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PubMedDate not supplied

The effect of simvastatin and bezafibrate on bile composition and gall-bladder emptying in female non-insulin-dependent diabetics.

Female non-insulin-dependent diabetics have a high prevalence of gallstones. Treatment of hyperlipidaemia in these patients may modify the risk. Seventeen female non-insulin-dependent diabetics (age 35-65) were treated with simvastatin (n = 10) or bezafibrate (n = 7) and had the cholesterol saturation index (CSI) of bile and gall-bladder emptying measured before and after 3 months therapy. In both groups, there was a significant reduction in serum cholesterol following treatment. The mean pretreatment cholesterol saturation indices of bile did not differ between the two groups but, after 3 months therapy, there was a highly significant difference in CSI between the bezafibrate group (2.0 +/- 0.33) and the simvastatin group (1.1 +/- 0.14) P < 0.002. Whereas the increase in the CSI (42%) observed with bezafibrate therapy was significant, the decrease in the simvastatin group (14%) was only significant in those whose pretreatment cholesterol saturation indices were elevated. Despite the differences in CSI observed between the two treatment groups, no changes in gall-bladder emptying were detected.

Adult↗
PubMed1992

Bezafibrate induced rhabdomyolysis.

The case is presented of a 70 year old woman with mild hypercholesterolaemia and hypertension who was readmitted to hospital six months after a previous admission for angina pectoris. The patient was treated with verapamil, nifedipine, and aspirin, and had been receiving bezafibrate (400 mg every 12 hours) for the previous 40 days. Twenty four hours after admission she developed podagra, which was treated with indomethacin (100 mg daily). Eight days after admission myocardial infarction was suspected, and the next day she presented with symptoms of rhabdomyolysis, which was confirmed by laboratory tests. Bezafibrate was withdrawn and the patient became asymptomatic after seven days. It is recommended that doctors should be aware of the possibility of patients, especially those with impaired renal function, developing rhabdomyolysis while being treated with bezafibrate.

Aged↗
PubMed1988

Combination treatment with cholestyramine and bezafibrate for heterozygous familial hypercholesterolaemia.

Cholestyramine and bezafibrate were compared individually and in combination in the treatment of 18 patients with heterozygous familial hypercholesterolaemia. The study used a double blind, placebo controlled block design with a placebo run in period of two months followed by three phases of active treatment, each of two months' duration. Patients were randomly allocated to one of the six possible sequences of medication so that three patients would be treated with each sequence. Two patients withdrew from the study before completion. The median concentration of total cholesterol decreased from 9.65 mmol/l (interquartile range 8.62 to 8.72) to 7.24 mmol/l (6.70 to 7.52) with cholestyramine, to 8.09 mmol/l (7.18 to 8.68) with bezafibrate, and to 6.31 mmol/l (5.84 to 7.27) with the combination. This fall was due almost entirely to a decrease in the low density lipoprotein cholesterol concentration, and the combination was significantly more effective than either drug alone. The 98% confidence intervals for the median differences between the combination and cholestyramine and the combination and bezafibrate were 0.04 to 1.49 mmol/l and 0.51 to 2.18 mmol/l respectively. These results suggest that this combination is an effective and useful treatment in heterozygous familial hypercholesterolaemia.

Adult↗
PubMed1989

Effect of bezafibrate on the sequelae of acute experimental focal cerebral ischaemia.

The possibility that the ability of bezafibrate to lower the oxygen affinity of haemoglobin might lead to an increased oxygen delivery to ischaemic cerebral tissue was explored in preliminary studies in two animal models. The combined morbidity and mortality of unilateral carotid ligation in the gerbil appeared to be reduced at two hours in bezafibrate treated animals. By four hours and thereafter the outcome was unaffected. Two hours after MCA occlusion bezafibrate-treated rats showed a significantly reduced rise in tissue lactate concentration (p less than 0.01) suggesting less anaerobic metabolism had occurred in the ischaemic tissue.

Acute Disease↗
PubMed1996

Comparative efficacy and safety of ciprofibrate and sustained-release bezafibrate in patients with type II hyperlipidaemia.

