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PubMed2001

Improvement in endothelial dysfunction in patients with hypoalphalipoproteinemia and coronary artery disease treated with bezafibrate.

Isolated low high-density lipoprotein cholesterol (HDLc) is a well-known risk factor for cardiovascular disease and is associated with arterial endothelium dysfunction. Several studies have shown that cholesterol lowering in patients with hypercholesterolemia improves endothelial function, but the effect of treating low HDLc levels remains unknown. We studied the effect of increasing HDLc on endothelial function in patients with coronary artery disease (CAD) and isolated low HDLc (HDLc) <0.91 mM, low-density lipoprotein cholesterol (LDLc) <4.1 mM, and triglycerides <2.8 mM. Flow-mediated endothelium-dependent dilatation (FMD) in response to reactive hyperemia was measured by brachial ultrasound, before and after bezafibrate treatment (400 mg daily for 6 months) in 16 patients with CAD and impaired FMD (<10%). After bezafibrate therapy, HDLc increased from 0.79-1.0 mM (p = 0.0008) at the expense of both HDL2 and HDL3 subfractions, apolipoprotein A-I increased from 1.04-1.19 g/l (p = 0.0012), and fibrinogen decreased from 4.45-3.39 g/l (p = 0.0007). The impaired FMD increased after bezafibrate treatment from a median of 2.5-12.3% (p = 0.0004). Endothelial function was normalized in eight patients (50%), improved in four (25%), and did not change in four (25%). These observations indicate that in patients with isolated low HDLc and CAD, bezafibrate treatment improves endothelial function of brachial arteries, increases HDLc and apolipoprotein A-I, and lowers fibrinogen concentrations.

Aged↗
PubMed1984

Effect of short-term treatment with bezafibrate and fenofibrate on biliary lipid metabolism in patients with hyperlipoproteinaemia.

Sixteen patients with different types of hyperlipoproteinaemia were treated with the clofibrate analogues, bezafibrate or fenofibrate. Serum lipids and lipid composition of gallbladder bile were measured before and after 3-4 weeks of treatment. Both bezafibrate and fenofibrate reduced serum lipids effectively but increased the lithogenic index of bile from 1.11 to 1.47 and 1.25 to 1.80 (P less than 0.01), respectively, by increasing molar percent of cholesterol and decreasing molar percent of bile acids. Measurements of biliary lipid secretion in three patients before and after bezafibrate administration revealed a marked and significant increase in cholesterol secretion (from 119 to 166, from 58 to 128, and from 149 to 172 mumol h-1, respectively; P less than 0.05) without altering bile acid and phospholipid output. These results indicate that bezafibrate and fenofibrate exhibit the same effect on biliary lipid metabolism as clofibrate and might therefore induce cholesterol gallstone disease.

Bezafibrate↗
PubMed1986

Change in very low-, low-, and high-density lipoproteins during lipid lowering (bezafibrate) therapy: studies in type IIA and type IIb hyperlipoproteinaemia.

The effects of lipid lowering therapy (bezafibrate) on plasma lipoproteins was investigated in twelve patients with familial hypercholesterolaemia (type IIA) and eight with familial combined hyperlipidaemia (type IIB). Bezafibrate caused a decrease of plasma cholesterol, plasma triglycerides, plasma apolipoprotein B, VLDL cholesterol and LDL cholesterol and an increase of HDL cholesterol. Post-heparin plasma lipoprotein and hepatic lipase activities increased in both groups (significant only in type IIB). Lipoprotein composition showed the following changes: Increased protein and phospholipids and decreased triglycerides and cholesteryl esters in VLDL. Decreased protein and triglycerides and increased free and esterified cholesterol in LDL. Decreased triglycerides and increased phospholipids in HDL. Cholesteryl ester to protein ratios decreased in VLDL and increased in LDL. The hydrated density of LDL (both groups) and of HDL3 (type IIB) decreased following bezafibrate therapy. These changes were in general similar to those observed in hypertriglyceridaemic patients and could be ascribed, at least in part, to the increase of plasma lipase activities and the decrease of lipid transfer reactions. Comparing the present data with that previously reported, it was found that bezafibrate caused decreased LDL cholesterol in types IIA and IIB but increased levels in type IV. This change was correlated with the initial plasma triglycerides (r = 0.74, P less than 0.0001) and initial plasma LDL cholesterol (r = 0.66, P less than 0.001). It is concluded that varied response of LDL to therapy reflects a complex interaction of metabolic events, including changing rates of VLDL conversion to LDL, lipoprotein compositional changes and effects of therapy on LDL degradation rates.

