adipose Tissue↗
PubMed1990

Reduction of BM 15.766-induced 7-dehydrocholesterol accumulation by bezafibrate and mevinolin in rats. A non-isotopic in vivo test system for compounds reducing cholesterol synthesis.

The effects of mevinolin, a 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor and bezafibrate, a modulator of lipoprotein metabolism, were measured on BM 15.766-induced 7-dehydrocholesterol (7-DHC) accumulation in liver and serum of rats. BM 15.766, an inhibitor of delta 7 sterol reductase, leads to an accumulation of 7-DHC, which can be used as a measure of cholesterol (CH) synthesis de novo. The investigations were carried out to evaluate the usefulness of this new non-isotopic in vivo method for testing compounds that affect directly and indirectly the CH-biosynthetic pathway. Mevinolin showed a dose-dependent reduction of BM 15.766-induced 7-DHC accumulation after a single oral dose. The dose range for reduction of 7-DHC in the liver of rats was comparable with that for serum CH-lowering in humans. Bezafibrate reduced the BM 15.766-induced 7-DHC accumulation in liver in a dose- and time-dependent manner. These findings agree with the reported reduced activity of HMG-CoA reductase and support the view, that bezafibrate reduces CH biosynthesis by modulation of lipoprotein metabolism. The 7-DHC levels in serum do not reflect those in the liver and cannot be used as a measure of CH biosynthesis. The investigations show that BM 15.766-induced 7-DHC accumulation in liver of rats is an appropriate measure for CH de novo synthesis and can be used for testing compounds that interfere directly and indirectly with the CH-biosynthetic pathway. In contrast to previously described methods, no radiolabelled precursors are necessary.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Effects of clofibric acid and bezafibrate administration on activities of alkaline phosphatase and other enzymes in livers of rats.

Administration of clofibric acid and bezafibrate to rats lowers plasma lipids, increases the liver weight, and causes a slight decrease in the activity of alkaline phosphatase in plasma. However, both these drugs increase the activity of alkaline phosphatase in liver over threefold. The activity of other enzymes did not change by the same magnitude. The increase in the alkaline phosphatase activity in liver tissue appears to be due to increase in the activity of this enzyme in parenchymal cells. Clofibric acid and bezafibrate increase the activity of bilirubin-glucuronyl transferase activity over twofold in liver microsomes. It is thus evident that both these drugs cause similar changes in various enzyme activities in liver even though bezafibrate has been reported to have a much shorter biologic halflife than clofibric acid.

Alkaline Phosphatase↗
PubMed1992

Differences in the response of Sprague-Dawley and Lewis rats to bezafibrate: the hypolipidemic effect and the induction of peroxisomal enzymes.

The effects of bezafibrate administered at 10 and 50 mg/kg/day for 7 days to male Sprague-Dawley (SD) and Lewis rats were investigated in order to determine the interrelation between the changes in serum and hepatic lipid contents and activities of selected peroxisomal, microsomal and mitochondrial enzymes in the two rat strains. In both strains, bezafibrate effectively reduced serum and hepatic lipids, increased the liver weight, induced a proliferation of peroxisomes, and selectively elevated the activities of carnitine acetyltransferase and of the enzymes of the peroxisomal beta-oxidation system. Moreover, immunoblotting revealed that the drug specifically enhanced the concentration of only those peroxisomal enzymes involved in fatty acid beta-oxidation. The data obtained demonstrate that although the responses initiated by bezafibrate are qualitatively similar in both strains, they differ in their magnitude in a dose-dependent manner, with the Lewis strain exhibiting a more pronounced response than the SD rats. These results show that dose-dependent strain differences as well as the generally known species differences should be taken into account in pharmacological and toxicological evaluations of fibrates in rodents. Furthermore, generalization and extrapolation from rodent studies should be treated with great caution.

Animals↗
PubMed1994

Treatment of primary hypercholesterolemia: fluvastatin versus bezafibrate.

