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PubMed1998

Bezafibrate down-regulates fibrinogen biosynthesis in human hepatoma HepG2 cells.

BACKGROUND: Bezafibrate reportedly lowers serum lipids and plasma fibrinogen in humans and rats, but the mechanism of this process has still to be clarified. We have addressed this problem by investigating the effects of bezafibrate on fibrinogen in the human hepatoma HepG2 cell line. METHODS: In cells cultured with and without bezafibrate, intra- and extracellular fibrinogen was quantified using an enzyme-linked immunosorbent assay (ELISA), and changes in the biosynthesis and secretion of bezafibrate were monitored by [35S]-methionine labelling. In addition, expression of the corresponding mRNA was investigated by Northern blotting. As fibrinogen is an acute-phase protein, HepG2 cells exposed to interleukin 6 were also analysed. RESULTS: Bezafibrate decreased fibrinogen biosynthesis by about 25%, regardless of whether or not the cultures were also exposed to interleukin 6. mRNA was reduced in proportion to the concentration of interleukin 6 to which the cells were exposed, but intracellular transport and release of the protein were not affected. CONCLUSION: Apparently, bezafibrate interferes with the biosynthesis of fibrinogen at the pretranslational level but does not affect the export of the protein.

Acute-Phase Reaction↗
PubMed1991

[Effectiveness of pravastatin and bezafibrate in primary hypercholesterolemia].

The efficacy and safety of pravastatin and bezafibrate (in retard form) were compared in a randomised double-blind trial comprising 96 patients (48 men, 48 women; mean age 52.5 [20-68] years) with primary hypercholesterolaemia types IIa and IIb. After four weeks' treatment 6 out of 38 patients (400 mg/d bezafibrate) and 27 out of 58 patients (20 mg/d pravastatin) reached a LDL cholesterol level of 190 mg/dl or less. In the other 31 patients of the pravastatin group the dose was raised to 40 mg/d. During the twelve-week course of pravastatin total cholesterol concentration fell from a mean of 364 +/- 75 mg/dl (initial value) to 281 +/- 61 mg/dl (P less than 0.01), while LDL-cholesterol fell from 288 +/- 81 mg/dl to 206 +/- 64 mg/dl (P less than 0.01) and triglyceride concentration from 168 +/- 83 mg/dl to 148 +/- 80 mg/dl (P less than 0.05). During the twelve-week course of treatment with 400 mg bezafibrate total cholesterol concentration fell from a mean of 363 +/- 91 mg/dl to 325 +/- 73 mg/dl (P less than 0.01), LDL-cholesterol level fell from 284 +/- 88 mg/dl to 242 +/- 70 mg/dl (P less than 0.01) and the triglyceride concentration from 173 +/- 91 mg/dl to 121 +/- 83 mg/dl (P less than 0.01). HDL cholesterol concentration rose by 9% in the bezafibrate group and by 8.4% in the pravastatin group (P less than 0.05). Except in the case of HDL-cholesterol, the falls were significantly different in the two treatment groups: pravastatin was superior to bezafibrate in terms of the reductions in both total and LDL-cholesterol (P less than 0.01 for each). However, bezafibrate produced a greater fall in serum triglycerides (P less than 0.05). No serious side effects were associated with either drug.

Adult↗
PubMed2001

Plasma concentrations of active lovastatin acid are markedly increased by gemfibrozil but not by bezafibrate.