Adult↗
PubMed1993

Disparate effects of a triglyceride lowering diet and of bezafibrate on the HDL system: a study in patients with hypertriglyceridaemia and low HDL-cholesterol levels.

The response of plasma triglyceride and of the high density lipoprotein (HDL) system to a triglyceride lowering diet and to a bezafibrate was compared in a group of 24 human subjects with mild to moderate hypertriglyceridaemia and low HDL-cholesterol levels. Post-heparin plasma lipoprotein (LPL) and hepatic (HL) lipase activities were determined before the initiation of the study and at the end of the diet (12 weeks) and bezafibrate (12 weeks) periods. HDL structure and composition were determined on a zonal centrifugation system at the end of the diet and bezafibrate periods. Diet caused a 9-20% reduction of plasma triglycerides but there was no change in LPL, HL or HDL levels. The individual responses between plasma triglycerides and HDL cholesterol levels however were highly correlated (r = 0.60 to 0.78). Combined diet plus bezafibrate therapy caused a further 38% decrease of plasma triglycerides with a 28% increase of HDL-cholesterol and a 47% increase of LPL activity. HDL3 density decreased and the contribution of cholesteryl ester to the HDL mass was increased while the contribution of proteins and triglycerides decreased. In the majority of the subjects (61%) HDL cholesterol levels increased by 20% or more and in these subjects the change of HDL was highly correlated with the change of the LPL/HL ratio (r = 0.74) but not with the change of the plasma triglyceride levels. In the remaining subjects (39%), HDL cholesterol levels remained unchanged or increased by less than 20%. The change of HDL cholesterol levels in these subjects was unrelated to the decrease of plasma triglycerides or the change of post-heparin lipase activities.(ABSTRACT TRUNCATED AT 250 WORDS)

Bezafibrate↗
PubMed1999

Relapsing acute pancreatitis induced by re-exposure to the cholesterol lowering agent bezafibrate.

We report a 75-yr-old patient, who presented three times with acute pancreatitis, accompanied by high temperature, shock, and multiorgan involvement and associated each time with exposure to the cholesterol lowering agent bezafibrate. Extensive workup excluded other possible causes for recurrent pancreatitis in this patient, further supporting bezafibrate as the cause of the patient's acute illness. Based on the short time elapsing between rechallenge and development of manifestations and the specific features of the attacks, we proposed hypersensitivity to bezafibrate as the underlying mechanism. The present report includes, for the first time, bezafibrate among definite causes of acute pancreatitis.

Acute Disease↗
PubMed1985

Double blind trial of bezafibrate in familial hypercholesterolaemia.

A six month, double blind, crossover controlled trial of bezafibrate was conducted in 14 children with familial hypercholesterolaemia all of whom had a strong family history of early coronary heart disease. The bezafibrate was given twice daily in a dose of 10 to 20 mg/kg/day. The mean plasma total cholesterol concentration on bezafibrate was 22% lower than during the period on placebo and there was a moderate rise in high density lipoprotein cholesterol. Bezafibrate may be a useful adjunct to treatment in these children.

Adolescent↗
PubMed1990

Lovastatin versus bezafibrate: efficacy, tolerability, and effect on urinary mevalonate.