The hypolipidaemic efficacy and safety of ciprofibrate were compared with a sustained-release formulation of bezafibrate (Bezalip Mono) in 174 patients with type II hyperlipidaemia. This multicenter, open, parallel-group study was conducted in general practice. A total of 83 patients received 100 mg ciprofibrate once daily and 91 received 400 mg bezafibrate once daily for eight weeks. Concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides were measured at baseline (after stabilisation on a lipid-lowering diet) and after eight weeks. Safety was assessed from reports of adverse events and by measuring haematological and biochemical parameters. After eight weeks, ciprofibrate produced a significantly greater decrease in total cholesterol (-17.8% vs -12.5%), low-density lipoprotein cholesterol (-22.4% vs -17.2%), and triglycerides (-33.9% vs -26.1%). High-density lipoprotein cholesterol concentrations were increased significantly by both drugs (19.6% with ciprofibrate, 24.9% with bezafibrate) but the differences between drugs were non-significant. Both drugs were well tolerated, with headache the most widely reported adverse event.

Adult↗
PubMed2006

Effects of peroxisome proliferator-activated receptor ligands, bezafibrate and fenofibrate, on adiponectin level.

OBJECTIVE: Adiponectin is adipose-specific secretory protein and acts as anti-diabetic and anti-atherosclerotic molecule. We previously found peroxisome proliferators response element in adiponectin promoter region, suggesting that peroxisome proliferator-activated receptor (PPAR) ligands elevate adiponectin. Fibrates are known to be PPARalpha ligands and were shown to reduce risks of diabetes and cardiovascular disease. Effect of fibrates on adiponectin has not been clarified, whereas thiazolidinediones enhance adiponectin. Thus, we explored the possibility and mechanism that fibrates enhance adiponectin in humans, mice, and cells. METHODS AND RESULTS: Significant increase of serum adiponectin was observed in bezafibrate-treated subjects compared with placebo group in patients enrolled in The Bezafibrate Infarction Prevention study. Higher baseline adiponectin levels were strongly associated with reduced risk of new diabetes. Fibrates, bezafibrate and fenofibrate, significantly elevated adiponectin levels in wild-type mice and 3T3-L1 adipocytes. Such an effect was not observed in PPARalpha-deficient mice and adipocytes. Fibrates activated adiponectin promoter but failed to enhance its activity when the point mutation occurred in peroxisome proliferators response element site and the endogenous PPARalpha was knocked down by PPARalpha-RNAi. CONCLUSIONS: Our results suggest that fibrates enhance adiponectin partly through adipose PPARalpha and measurement of adiponectin might be a useful tool for searching subjects at high risk for diabetes.

Adipocytes↗
PubMed1981

Effects of bezafibrate on low HDL-cholesterol in patients with ischaemic cerebrovascular disease: a pilot study.

Bezafibrate is a new lipid-lowering agent that quite constantly increases low HDL-cholesterol values in hyperlipoproteinaemic patients. The possible role fo HDL-cholesterol as an anti-atherogenic factor has been frequently discussed, mainly in patients with ischaemic heart disease but recently also in ischaemic cerebrovascular disease (ICD). This is the first pilot study in six selected patients suffering from ICD who had at the same time low HDL-cholesterol values (less than or equal to = 1.1 mmol/l) with otherwise normal lipids. After a wash-out period of 2 months duration these patients were treated with 200 mg bezafibrate t.i.d. for 2 months. They were then followed up for another 8 months. Bezafibrate therapy increased HDL-cholesterol (range 45-130%). Eight months after cessation of therapy five patients have returned to pathologically low HDL-levels and the sixth patient also has a relatively low value of 1.2 mmol/l. This small preliminary study cannot, however, provide evidence about the possible beneficial role of increasing HDL-cholesterol in patients with ICD. Further investigations are therefore in progress.

Adult↗
PubMed2001

Effect of bezafibrate on soluble adhesion molecules and platelet activation markers in patients with connective tissue diseases and secondary hyperlipidemia.

We evaluated the plasma concentrations of soluble adhesion molecules, platelet activation markers, and platelet-derived microparticles (PMPs) in patients with connective tissue diseases who had secondary hyperlipidemia caused by long-term steroid administration (n = 22) before and after treatment with bezafibrate. There were differences in levels of platelet activation markers both before and after treatment (platelet CD62p: 15.11+/-2.03 vs 10.38+/-8.53%, P < 0.05; platelet CD63: 12.12+/-9.17 vs 9.90+/-7.20%, P < 0.05). There were also differences in the levels of PMPs and soluble adhesion molecules both before and after treatment (PMP: 514+/-273 vs 401+/-201 /10(4) platelet. P < 0.05; soluble vascular cell adhesion molecule-1: 724+/-191 vs 666+/-157 ng/mL, P < 0.01). After 6 months of treatment, serum lipid concentrations were reduced by 9% for total cholesterol (TC) and 32% for triglyceride (TG). The level of PMPs, activated platelets, and soluble adhesion molecules were all significantly decreased after treatment with bezafibrate. These findings suggest that bezafibrate may be useful for inhibiting both PMP-dependent and -independent vascular damage in patients with connective tissue diseases complaining of secondary hyperlipidemia.

