SEARCH · Search PubMed

Results for “Bezafibrate”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources

PubMed1991

Bezafibrate fails to directly modulate HMG-CoA reductase or LDL catabolism in human mononuclear cells.

The effect of bezafibrate on HMG-CoA reductase, the key enzyme of cholesterol synthesis, and LDL metabolism was studied in human mononuclear cells. Bezafibrate at concentrations achieved during administration in patients did not suppress preformed reductase in mononuclear cells. Similarly, the drug was ineffective in regulating reductase when added to the medium of cultured cells. Also, the fibrate did not modulate the enzyme suppression mediated by LDL. At very high concentrations bezafibrate enhanced LDL binding, but both total cell association and degradation were unchanged. Thus, the previously observed decrease of HMG-CoA reductase activity in mononuclear cells of patients treated with fibrates is likely to be indirect and probably due to changes in LDL structure.

Bezafibrate↗

PubMed1990

The effect of a slow release formulation of bezafibrate on lipids, glucose homeostasis, platelets and fibrinogen in type II diabetics: a pilot study.

A double-blind placebo-controlled prospective trial assessed the effect of a slow release formulation of bezafibrate (Bezalip Mono) on lipids, glucose homeostasis, platelet function and plasma fibrinogen in non-insulin dependent (type II) diabetics. Twenty-four patients completed the trial. There was a significant improvement in the cholesterol and triglyceride levels and in the fasting blood glucose and glycated haemoglobin levels of those who received the active preparation but not in those who received placebo. Treatment, but not placebo, also resulted in a significant fall in plasma fibrinogen concentration and a trend towards inhibition of platelet aggregation. Bezafibrate was well tolerated and only one patient withdrew from the trial possibly because of side-effects of the drug. A larger study is needed to establish whether bezafibrate can reduce non-lipid risk factors (e.g., plasma fibrinogen concentration; glucose intolerance--hyperinsulinaemia) in normo- and hyperlipidaemic patients.

Adenosine Diphosphate↗

PubMed1989

[Acute severe myositis due to bezafibrate treatment].

The second generation fibric acid derivative, bezafibrate (Bezalip, Norlip) is widely used as a hypolipemic agent throughout Europe and Israel. Its side-effects are well documented, and include myositis, which is considered very rare. We report a 55-year-old diabetic woman with hypertension who had mild renal dysfunction (creatinine 2.0 mg/dl) who received 400 mg/d bezafibrate because of combined (Type IIb) hyperlipoproteinemia. She developed acute myositis, with extreme muscle weakness, pain and CPK levels of up to 3500 units. On discontinuation of the drug all clinical and biochemical features ceased and complete cure followed. No other symptoms have appeared during 2 years of followup. The few reports of such cases in the German literature point to a greater prevalence of myositis in those with renal dysfunction. Early diagnosis of bezafibrate-induced myositis is crucial, a discontinuation of the drug results in cure.

Acute Disease↗

PubMed1989

Effects of treatment with clofibrate, bezafibrate, and ciprofibrate on the metabolism of cholesterol in rat liver microsomes.

The effects of treatment of rats with clofibrate, bezafibrate, and ciprofibrate on the hepatic metabolism of cholesterol were studied in rat liver microsomes. HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase activity, regulating cholesterol biosynthesis, was unaffected by clofibrate and ciprofibrate and slightly decreased (20%) by bezafibrate. Also cholesterol 7 alpha-hydroxylase activity, governing bile acid biosynthesis, was unaffected by clofibrate and was reduced by 25-30% in the two other groups of rats. A major new finding was that all three fibric acid derivatives reduced ACAT (acyl-coenzyme A:cholesterol acyltransferase) activity, catalyzing the esterification of cholesterol, by 50-70%. The hepatic content of free and esterified cholesterol was determined in the bezafibrate-treated rats. The concentration of microsomal cholesteryl ester was about 60% lower in the treated rats compared to the controls whereas the concentration of total cholesterol was unchanged.

Animals↗

PubMed1988

Selective induction of peroxisomal enzymes by the hypolipidemic drug bezafibrate. Detection of modulations by automatic image analysis in conjunction with immunoelectron microscopy and immunoblotting.