Lovastatin and benzafibrate have proved effective in lowering low-density-lipoprotein (LDL) cholesterol and elevating high-density-lipoprotein (HDL) cholesterol. We compared their tolerability, safety, and effects on lipoproteins and urinary mevalonate excretion in a short-term study. Forty patients with primary hypercholesterolemia were enrolled in a single-blind randomized study with a diet/placebo period of 8 weeks and a treatment period of 12 weeks. Twenty patients received lovastatin (final average dose 70.5 mg/day), and 20 patients received bezafibrate 400 mg/day. LDL cholesterol was lowered by 35% (from 323 to 208 mg/dl) with lovastatin and by 8% (from 289 to 264 mg/dl) with benzafibrate. HDL cholesterol increased by 21 and 20% with lovastatin and benzafibrate, respectively. Twenty-four-hour urinary mevalonic acid output decreased by 37% during treatment with lovastatin and by 2% during treatment with bezafibrate. Thus, the lowering of cholesterol by lovastatin, but not by bezafibrate, can be attributed to inhibition of HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase. Both lovastatin and bezafibrate are well tolerated.

Adult↗
PubMed2000

Bezafibrate increases prebeta 1-HDL at the expense of HDL2b in hypertriglyceridemia.

Prebeta1-high density lipoprotein (prebeta1-HDL), the initial acceptor of cell-derived cholesterol, can be generated from HDL(2) by hepatic lipase. Because bezafibrate elevates lipase activity, it may increase prebeta1-HDL at the expense of HDL(2). To answer this question, we determined the apolipoprotein A-I (apoA-I) distribution in 20 hypertriglyceridemics (triglycerides>2.26 mmol/L) and 20 sex-matched normolipidemics by native 2-dimensional gel electrophoresis. At baseline, prebeta1-HDL was 70% higher in hypertriglyceridemics than in normolipidemics (123.5+/-49.9 versus 72.5+/-34.1 mg/L apoA-I, P<0.01). Prebeta1-HDL was positively correlated with triglyceride (r=0.624, P<0.0001). A 4-week bezafibrate treatment (400 mg daily) increased prebeta1-HDL by 30% (160.2+/-64.5 mg/L apoA-I, P<0.05) but decreased HDL(2b) by 31% (from 188.8+/-94.9 to 129.3+/-78.7 mg/L apoA-I, P<0.05). Hepatic lipase activity increased by 24% (P<0.005). Prebeta1-HDL was generated either from ultracentrifugally isolated HDL(2) or from plasma during incubation with triglyceride lipase. In conclusion, bezafibrate increases prebeta1-HDL at the expense of HDL(2). We speculate that such an effect might partly contribute to the antiatherogenic action of bezafibrate.

Adult↗
PubMed2006

Effects of bezafibrate on HDL2/HDL3 ratio in postmenopausal hypertriglyceridemic women.

The short-term effects of bezafibrate on high-density lipoprotein cholesterol quality and triglyceride-rich lipoprotein metabolism in 186 postmenopausal hypertriglyceridemic women were investigated. Patients were randomized to an untreated group and to bezafibrate (400 mg/d) for 6 months. Fasting lipid concentrations, high-density lipoprotein 2, and high-density lipoprotein 3 levels were measured at baseline and after 3 and 6 months. At 3 months, bezafibrate had significantly decreased mean serum triglycerides and remnant-like particle cholesterol levels (105.7 +/- 43.4 mg/dL and 5.33 +/- 2.1 mg/dL, P < .001, respectively) from baseline values (232.5 +/- 63.9 mg/dL and 9.69 +/- 3.8 mg/dL, respectively). It also maintained lower total cholesterol, low-density lipoprotein cholesterol, triglycerides, and remnant-like particle cholesterol concentrations to 6 months. After 3 months, it significantly increased mean serum high-density lipoprotein cholesterol (55.1 +/- 14.7 vs 64.8 +/- 12.1 mg/dL; P < .0001) and maintained higher high-density lipoprotein cholesterol at 6 months. The high-density lipoprotein 2-high-density lipoprotein 3 ratio was decreased after 3 months of therapy with bezafibrate (2.13 +/- 0.68) from the baseline (2.42 +/- 0.71) (P < .01).