Bezafibrate↗
PubMed1988

Changes in lipid and lipoprotein levels and Achilles tendon diameters and indices in familial hypercholesterolaemic patients with tendinous xanthomatosis treated by diet and bezafibrate for 2 years.

Thirteen young adult patients suffering from heterozygotic familial hypercholesterolaemia with tendinous xanthomatosis, previously treated with a suitable special diet, were studied to assess the effect of bezafibrate, given for 2 years at a dose of 800 mg/day, on plasma lipid and lipoprotein levels and on changes in size of the Achilles tendon xanthomas. Measurements were made before and at intervals during treatment, the tendinous xanthomas being measured by an echographic procedure to give data on antero-posterior and lateral diameters, thus enabling an Achilles tendon index to be defined. The results confirm the hypolipidaemic activity of bezafibrate, changes in the levels of total cholesterol, triglycerides, lipids and lipoproteins (LDL, VLDL and HDL) being similar in direction and magnitude to those reported previously. A significant regression in the size of the Achilles tendon xanthomas was observed in 11 of the 13 patients, and the regression in the Achilles tendon index correlated significantly with a favourable change in the ratio HDL/LDL + VLDL. It is suggested that, as a result of this objective observation, a favourable effect of bezafibrate treatment would possibly be seen on the anatomical atheromatous lesions which are usual in this type of hyperlipidaemia.

Achilles Tendon↗
PubMed2003

Correction of fatty acid oxidation in carnitine palmitoyl transferase 2-deficient cultured skin fibroblasts by bezafibrate.

Carnitine palmitoyltransferase 2 (CPTII) deficiency is among the most common inborn errors of mitochondrial fatty acid beta-oxidation (FAO). Clinical phenotype varies in relation to the metabolic block, as assessed by studies of FAO in patient fibroblasts. Thus, fibroblasts from patients with mild manifestations have appreciable residual CPTII enzyme activity, in contrast to those from severely affected patients. In the present study, we hypothesized that the hypolipidemic drug bezafibrate, acting as an activator of the peroxisome proliferator-activated receptor alpha might stimulate FAO in CPTII-deficient cells. Data obtained show that bezafibrate treatment of mild-type CPTII-deficient cells resulted in a time- and dose- dependent increase in CPTII mRNA (from +47% to +66%) and residual enzyme activity (from +54% to 135%), and led to normalization of 3H-palmitate and 3H-myristate cellular oxidation rates. Bezafibrate did not correct FAO in fibroblasts from patients with severe phenotype. This study establishes for the first time that peroxisome proliferator-activated receptor activators, acting via stimulation of gene expression, can stimulate CPTII residual activity to a level sufficient to allow normal FAO flux in deficient human fibroblasts, and suggests that this approach should be tested in other inborn errors of mitochondrial beta-oxidation.

Bezafibrate↗
PubMed1996

A lipid lowering drug (bezafibrate) has a favorable effect on liver enzymes (Al-P and gamma-GTP).

We administered 400 mg of bezafibrate daily to 27 patients with hyperlipidemia for seven moths. Most biochemical parameters remained unchanged, whereas levels of alkaline phosphatase (Al-P)and gamma-glutamyl transpeptidase (gamma-GTP), which are the hepatobiliary enzymes, were significantly decreased. Blood lipid levels were improved. Al-P levels decreased significantly from the baseline level of 174.5 IU/l to 116.7 IU/l (-26.5%) and gamma-GTP levels also decreased from 64.4 IU/l to 34.4 IU/l (-29.5%) (p < 0.001). When we compared the changes in serum lipid levels with those in Al-P and gamma-GTP levels following bezafibrate therapy, we found a slight degree of correlation between changes in gamma-GTP and triglyceride (T-G) levels, but no correlation at all between the changes of Al-P and total-cholesterol (T-cho), T-G or high density lipoprotein cholesterol (HDL-C). A close correlation was observed between both Al-P and gamma-GTP (r = 0.81, p < 0.001). From these results it was suggested that bezafibrate has not only a lipid lowering effect but has a favorable efficacy on the hepatobiliary enzymes.