BACKGROUND: Concomitant use of fibrates with statins has been associated with an increased risk of myopathy, but the underlying mechanism of this adverse reaction remains unclear. Our aim was to study the effects of bezafibrate and gemfibrozil on the pharmacokinetics of lovastatin. METHODS: This was a randomized, double-blind, 3-phase crossover study. Eleven healthy volunteers took 400 mg/day bezafibrate, 1200 mg/day gemfibrozil, or placebo for 3 days. On day 3, each subject ingested a single 40 mg dose of lovastatin. Plasma concentrations of lovastatin, lovastatin acid, gemfibrozil, and bezafibrate were measured up to 24 hours. RESULTS: Gemfibrozil markedly increased the plasma concentrations of lovastatin acid, without affecting those of the parent lovastatin compared with placebo. During the gemfibrozil phase, the mean area under the plasma concentration-time curve from 0 to 24 hours [AUC(0-24)] of lovastatin acid was 280% (range, 131% to 1184%; P < .001) and the peak plasma concentration (Cmax) was 280% (range, 123% to 1042%; P < .05) of the corresponding value during the placebo phase. Bezafibrate had no statistically significant effect on the AUC(0-24) or Cmax of lovastatin or lovastatin acid compared with placebo. CONCLUSIONS: Gemfibrozil markedly increases plasma concentrations of lovastatin acid, but bezafibrate does not. The increased risk of myopathy observed during concomitant treatment with statins and fibrates may be partially of a pharmacokinetic origin. The risk of developing myopathy during concomitant therapy with lovastatin and a fibrate may be smaller with bezafibrate than with gemfibrozil.

Adult↗
PubMed2005

Effect of bezafibrate on incidence of type 2 diabetes mellitus in obese patients.

AIMS: To assess the effect of fibric acid derivative bezafibrate on incidence of type 2 diabetes in obese patients over a median 6.3 years follow-up period. METHODS AND RESULTS: The study sample comprised 339 non-diabetic obese patients (body mass index > or = 30.0 kg/m2) aged 42-74. Patients received either bezafibrate retard 400 mg (178 patients) or placebo (161 patients) once daily. Development of new diabetes was recorded in 98 patients: in 56 (37.0%) from the placebo group vs. 42 (27.1%) from the bezafibrate group, (P log-rank=0.01). The median time (interquartile range) until onset of new diabetes was significantly delayed in patients on bezafibrate when compared with those on placebo: 4.0 (2.1-5.0) vs. 2.0 (0.5-3.5) years, P=0.002. Multivariable analysis identified bezafibrate treatment as an independent predictor of reduced risk of new diabetes with hazard ratio (HR) 0.59 [95% confidence interval (CI) 0.39-0.91]. Other significant variables associated with future overt type 2 diabetes in obese patients were triglycerides (50 mg/dL increment) with HR 1.15 (95% CI 1.02-1.28) and fasting glucose (10 mg/dL increment) with HR 2.27 (95% CI 1.83-2.81). CONCLUSION: Bezafibrate, when compared with placebo, reduced the incidence and delayed the onset of type 2 diabetes in obese patients over a long-term follow-up period.

Adult↗
PubMed2006

Effects of bezafibrate in patients with chronic hepatitis C virus infection: combination with interferon and ribavirin.

An association of hepatitis C virus (HCV) with low-density lipoproteins (LDL) in serum of patients with chronic hepatitis C (CHC) has been suggested. We conducted a prospective study in CHC patients complicated with hyperlipidaemia, to examine whether bezafibrate, which is commonly used for treatment of hyperlipidaemia, reduces serum HCV-RNA titre and improves liver dysfunction. Fifteen patients received daily oral bezafibrate treatment (400 mg/day) for 8 weeks, and its effects on serum lipids, transaminases, HCV-RNA titres, and HCV-RNA titres bound to LDL were evaluated. Fifteen untreated patients with CHC and hyperlipidaemia were used as controls. The mean serum alanine aminotransferase levels and HCV-RNA titres significantly decreased at the end of bezafibrate therapy in the treated group (105 +/- 34 to 80 +/- 32 IU/L, P = 0.02 and 2.23 +/- 2.71 to 1.78 +/- 2.38 x 10(7) copies/mL, P < 0.01 respectively), but no changes were observed in the control group. Serum HCV-RNA titres bound to LDL, as quantified by immunoprecipitation using anti-LDL antibody, also decreased in all 15 treated patients [5.55 +/- 6.59 to 1.07 +/- 1.58 x 10(6) copies/ml, P < 0.01 (mean reduction rate was -78.5 +/- 17.0%)]. Sucrose density-gradient ultracentrifugation study revealed that HCV-RNA-decreased density fractions after the bezafibrate were identical to LDL-density fractions (1.015-1.062 g/mL). Eight CHC patients were treated with bezafibrate, interferon, and ribavirin triple therapy for 32 weeks, and four patients achieved sustained virological response to therapy. This pilot study provides further evidence of an association between HCV and LDL in serum and suggests the potential usefulness of bezafibrate as an anti-HCV reagent for the treatment of CHC patients.