The effects of fluvastatin and bezafibrate on lipids, lipoproteins, and apoproteins (apo) were investigated in a multicenter randomized, double-blind, parallel-group study. After 8 weeks of strictly controlled (computer-based assessment) dietary stabilization, patients with primary hypercholesterolemia (low-density lipoprotein cholesterol [LDL-C] > or = 160 mg/dL; triglycerides < or = 300 mg/dL) were enrolled into a 6-week placebo phase. Altogether, 131 patients were randomized to receive either fluvastatin at 40 mg once daily (n = 64; mean age 53 years) or bezafibrate at 400 mg once daily (n = 67; mean age 52 years) for 12 weeks. Compliance with the diet was monitored (3-day food records) after 6 and 12 weeks. Fluvastatin led to significant reductions in LDL-C (-23%), total cholesterol (-17%), LDL-C/high-density lipoprotein cholesterol (HDL-C) (-24%) and apo B (-19%). Fluvastatin significantly increased LpA-I (+8%) and apo E (+20%). Bezafibrate produced significant reductions in LDL-C (-17%), total cholesterol (-13%), LDL-C/HDL-C (-24%), triglycerides (-28%), apo B (-15%), and LpA-I (-10%) and significantly increased HDL-C (+12%), apo A-I (+9%), apo A-II (+30%), apo E (+14%), and Lp(a) (+3%). No clinically notable increases in levels of liver enzymes or creatine phosphokinase were observed with either treatment. Both treatments were well tolerated. There was a low incidence of adverse events that tended to be mild and included headache, muscular pain, angina, and dyspepsia. The frequency of adverse events was similar in both treatment groups, and no significant differences in dietary behavior were observed. In conclusion, fluvastatin is a well tolerated 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment of primary hypercholesterolemia. Effects of fluvastatin on LpA-I occur irrespective of changes in HDL-C.

Adult↗
PubMed1984

Analysis of the effect of bezafibrate on the oxygen dissociation curve of human hemoglobin.

Analysis of the effects of a range of concentrations of the antihyperlipoproteinemia drug, bezafibrate, on the oxygen dissociation curve of dilute hemoglobin solutions indicates a 4:1 binding stoichiometry with a site binding constant of 434 mol-1 for deoxyhemoglobin. Analysis of the combined effects of a range of bezafibrate and 2,3-diphosphoglycerate (DPG) concentrations indicates that 2 of the 4 bezafibrate sites are in the vicinity of the DPG binding site, and competitive with DPG binding, and 2 of the sites are remote from the DPG binding site.

2,3-Diphosphoglycerate↗
PubMed1981

Reduced LDL- and increased HDL-apoproteins in patients with hypercholesterolaemia under treatment with bezafibrate.

The effect of bezafibrate on serum lipids, lipoproteins and the apoproteins A-I, A-II and B was studied in 18 patients with primary hypercholesterolaemia. Total cholesterol was lowered by 20% (P less than 0.05), LDL-cholesterol by 24% (P less than 0.05), and apo B by 14% (P less than 0.05), which is comparable to the effect obtained with anion exchange resins but with far fewer side-effects. HDL increased significantly during bezafibrate treatment both by measurement of HDL-cholesterol (+54%, P less than 0.05) and by the determination of HDL-apoproteins A-I (+ 19%, P less than 0.05) and A-II (+ 23%, P less than 0.05). This increase of HDL and the decrease of triglycerides was maintained for 6 weeks of placebo treatment after cessation of bezafibrate, while serum total and LDL cholesterol as well as apo B returned to their baseline levels.

Adult↗
PubMed1982

Effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B and LCAT activity in hyperlipidemic, non-insulin-dependent diabetics.

The effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B, and LCAT activity was investigated in 16 hyperlipidemic, non-insulin-dependent diabetes, who were treated for 8 weeks with either placebo or bezafibrate in a double-blind cross-over design. Bezafibrate induced a significant decrease in plasma triglycerides (P less than 0.01), cholesterol (P less than 0.05), VLDL triglycerides (P less than 0.05) and VLDL cholesterol (P less than 0.01), and a significant increase in HDL cholesterol (P less than 0.01), whereas LDL cholesterol remained unchanged. The apolipoprotein AI/apolipoprotein B ratio increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.0001) and the apolipoprotein AI/apolipoprotein AII ratio decreased (P less than 0.0001), indicating an increase in the HDL3 rather than the HDL2 fraction. No significant change in LCAT activity was observed.

Aged↗