Aged↗
PubMed1996

Ultrastructural observation of changes in (hepatic) peroxisomes by 3 to 90 days administration of bezafibrate in male rats.

Although many reports are available to indicate the increase in number and size of peroxisomes by oral administration of hypolipidemic reagents such as clofibrate and bezafibrate, the decrease in number and size of proliferated peroxisomes even during administration of these chemicals has not been well documented. The present study was aimed to detect when the decrease in number and size of peroxisomes would occur. In the present study, ultrastructural changes in hepatocytes of male Wistar rats during 3 to 90 days of oral administration of bezafibrate were analyzed by morphometric and cytochemical methods. By 3-day administration, the weight of the liver and the number and size of peroxisomes were significantly increased. These parameters began to decline from the time 14 days of administration when the weight of the liver and the size of peroxisomes attained the peak. Heterogeneous catalase staining was most remarkable by 7-day administration. Mitochondria were another target cell organelle by bezafibrate. The total area of mitochondria was decreased by 3-day administration. However, by subsequent 7 to 90-day administration, it recovered almost the level of controls. By 90-day administration, many mitochondria had expanded cristae which contained filamentous substances.

Administration, Oral↗
PubMed1998

Cardiovascular outcomes in type 2 diabetes. A double-blind placebo-controlled study of bezafibrate: the St. Mary's, Ealing, Northwick Park Diabetes Cardiovascular Disease Prevention (SENDCAP) Study.

OBJECTIVE: To determine whether serum lipid intervention, in addition to conventional diabetes treatment, could alter cardiovascular outcomes in type 2 diabetes. RESEARCH DESIGN AND METHODS: There were 164 type 2 diabetic subjects (117 men, 47 women) without a history of clinical cardiovascular disease randomized to receive either bezafibrate or placebo daily on a double-blind basis in addition to routine diabetes treatment and followed prospectively for a minimum of 3 years. Serial biochemical and noninvasive vascular assessments, carotid and femoral artery B-mode ultrasound measurements, and those pertaining to coronary heart disease (CHD)--clinical history, the World Health Organization (WHO) cardiovascular questionnaire, and resting and exercise electrocardiogram (ECG)--were recorded. RESULTS: Bezafibrate treatment was associated with significantly greater reductions over 3 years in median serum triglyceride (-32 vs. 4%, P = 0.001), total cholesterol (-7 vs. -0.3%, P = 0.004), and total-to-HDL cholesterol ratio (-12 vs. -0.0%, P = 0.001), and an increase in HDL cholesterol (6 vs. -2%, P = 0.02) as compared with placebo. There was a trend toward a greater reduction of fibrinogen (-18 vs. -6%, P = 0.08) at 3 years. No significant differences between the two groups were found in the progress of ultrasonically measured arterial disease. In those treated with bezafibrate, there was a significant reduction (P = 0.01, log-rank test) in the combined incidence of Minnesota-coded probable ischemic change on the resting ECG and of documented myocardial infarction. CONCLUSIONS: Improving dyslipidemia in type 2 diabetic subjects had no effect on the progress of ultrasonically measured arterial disease, although the lower rate of "definite CHD events" in the treated group suggests that this might result in a reduction in the incidence of coronary heart disease.

Adult↗
PubMedDate not supplied

Influence of bezafibrate on total antioxidant activity of serum and deformability of blood cells in hypercholesterolaemic patients.

Fourteen patients with hypercholesterolaemia were treated with bezafibrate (600 mg/day) for a month. Before and after the treatment some biochemical and physical parameters were investigated. Plasma cholesterol levels, elevated before treatment, significantly decreased after one month (p<0.001). Deformability of red blood cells increased significantly in this time (p<0.05). Total antioxidant status of serum decreased statistically significantly (p<0.01). It is concluded that the mechanism of action of bezafibrate is not connected with resistance to oxygen free radicals since the drug has no antioxidant activity. A main mechanism of action of bezafibrate seems to be lowering the cholesterol level. An increase in deformability of red blood cells may make some contribution to this mechanism.

Adult↗
PubMed1992

[Long-term bezafibrate treatment in a lipid clinic].