Quantitative immunoelectron microscopy in conjunction with quantitative analysis of immunoblots have been used to study the effects of bezafibrate (BF), a peroxisome-proliferating hypolipidemic drug, upon six different enzyme proteins in rat liver peroxisomes (Po). Antibodies against following peroxisomal enzymes: catalase, urate oxidase, alpha-hydroxy acid oxidase, acyl-CoA oxidase, bifunctional enzyme (hydratase-dehydrogenase) and thiolase, were raised in rabbits, and their monospecificities were confirmed by immunoblotting. Female Sprague-Dawley rats were treated for 7 days with 250 mg/kg/day bezafibrate and liver sections were incubated with the appropriate antibodies followed by the protein A-gold complex. The labeling density for each enzyme was estimated by automatic image analysis. In parallel experiments immunoblots prepared from highly purified peroxisome fractions of normal and BF-treated rats were incubated with the same antibodies. The antigens were visualized by an improved protein A-gold method including an anti-protein A step and silver amplification. The immunoblots were also quantitated by an image analyzer. The results revealed a selective induction of beta-oxidation enzymes by bezafibrate with thiolase showing the most increase followed by bifunctional protein and acyl-CoA oxidase. The labeling density for catalase and alpha-hydroxy acid oxidase was reduced, confirming fully the quantitative analysis of immunoblots which in addition revealed reduction of uricase. These observations demonstrate that hypolipidemic drugs induce selectively the beta-oxidation enzymes while other peroxisomal enzymes are reduced. The quantitative immunoelectron microscopy with automatic image analysis provides a versatile, highly sensitive and efficient method for rapid detection of modulations of individual proteins in peroxisomes.

Acetyl-CoA C-Acetyltransferase↗

PubMed1988

Blood rheology changes during bezafibrate treatment.

To evaluate the effect of bezafibrate on the haemorheological pattern, 30 atherosclerotic non-diabetic patients were enlisted in a double-blind, comparative, parallel group trial with bezafibrate (600 mg daily) or placebo being randomly assigned. The 45-day treatment period was preceded by a three week pharmacological wash-out. Haemorheological parameters such as whole-blood, plasma and serum viscosity, haematocrit, fibrinogen, fibrinogen/albumin ratio and erythrocyte filterability were evaluated before and at the end of treatment. The results showed no change in haemorheological determinants in the placebo-treated group but a significant reduction in whole-blood viscosity, in haematocrit, in fibrinogen and fibrinogen/albumin ratio was observed in the bezafibrate treated patients. No variation was present in the plasma and serum viscosity and in the erythrocyte filterability.

Aged↗

PubMed1986

Effects of bezafibrate on apolipoprotein B metabolism in type III hyperlipoproteinemic subjects.

This study was designed to investigate the response of Type III hyperlipoproteinemic subjects to bezafibrate therapy. The metabolism of apolipoprotein B was examined in four lipoprotein subclasses of Sf 60-400 (large very low density lipoprotein (VLDL)), Sf 20-60 (small VLDL), Sf 12-20 (intermediate density lipoprotein (IDL)), and Sf 0-12 (low density lipoprotein (LDL)) before and during bezafibrate therapy. Treatment reduced the plasma concentration of VLDL and raised high density lipoprotein (HDL) cholesterol. There was no net change in LDL cholesterol or its associated apolipoprotein B. The decrease in plasma VLDL derived mainly from an inhibition of synthesis of both large and small subfractions which reduced the number of particles in the circulation without normalizing their lipid composition. Catabolism of the larger VLDL also increased, presumably as a result of lipoprotein lipase activation. Although the plasma concentration of LDL was unchanged, both its synthesis and catabolism were perturbed. Its fractional catabolic rate fell by 50%, but the impact that this would have had on its steady state level in the circulation was apparently blunted by a decrease in its synthesis from Sf 12-20 IDL. In the control phase of the study, most IDL apolipoprotein B was converted to LDL. Bezafibrate therapy channelled this material towards direct catabolism.

Adult↗

PubMed1985

[Effective long-term treatment of primary hyperlipoproteinemias with bezafibrate].