Adult↗
PubMedDate not supplied

Double-blind placebo-controlled study of the effects of bezafibrate on blood lipids, lipoproteins, and fibrinogen in hyperlipidaemic type 1 diabetes mellitus.

The effects of bezafibrate 400 mg day-1 or placebo administered for 3 months, were compared in 36 patients with stable Type 1 diabetes and hypercholesterolaemia and/or hypertriglyceridaemia. Baseline characteristics of the 17 bezafibrate- and 19 placebo-treated patients were comparable in most respects with the exception of concentrations of fasting serum triglycerides and blood glucose which were lower (NS) and plasma fibrinogen which were higher (p less than 0.05), in those later treated with bezafibrate. Serum cholesterol concentrations decreased after 3 months bezafibrate treatment (from 7.1(0.2) (SE) to 6.3 (0.3) mmol l-1, p less than 0.05), predominantly due to a reduction in low density lipoprotein (LDL) cholesterol (from 4.8(0.3) to 4.2(0.3) mmol l-1, p less than 0.05). Over the same period bezafibrate reduced serum triglycerides from 1.78 (95% Cl 1.23-2.57) to 1.26(1.02-2.09) mmol l-1 (p less than 0.05), and plasma fibrinogen from 4.1(0.2) to 2.9(0.2) g l-1, p less than 0.001. Serum apolipoprotein B and apolipoprotein (a) showed no statistically significant changes. Overall there was no change in high density lipoprotein (HDL) cholesterol. However, in patients who were initially hypertriglyceridaemic there was significant increase in the cholesterol content of HDL and the HDL2-cholesterol subfraction (both p less than 0.05). After 3 months treatment with bezafibrate, fasting blood glucose levels were reduced from 8.5(1.1) to 6.4(0.7) mmol l-1, p less than 0.05, without any change in glycosylated haemoglobin (9.2(0.4) to 9.1(0.5)%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Normal oxidative stress and enhanced lipoprotein resistance to in vitro oxidation in hypertriglyceridemia: effects of bezafibrate therapy.

Although there is evidence that hyperlipidemia and predominance of small dense low density lipoproteins (LDLs) are associated with increased oxidative stress, the oxidation status in patients with hypertriglyceridemia (HTG) has not been studied in detail. Therefore, we studied urinary levels of F(2)-isoprostanes (8-isoprostaglandin F(2alpha) and 2,3-dinor-5,6-dihydro-8-isoprostaglandin F(2alpha)) and susceptibility of very low density lipoproteins (VLDLs) and LDLs to oxidation ex vivo in 18 patients with endogenous HTG and 20 matched control subjects. In addition, the effects of 6 weeks of bezafibrate therapy were assessed in a double-blind, placebo-controlled, crossover trial. Urinary levels of F(2)-isoprostanes were similar in the HTG and normolipidemic group. Bezafibrate caused an increase in 8-isoprostaglandin F(2alpha) (762+/-313 versus 552+/-245 ng/24 h for bezafibrate and placebo therapy, respectively; P=0.03), whereas 2,3-dinor-5, 6-dihydro-8-isoprostaglandin F(2alpha) levels tended to be increased (1714+/-761 versus 1475+/-606 ng/24 h for bezafibrate and placebo therapy, respectively; P=0.11). VLDLs and LDLs were more resistant to copper-induced oxidation in patients with HTG than in control subjects. Bezafibrate reversed the oxidation resistance to the normal range. In conclusion, these results indicate the following: (1) HTG is associated with normal in vivo oxidative stress and enhanced ex vivo resistance of lipoproteins to oxidation. (2) Bezafibrate reduces the resistance of lipoproteins to copper-induced oxidation and enhances oxidative stress in HTG patients.

Bezafibrate↗
PubMed1985

Comparative study of bezafibrate and fenofibrate in patients with primary hyperlipoproteinaemia.