The files of 122 patients treated for at least 6 months with bezafibrate, a second generation fibric acid derivative, were reviewed. Our indications for bezafibrate treatment included cases of type IIb, IV and V hyperlipidemia which did not respond to a serious dietetic trial. Mean decrease in plasma triglycerides was 45% and in cholesterol 1012%, while in HDL-cholesterol there was a mean increase of 8%. The drug was usually well tolerated. Thorough review of patient files for side effects revealed gastrointestinal disturbances in 6.5%. There was a decrease in libido in 4%. 2 patients developed gynecomastia, 1 abnormal liver function tests and 1 severe myositis. All side effects were fully reversed on discontinuing the drug. Bezafibrate seems to be well-tolerated and suitable for treating type IIb, IV and V hyperlipidemia unresponsive to diet.

Bezafibrate↗
PubMedDate not supplied

[Progression of lesions of the arterial wall evaluated by ultrasonic biopsy in asymptomatic subjects and in diabetic and hyperlipidemic patients treated with bezafibrate. A 4-year follow-up].

Non-invasive arterial ultrasonic biopsy (UB) has been used to evaluate and follow-up arterial wall changes in four years in asymptomatic subjects, hyperlipidemics and diabetics. Both groups of patients were randomised in a treatment group (bezafibrate 400 mg daily) and in a control group. The rate of progression (ROP) into the next higher UB class was recorded by UB scans repeated every six months. In diabetics and hyperlipidemics the rate of progression (ROP, namely the percent of patients progressing to the next class) was significantly higher than the ROP in the asymptomatic subjects. However in the bezafibrate group the ROP was significantly lower than that observed in the controls. As each UB class corresponds to different levels of risks of occult coronary ischemia and cardiovascular events in the following four years, the reduction of ROP with bezafibrate was an important and positive achievement.

Adult↗
PubMed1990

Effect of bezafibrate on metabolic profiles in non-insulin-dependent diabetes mellitus.

Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by hyperglycemia secondary to increased hepatic glucose output and impaired extrahepatic insulin sensitivity. Many NIDDM patients also have raised serum triglyceride and low-density lipoprotein (LDL) cholesterol levels, which may require drug therapy, as well as increased plasma nonesterified fatty acid concentrations. Some hypolipidemic agents such as bezafibrate lower fatty acid levels as well as LDL cholesterol and triglycerides. It has been suggested that raised fatty acid levels may be responsible in part for the increased hepatic glucose output and insulin insensitivity of NIDDM. Several groups have therefore sought to examine the effects of fibrates on glycemic control in NIDDM. In our own studies, we used bezafibrate (200 mg t.i.d.) in a double-blind, placebo-controlled design for 3 months. Fasting blood glucose, serum insulin, C-peptide, plasma nonesterified fatty acids, blood lactate and alanine, serum triglycerides, and LDL cholesterol were all lowered. HbA1 showed no significant change. Meal hormone and metabolite profiles were all improved although this reflected mainly the lower premeal values. The results of our and other studies are sufficiently encouraging to suggest that bezafibrate could provide alternative first-line drug therapy in hyperlipidemic NIDDM patients when diet alone has failed.

Bezafibrate↗
PubMed1990

Bezafibrate retard in type II diabetic patients: effects on hemostasis and glucose homeostasis.

A double-blind, placebo-controlled trial assessed the effect of a slow-release formulation of bezafibrate (Bezalip Mono, 400 mg daily for 3 months) on lipid profile, glucose homeostasis, platelet function, and plasma fibrinogen concentration in non-insulin-dependent (type II) diabetics. Twenty-four patients completed the trial. There was a significant improvement in the cholesterol (p less than 0.02), triglyceride (p less than 0.01), and nonesterified fatty acid (p less than 0.05) concentrations and in the fasting blood glucose (p less than 0.03) and glycosylated hemoglobin (p less than 0.01) levels of those (n = 11) who received the active preparation but not in those (n = 13) who received placebo. Treatment, but not placebo, also resulted in a significant (p less than 0.01) fall in plasma fibrinogen concentration and a trend towards inhibition of platelet aggregation. Bezafibrate was well tolerated; only one patient (not included in the analysis of results) withdrew from the trial possibly because of side effects of the drug. A larger study is needed to establish whether bezafibrate can reduce nonlipid risk factors (e.g., plasma fibrinogen concentration, glucose intolerance, and hyperinsulinemia) in normo- and hyperlipidemic subjects.

Adult↗