Bezafibrate, a new hypolipidemic agent, was evaluated in a single blind, placebo-controlled study lasting 14 months to 3 years in 40 patients with primary hyperlipoproteinemia of various types (23 patients with type II, 15 with type IV and 2 with type V). Bezafibrate in a dose of 200 mg 3 times daily reduced total serum cholesterol by an average of 17% (p less than 0.001) in hyperlipoproteinemia type II and by 24% (p less than 0.001) in type IV or V, lowered serum triglycerides by 31% (p less than 0.001) in hyperlipoproteinemia type II and by 58% (p less than 0.001) in type IV or V, while high-density-lipoprotein-cholesterol was increased by 17% (p less than 0.001) in type II and by 36% (p less than 0.001) in type IV or V. The few side effects encountered were only mild and transient. These findings show that bezafibrate affords safe and effective long-term treatment of patients with hyperlipoproteinemia.

Adult↗

PubMed1984

[The somatostatin infusion test for the evaluation of glucose utilization in bezafibrate medication].

The utilisation of blood glucose may be used for definition of insulin resistance in type II diabetes mellitus. To evaluate this possibility we adapted an infusion test of somatostatin in 10 normal persons (age 26 +/- 3 years, relative body weight 26 +/- 10% according to Broca) in a randomized cross-over therapy with bezafibrate (3 X 200 mg/die). As the coefficient of variation (VC) of measured blood glucose continuously increased the best time of a steady state was between 90 and 130 min after beginning the infusion (mean VC 8.9%). While insulin remained nearly constant (41 (45; 38) microU/ml) blood glucose dropped by about 14% and reached a steady state of 89 (134; 45) mg/dl. During the therapy of bezafibrate blood glucose was significantly decreased by 36% 130 min after beginning the infusion. Although the effect was not significant during the whole time of the steady state it became evident by a negative correlation with lactate (r = -0.687) and pyruvate (r = -0.843). A correlation with a concomitant decrease of triglyceride and cholesterol also induced by bezafibrate could not be proven. The results show that the infusion test of somatostatin is fitted to measure a steady state of blood glucose and insulin and that it is possible by this technique to quantify a changed utilisation of blood glucose induced by specific therapy.

Adult↗

PubMed1983

Changes in the concentration and composition of lipids and lipoproteins in primary hyperlipoproteinemia during treatment with bezafibrate.

The effect of 2-(4-chlorobenzoyl-aminoethyl-phenoxy)-2-methylpropionic acid (bezafibrate, Cedur) at doses of 3 x 150 mg and 4 x 150 mg daily on lipids and lipoproteins in 27 patients (3 type IIa, 7 type IIb, 1 type III, 12 type IV and 4 type V) was investigated over a period of 24 weeks in a single-blind study. The lower dose was administered for the first 12 weeks and then the higher dose was given. Plasma triglycerides were reduced in all types. This was mainly caused by a massive reduction in VLDL triglycerides. Plasma cholesterol decreased in the types IIa, IIb, III as a result of the reduction of the LDL cholesterol. In type IV, the plasma cholesterol concentration remained unchanged because of a significant rise in the LDL cholesterol (+14%). The HDL cholesterol rose in all types, statistically significantly in the type IV. Phospholipids and protein behaved in an analogous fashion. In comparison with a control group, the lipoprotein fractions VLDL, LDL and HDL retained their abnormal composition in the types IIa, IIb and IV even when the lipid concentrations were massively lowered by bezafibrate. The drug treatment only led to a reduction of circulating lipoproteins in the blood, but didn't contribute to a normalisation of the lipoprotein composition. In the type V, a shift in the direction of type IV was observed. Bezafibrate proved to be well tolerated.

Aged↗

PubMed1980

[The therapeutic efficacy of bezafibrate in hyperlipoproteinemias of various types].