A study was carried out in 40 patients with primary hyperlipoproteinaemia to compare the efficacy and tolerance of bezafibrate and fenofibrate, combined with a dietary regimen, in reducing lipid levels. Patients were allocated at random to receive treatment for 4 months with either 600 mg bezafibrate or 300 mg fenofibrate per day. Efficacy of treatment was assessed from measurement before and after treatment of the levels of total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides and blood glucose. Tolerance was monitored by monthly clinical examinations and routine investigation of blood chemistry and urinalysis before and after treatment. The results indicated that bezafibrate was a more effective normolipaemic agent than fenofibrate. Whilst both drugs reduced triglyceride levels significantly, only in the bezafibrate group were they decreased to within the risk-free range. Bezafibrate also produced a significant decrease in total cholesterol and LDL-cholesterol to near the risk-free level and an increase in HDL-cholesterol. With fenofibrate, total cholesterol and LDL-cholesterol levels remained within the range necessitating treatment and HDL-cholesterol showed little if any change. Although there were decreases in alkaline phosphatase and significant decreases in gamma-glutamyl transpeptidase levels in both groups after treatment, there was a tendency for SGPT, SGOT, total bilirubin and direct bilirubin levels to increase after fenofibrate but to decrease after bezafibrate.

Adult↗
PubMed2003

Bezafibrate improves hypertension and insulin sensitivity in humans.

We examined cellular membrane fatty acid composition and insulin sensitivity in patients with mild essential hypertension and hyperlipidemia, and investigated whether bezafibrate, a lipid-lowering drug, could improve elevated blood pressure and insulin sensitivity in these subjects by ameliorating cellular membrane fatty acid composition. Twenty-seven subjects were recruited. Twelve men with mild essential hypertension [systolic blood pressure (SBP) between 140 mmHg and 160 mmHg] and hypertriglyceridemia (plasma triglyceride concentration over 150 mg/dl) were designated the HL group. Fifteen men with mild essential hypertension and normotriglyceridemia (plasma triglyceride concentration below 150 mg/dl) were designated the NL group. Subjects in the HL group were given bezafibrate 400 mg/dl and those in the NL group were given placebo for 3 months. Bezafibrate significantly reduced SBP (140 +/- 2.6 to 131.8 +/- 2.6 mmHg, mean +/- SEM), diastolic blood pressure (DBP) (87.8 +/- 2.0 to 82.8 +/- 2.6 mmHg), fasting plasma triglyceride concentration (225.5 +/- 23.5 to 102.9 +/- 10.9 mg/dl), fasting plasma insulin concentration (9.6 +/- 0.8 to 7.1 +/- 0.8 microU/ml), and homeostasis model assessment scores (HOMA-R, 2.4 +/- 0.2 to 1.7 +/- 0.2), and significantly improved the insulin sensitivity index (56.0 +/- 3.0 to 70.7 +/- 4.8 mg x l2/mmol x mU x min) in the HL group. Regarding erythrocyte membrane fatty acid composition, bezafibrate reduced the percentages of saturated fatty acids (SFA) and increased the percentage of polyunsaturated fatty acids (PUFA). Plasma triglyceride concentrations were positively correlated with HOMA-R (r = 0.50, p < 0.01) and SFA (r = 0.39, p < 0.05), and negatively correlated with PUFA (r = -0.45, p < 0.05) before administration of placebo or bezafibrate. In conclusion, an improvement of hyperlipidemia by bezafibrate may be attributed to reduction of blood pressure and amelioration of insulin sensitivity. Abnormalities in membrane lipid composition may play an important role in these metabolic disorders.

Adult↗
PubMed1997

Morphometry of abnormal peroxisomes induced by withdrawal of bezafibrate, a hypolipidemic drug in male rat hepatocytes.