Bezafibrate↗
PubMed1994

Effects of oral administration of bezafibrate on peroxisomes and carnitine acetyltransferase in rat hepatocytes.

Changes in fine structure of peroxisomes and mitochondria were examined by electron microscopy in the hepatocyte of rats administered with bezafibrate, a hypolipidemic reagents. Peroxisomes increased to approximately 4.8 times in number one week after oral administration of bezafibrate in male rats. Newly induced peroxisomes showed paler matrix with frequent absence of core structure at two weeks after administration, peroxisomes further increased in number, 5.8 times in males, and were mostly devoid of core structure. Mitochondrial cristae were occasionally arranged along the long axis of mitochondria. Activity of carnitine acetyltransferase (CAT), one of the enzymes involved in beta oxidation of fatty acids, increased significantly after oral administration of bezafibrate. At two weeks after administration, it increased up to 12.0 times in males, 8.4 times in castrated males, 3.8 times in females and 5.5 times in castrated females, respectively. Cytochemically, CAT was localized in the outer compartment and inner membrane of mitochondria. CAT activity was also detected in the matrix of peroxisomes at two weeks after oral administration of bezafibrate.

Administration, Oral↗
PubMedDate not supplied

Effect of lipoprotein lipase activators bezafibrate and NO-1886, on B16 melanoma-induced cachexia in mice.

Our recent study has demonstrated that B16 melanoma-induced cachexia in mice is inhibited by ponalrestat, an aldose reductase inhibitor, which has the ability to activate lipoprotein lipase (LPL) activity both in vitro and in vivo. In this study, the effect of bezafibrate and NO-1886, LPL activators, on B16 melanoma-induced cachectic symptoms was investigated in mice. Treatment with bezafibrate resulted in an attenuation of the decrease in the weight of epididymal fat and whole body lipid observed in mice following intraperitoneal inoculation of B16. The increase in the levels of triglyceride and non-esterified fatty acid, and a decrease in the level of glucose in the blood, which was induced by the presence of tumor, were also restored to that of normal mice after treatment with bezafibrate. The reduction in the weight of epididymal fat and whole body lipid induced by B16 was also ameliorated by NO-1886. Overall, this study demonstrated that cachexia induced by B16 melanoma in mice was alleviated by the LPL activators bezafibrate and NO-1886, suggesting the involvement of the impaired LPL activity in the establishment of cachexia syndrome in mice bearing B16 melanoma.

Adipose Tissue↗
PubMedDate not supplied

Effectiveness of nicotinic acid and bezafibrate alone and in combination for reducing serum triglyceride level.

OBJECTIVE: To study the effectiveness of nicotinic acid and Bezafibrate alone and in combination for reducing triglyceride level. DESIGN: It was a randomised, prospective, longitudinal study. SETTING: Patients attending a private clinic, and medical department of Kathmandu Medical College, Sinamangal. METHODS: This study included 83 consecutive patients, 19 females and 64 males with hypertriglyceridaemia (defined as serum triglyceride >200mg/dl) attending the department of medicine, Kathmandu Medical College, Sinamangal and private clinic. MAIN OUTCOME MEASURES: Statistically significant reduction of serum triglyceride level. RESULT: 51 out of 83 patients completed the study in which Nicotinic acid alone reduced the serum trygleceride level from 320.62 +/- 104.23 to 182.55 +/- 46.21, which is a reduction of 138.07 +/- 85.69 (P. value = 001). Bezafibrate when given alone also reduced triglyceride level significantly from 345.25 +/- 181.03 to 203.30+/-93.59 which is a reduction of 141.95 +/- 121.130 (P value= .001). When a combination of both drugs was given the reduction of 472.73+/-247.53 (P value =.002) was achieved. CONCLUSIONS: Nicotinic acid is a very effective drug in reducing serum triglyceride level and its effectiveness is similar to Bezafibrate. There is no added benefit of giving a combination of nicotinic acid and Bezafibrate in reducing serum triglyceride level.