17 patients with hyperlipoproteinemia of type 11 (9 type IIa and 8 type IIb), 4 with hyperlipoproteinemia of type IV and 1 with hyperlipoproteinemia of type V were treated for 4.6 +/- 0.7 months with the new lipid lowering agent bezafibrate in a dose of 200 mg three times daily. Bezafibrate markedly lowered total serum cholesterol and triglycerides and increased HDL-cholesterol in each of these types of hyperlipoproteinemia. These data suggest that bezafibrate may be effective in reducing the possibly atherogenic LDL- and VLDL-fractions while increasing the antiatherogenic HDL-fraction.

Bezafibrate↗

PubMedDate not supplied

[The inhibition of bile acid synthesis in cultured rabbit hepatocytes by bezafibrate].

Primary culture of rabbit hepatocytes was used for study the influence of hypolipidemic drug bezafibrate on bile acid production. Bezafibrate inhibits bile acid synthesis from endogenous and exogenous (lipoprotein) cholesterol at concentration range 1-10 micrograms/ml. Such inhibitory action of bezafibrate on bile acid synthesis should be kept in mind while applying hypolipidemic treatment.

Animals↗

PubMed1996

Photodegradation of bezafibrate in aqueous media. Studies of its in vitro phototoxicity.

Aqueous solutions of the antihyperlipoproteinemic drug bezafibrate (CAS 41859-67-0) are photolabile towards UV-B light under aerobic conditions. Two compounds were isolated and identified spectroscopically as well as by alternative synthesis as the only photoproducts formed. Their formation involves primary cleavage of the aryloxy-carbon bond and decarboxylation followed by hydrogen abstraction or dimerization. Bezafibrate is phototoxic in vitro as indicated by the photohemolysis test. Furthermore bezafibrate photo-sensitizes peroxidation of linoleic acid as monitored by the UV detection of dienic hydroperoxides. Partial inhibition of these processes on addition of butylated hydroxyanisole (BHA), reduced glutathione (GSH), sodium azide (NaN3) or 1,4-diazabicyclo [2.2.2] octane (DABCO) suggests the involvement of type I as well as type II mechanisms.

Aerobiosis↗

PubMed1995

Effect of bezafibrate on HDL with APO A-I and APO A-II and on HDL with APO A-I without APO A-II in hyperlipidaemic patients.

On the basis of apoprotein composition, high-density lipoprotein (HDL) particles may be subdivided into two main subpopulations defined by the presence in the lipoprotein molecule of apo A-I (Lp A-I) and of both apo A-I and apo A-II (Lp A-I:A-II). The effect of slow-release bezafibrate 400 mg a day on Lp A-I and Lp A-I: A-II was evaluated in 34 hyperlipidaemic patients (19 with hypercholesterolaemia and 15 with hypertriglyceridaemia). Seventeen patients on low-fat low-cholesterol diet only were taken as the reference group. In the reference group, no change in HDL-C, apo A-I, apo A-II, Lp A-I and Lp A-I:A-II occurred during the 3 months of observation. In patients on bezafibrate, HDL-C, apo A-I and apo A-II significantly increased. Lp A-I:A-II increased by 33% in hypercholesterolaemic and by 29% in hypertriglyceridaemic patients. Lp A-I decreased by 15% in hypercholesterolaemic patients and did not change significantly in hypertriglyceridaemic patients. This differential effect of bezafibrate on apo-A-defined HDL subpopulations in hypertriglyceridaemia and in hypercholesterolaemia is in accord with previous studies on the effect of the drug on HDL subfractions defined by their density.

Apolipoprotein A-I↗

PubMed1996

Effect of fluvastatin or bezafibrate on the distribution of high density lipoprotein subpopulations in patients with familial hypercholesterolemia.

In eight patients with familial hypercholesterolemia the effects of two lipid reducing drugs on subpopulations of high density lipoproteins (HDL) were examined. After a 14-week period of diet and diet/placebo a 12-week therapy followed with either bezafibrate (CAS 41859-67-0) or fluvastatin (CAS 93957-55-2). Throughout both treatments a significant decrease of total and low density lipoprotein (LDL)-cholesterol, apolipoprotein B and triglycerides during both therapies were noted as well as an insignificant increase of HDL-cholesterol during bezafibrate. The nondenaturating gradient gel electrophoresis is a valid method for the investigation of the behaviour of HDL and was therefore chosen for this investigation. The individual HDL pattern and HDL diameters did not change in these subjects. The effect on the amounts of HDL 3b and HDL 3c was significantly more extensive during fluvastatin (+2.4% resp. + 2.9%) as compared to during bezafibrate therapy (+1.7% resp. + 2.9%). The changes noted in the HDL subclasses are probably due to a variable lipoprotein metabolism, for example increased activity of lipoprotein lipase, hepatic triglyceride lipase, lecithin-cholesterol acyltransferase and cholesterol ester transfer protein.