Peroxisomes containing fibrillar structures were induced after 1 week withdrawal of bezafibrate, a peroxisome proliferator. In this report, the relation between the duration of bezafibrate treatment and the induction of abnormal peroxisomes in rat hepatocytes was studied morphometrically. The abnormal peroxisomes did not appear during 3 to 90 days of treatment with bezafibrate, but they appeared after 1 week withdrawal of it. The number and frequency of abnormal peroxisomes were prominent in 3, 7, and 14 days of treatment followed by 1 week of withdrawal of bezafibrate. It was evident that the frequency of abnormal peroxisomes decreased with 30-90 days administration of bezafibrate. This means that long-term (30-90 days) treatment with bezafibrate suppresses the induction of abnormal peroxisomes.

Animals↗
PubMed1990

Lowering of plasma glucose concentrations with bezafibrate in patients with moderately controlled NIDDM.

The goal of this study was to investigate whether treatment with bezafibrate improves glucose tolerance in non-insulin-dependent diabetes mellitus (NIDDM). The study included 37 NIDDM patients with HbA1 concentrations greater than 8.5% and normal kidney and liver function who were being treated with diet alone or diet together with a sulfonylurea drug. One patient withdrew because of constipation. At randomization and after 3 mo of treatment, patients were given a standard mixed-test-meal tolerance test (MTT; 500 cal) after an overnight fast, and plasma glucose, insulin, C-peptide, metabolite, nonesterified fatty acid (NEFA), and triglyceride concentrations were measured at 15- to 30-min intervals. Serum lipid, HbA1, and fructosamine concentrations were measured at monthly intervals. Glucose, NEFA, and triglyceride concentrations were significantly lower throughout the second MTT in bezafibrate patients (P less than 0.01-0.001) but not in the placebo group. Fasting serum insulin and C-peptide levels, but not postprandial concentrations, were reduced only in bezafibrate patients (P less than 0.05). After 3 mo, mean fasting serum triglyceride concentrations fell from 2.2 to 1.4 mM (P less than 0.001), total serum cholesterol concentrations from 6.3 to 5.5 mM (P less than 0.001), and low-density lipoprotein cholesterol concentrations from 4.2 to 3.5 mM (P less than 0.001) in bezafibrate patients. There were no changes in serum lipid concentrations in the placebo group. Treatment of patients with moderately controlled NIDDM with bezafibrate improves glucose tolerance and the serum lipid profile. Bezafibrate treatment may be a useful adjunct to hypoglycemic therapy in patients with NIDDM.

Bezafibrate↗
PubMed1997

Influence of apolipoprotein E polymorphism on bezafibrate treatment response in dyslipidemic patients.

To examine the significance of apolipoprotein E (apo E) polymorphism in the hypolipidemic effect of bezafibrate, we evaluated the influence of different apo E phenotypes on serum lipid response to bezafibrate treatment in 58 dyslipidemic patients with WHO phenotypes of IIb, IV, or isolated hypo HDL cholesterolemia. Patients were categorized into one of three groups according to apo E phenotypes of E2 (E2/3, n=5), E3 (E3/3, n=35), and E4 (E3/4 and E4/4, n=18). After 3 months daily administration of 400 mg bezafibrate, serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC) levels changed on average in the E3 group [-8.0%; p<0.05 and +1.1%; not significant (ns), respectively], the E2 group (-18.3%; p<0.005 and -26.9%; p<0.05, respectively) and the E4 group (+3.8%; ns and +10.1%; ns, respectively). The changes in TC and LDLC levels in the E4 group was significantly less effective compared with those in the E3 (p<0.05) and E2 groups (p<0.01). Bezafibrate induced a reduction in serum triglyceride (TG) levels in the E3 group (-50.1%; p<0.0001), the E2 group (-46.9%; p<0.05) and the E4 group (-44.8%; p<0.005). An increase in high-density lipoprotein cholesterol (HDLC) levels was also observed in the E3 group (+27.5%; p<0.0001), the E2 group (+35.0%; ns) and the E4 group (+38.8%; p<0.005). However, there was no significant difference in the changes of TG and HDLC levels between the groups. These results suggest an important role of apo E polymorphism in modulating serum lipid response to bezafibrate, and phenotyping of apo E helps predict the therapeutic effect of bezafibrate treatment.

Aged↗
PubMed1992

[Bezafibrate myopathy in two patients with chronic renal failure].