Bezafibrate↗
PubMed1991

[Effect of bezafibrate in isolated hypercholesterolemia and mixed hyperlipidemia on infarct risk (Stepwise Program for Individual Risk Identification and Therapy): an open multicenter study].

The therapeutic effect of bezafibrate (1 x 400 mg/day) on plasma lipids and coronary risk was evaluated in an open, prospective multicenter study in 763 patients with isolated hypercholesterolemia or mixed hyperlipidemia. During the 16 weeks of treatment (712 patients were included in the evaluation) bezafibrate lowered total cholesterol (C) by 22%, triglycerides (TG) by 32% and LDL-C by 20% and increased HDL-C by 29.6%. The ratio of C/HDL-C decreased from 8.8 +/- 2.0 to 5.4 +/- 1.5, i.e. a reduction of 36%. A comparable hypolipemic effect of bezafibrate was seen in all the subgroups of isolated hypercholesterolemia (C -21%, LDL-C -31%, HDL-C + 28%, TG -10%) and mixed hyperlipidemia (C -22%, LDL-C -16%, HDL-C + 30%, TG -37%). During treatment the coronary risk factor estimated by the SPIRIT calculator decreased from 5.5 to 2.5 (-54.5%) in male patients (n = 499). The calculated incidence of myocardial infarction thereby decreased from 225.7 to 111.9 (-50.4%). This study shows that bezafibrate effectively improves lipid metabolism in both isolated hypercholesterolemia and mixed hyperlipidemia and results in a decreased coronary risk.

Adult↗
PubMed1990

Bezafibrate and simvastatin (MK-733) in the treatment of primary hypercholesterolaemia.

Simvastatin, a new 3-hydroxy-3-methylglutaryl co-enzyme A reductase inhibitor, was compared to bezafibrate, a fibric acid derivative, in an open cross-over placebo-controlled study. Bezafibrate was administered as a 200 mg dose 3 times daily, while simvastatin dosage ranged from 10 mg to 40 mg once daily at night. Bezafibrate produced a non-significant 13.1% (P = 0.113) decrease in total cholesterol (TC), a 20.7% (P less than 0.05) decrease in low-density lipoprotein cholesterol (LDL-C), an increase of 26.5% (P less than 0.01) in high-density lipoprotein cholesterol (HDL-C) and an improvement in the HDL:LDL ratio of 77.3% (P less than 0.01). Simvastatin 10 mg and 20 mg daily reduced TC by 18.6% and 22.6%, respectively, and LDL-C by 23.9% and 28.6% respectively (P less than 0.01), while no significant increase was noted in HDL-C. Simvastatin 40 mg daily reduced TC and LDL-C by 27.1% and 37.6%, respectively (P less than 0.01), increased HDL-C by 32.0% (P less than 0.05) and improved on the HDL:LDL ratio by 130.8% (P less than 0.01). This showed improvements over bezafibrate of 13.5% for TC, 18.9% for LDL-C, 6.0% for HDL-C and 55.8% for HDL:LDL ratio. It was concluded that simvastatin was well tolerated and had significant hypocholesterolaemic effects when taken once daily.

Adult↗
PubMed1988

Effects of bezafibrate and gemfibrozil on serum lipoproteins in primary hypercholesterolemia.