Adult↗

PubMed1997

Comparative effects of bezafibrate and micronised fenofibrate in patients with type III hyperlipoproteinemia.

Type III hyperlipoproteinemia (HLP) is characterized by elevated concentrations of plasma cholesterol and triglycerides due to an increase in atherogenic beta-very low density lipoproteins (beta-VLDL). As a consequence, affected individuals develop premature and accelerated atherosclerosis. Fibrates have been shown to be most effective in treatment of the dyslipidemia in type III HLP. However, comparative data on the efficacy of different fibrates in this disorder are very limited; to assess this further we have compared in a prospective study the hypolipidemic effects of bezafibrate (400 mg once daily) and micronised fenofibrate (200 mg once daily) in 23 patients with well-characterized type III HLP. Baseline values were obtained after 4 weeks on diet and treatment values were obtained after 12 weeks of treatment with each drug. Treatment with bezafibrate and micronised fenofibrate both resulted in significant reductions in the serum concentrations of total cholesterol (26.0% and 38.7%), VLDL cholesterol (41.5% and 54.1%) and total triglycerides (27.5% and 39.1%), as well as a significant increase in high density lipoprotein (HDL) cholesterol (15.0% and 27. 8%). Micronised fenofibrate was, however, significantly (P < 0.05) more effective in reducing serum concentrations of total cholesterol and VLDL cholesterol and increasing HDL cholesterol than was bezafibrate in the same patients.

Bezafibrate↗

PubMed1998

[Bezafibrate in the treatment of familial combined hyperlipidemia and its effect on certain parameters of lipid metabolism, particularly fibrinogen].

Fibrates are a standard in the treatment impaired lipid metabolism, in particular in combined disorders. The classical Helsinki trial provided evidence of a decreased incidence of IHD in the treated group as compared with the group on placebo. Moreover there is some recent work which proved by statistical methods regression of atherosclerosis after fibrate administration, e.g. the angiographic study BECAIT with bezafibrate. The objective of the present study was to test the effectiveness of bezafibrate (Regadrin B, 200 mg tablets, Berlin-Chemie, FRG) in patients with combined familial hyperlipidaemia. The total cholesterol concentration dropped by 12.7% the LDL-cholesterol concentration by 8.8%. There was a significant drop of triacylglycerols by 37% and a rise of HDL-cholesterol by 24.2%. The apoB concentration declined by 11.3% and apo A-1 increased by 19.6%. The fibrinogen value dropped significantly by 15.2%, the Lp(a) value did not change significantly. The body weight in the two groups did not change significantly. The achieved results resemble those of work published abroad. In the authors opinion it is a positive feature that it proved possible to engage the patients in regular aerobic physical activity. Bezafibrate, Regadrin B was well tolerated by the patients, neither clinical nor laboratory tests revealed significant undesirable effects.

Adult↗

PubMed1979

[Dose-effects studies with bezafibrate in patients with hypercholesterolemia and hypertriglyceridemia (author's transl)].

The dose-effect relationship of bezafibrate, a new clofibrate derivative, was investigated in 24 outpatients with a primary hyperlipidemia and a Type lla lipoprotein pattern. The patients were divided into two groups at random and in each case received 3 X 50, 3 X 100, 3 X 150 and 3 X 200 mg bezafibrate daily in increasing or falling dosage for four weeks. For rising doses a statistically significant dose-effect relationship could be demonstrated for cholesterol and triglycerides. This was only true for cholesterol with falling doses while triglycerides remained at a low level. The optimal dose was found to be 600 mg bezafibrate daily. The substance was well tolerated, and the usual laboratory parameters remained within the normal range in all patients.

Cholesterol↗