29 patients with primary hypercholesterolemia were treated for 8 weeks each with either bezafibrate (200 mg t.i.d.) or gemfibrozil (600 mg b.i.d.) in a randomized cross-over trial. Compared to placebo bezafibrate was significantly more effective on low density lipoprotein (LDL)-cholesterol (-28% versus -18%) and the LDL/high density lipoprotein (HDL) ratio (-34% versus -24%) by exploratory statistics. There was also a trend for a more marked reduction of bezafibrate on total cholesterol and apoliproprotein B as well as more pronounced increase in HDL-cholesterol and apolipoprotein A-I. The triglyceride reduction tended to be more extensive with gemfibrozil. Complicance to both drugs was good. No side-effects were observed. The results are considered important with respect to the potential of bezafibrate in reducing the risk of cardiovascular disease.

Adult↗
PubMed1988

Effects of a bezafibrate sustained release formulation on plasma lipoproteins in patients with hypercholesterolemia. Importance of timing of tablet intake for efficacy.

The therapeutic effect of a single sustained release tablet of bezafibrate (Cedur retard, 400 mg) in primary hypercholesterolemia type IIa and type IIb was investigated in a placebo-controlled randomised study comparing the efficacy of morning vs. evening intake. The decrease in total cholesterol with the morning intake was 18.5% vs. 16.5% for the evening intake (n.s.). HDL-cholesterol increased more in patients taking bezafibrate retard at morning (29.6% vs. 22.4%, p less than 0.05). Bezafibrate was well tolerated. Animal experiments and precursor studies of cholesterol synthesis in man indicate peak activity of HMG-CoA reductase between 1 a.m. and 3 a.m. The data suggest that with normal eating habits during day time other modes of action of bezafibrate besides HMG-CoA reductase inhibition such as reduction of VLDL-synthesis in the liver and an increased fractional catabolic rate, could contribute to the therapeutic effect.

Alkaline Phosphatase↗
PubMed1986

[Effect of bezafibrate on lipoprotein secretion by cultured human hepatocytes].

The rate of synthesis and secretion of lipid and apoprotein components of lipoprotein fractions and of proteins of the nonlipoprotein fraction d greater than 1.21 g/ml by human hepatocytes in culture was determined. The cells were incubated for 18 hours in the media containing [14C] acetate or [3H]-marked leucine in the presence of bezafibrate or without it. VLDL, HDL and d greater than 1.21 g/ml fractions were separated by differential ultracentrifugation. The lipids were divided using thin-layer chromatography, and the apoprotein-using SDS-electrophoresis in polyacrylamide gel. Bezafibrate in the therapeutic concentration of 10 microM specifically inhibits apoprotein and VLDL lipid secretion. Lowered secretion of all VLDL apoproteins was revealed, which points to a decrease in the number of secreted particles. The effect of bezafibrate was found to be associated with the inhibition of the intracellular synthesis of lipids. The secretion of HDL proteins and of d greater than 1.21 g/ml fraction proteins was unchanged with 10 microM of bezafibrate.

Adult↗
PubMed1985

Diurnal lipid and lipoprotein profiles with bezafibrate and clofibrate in healthy volunteers.

Diurnal lipid and lipoprotein profiles were measured in 28 healthy volunteers after 10-day treatment periods with placebo, bezafibrate (200 mg 3-times daily) or clofibrate (500 mg 3-times daily) in a double-blind, parallel trial. The two drugs lowered fasting triglyceride and cholesterol levels (p less than or equal to 0.05 for cholesterol with bezafibrate vs placebo). Diurnal triglyceride profiles were lowest with bezafibrate due to lowest fasting triglycerides. Alimentary lipaemia with placebo was mild and due to increased VLDL-triglycerides, while the other lipoprotein lipids and total plasma cholesterol remained virtually unchanged during the day. Bezafibrate (half-life 2 hours) and clofibrate (half-life 15 hours) gave similar diurnal triglyceride patterns. The diurnal values were dependent on the fasting values. Changes in the cholesterol/phospholipid ratio during the day may be related to altered post-prandial composition of HDL.

Adult↗