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.

Aged↗
PubMed1990

Bezafibrate retard in patients with insulin-dependent diabetes: effect on serum lipoproteins, fibrinogen, and glycemic control.

The effects of a sustained-release preparation of bezafibrate (Bezalip Mono) 400 mg once daily and placebo administered for 3 months were compared in 36 patients with stable type 1 diabetes and hypercholesterolemia and/or hypertriglyceridemia. There was a significant decrease in fasting glucose levels with bezafibrate, but not in glycosylated hemoglobin. The serum cholesterol concentration decreased on bezafibrate [from 7.1 +/- 0.2 (mean +/- SEM) to 6.3 +/- 0.3 mmol/L; p less than 0.05] predominantly due to a reduction in low-density lipoprotein (LDL) cholesterol [from 4.8 +/- 0.3 to 4.2 +/- 0.3 mmol/L; p less than 0.05. There was also a decrease in fasting serum triglycerides with bezafibrate [1.82 to 1.26 mmol/L (geometric mean)] and in very-low-density lipoprotein (VLDL) cholesterol. Plasma fibrinogen decreased significantly with bezafibrate (from 4.1 +/- 0.2 to 2.9 +/- 0.2 g/L; p less than 0.001). Serum apolipoproteins B and A showed no statistically significant changes. Overall, there was no change in high-density lipoprotein (HDL). However, in patients who were initially hypertriglyceridemic, there was a significant increase in the cholesterol content of total HDL and the HDL2 subfraction (both p less than 0.05). It is concluded that in insulin-dependent diabetic patients with hyperlipidemia, bezafibrate is effective in lowering both serum VLDL and LDL. In addition, it has a potentially important action in decreasing plasma fibrinogen levels.

Adolescent↗
PubMed1992

Long-term treatment of severe familial hypercholesterolemia in children: effect of sitosterol and bezafibrate.

Seven prepubertal children (age range 5.3 to 10.8 years) with severe heterozygous familial hypercholesterolemia (serum cholesterol concentration 416 +/- 85 mg/dL and low-density lipoprotein [LDL] cholesterol concentration 360 +/- 90 mg/dL) were first treated by dietary intervention, second by sitosterol (3 x 2 g/d), and third by bezafibrate (2 x 200 mg/d). Each treatment period lasted 3 months. Subsequently, a treatment combining half the dose of sitosterol and bezafibrate was administered for the following 24 months. Diet alone reduced total and LDL cholesterol values by 4.5% (not significant) and 6.6% (P less than .05), respectively. Sitosterol lowered total and LDL cholesterol values by 17% (P less than .05) when compared with diet alone. Compared with sitosterol, bezafibrate produced a more pronounced effect on total and LDL cholesterol values (-18% and -28%, P less than .05), and high-density lipoprotein cholesterol concentration increased significantly from 48 mg/dL to 55 mg/dL. Combined treatment with half the dose each of sitosterol and bezafibrate was as effective as the higher dose of bezafibrate, and reduction averaged almost 40% and 50% for total and LDL cholesterol values; this lipid-lowering effect persisted for the next 24 months. Laboratory safety parameters and physical examination revealed no obvious side effects. This study indicates that the combination of sitosterol (3 x 1 g/d) plus bezafibrate (1 x 200 mg/d) is an alternate, acceptable, safe, and effective therapeutic approach for treatment of severe hypercholesterolemia in children with high-risk familial hypercholesterolemia.

Apolipoprotein A-I↗
PubMed1987

Effect of bezafibrate and colestyramine in patients with primary hypercholesterolemia.

40 patients with primary hypercholesterolemia were included in a randomized cross-over trial comparing effects and tolerance of bezafibrate (Cedur) (200 mg t.i.d.) and colestyramine (4 g t.i.d.). Gastrointestinal side-effects led to the discontinuation of colestyramine in 11 patients. No adverse events were observed with bezafibrate. Both drugs had similar effects on total and low density lipoprotein cholesterol (bezafibrate: -15% and -12%, respectively; colestyramine: -10% and -11%, respectively). While the high density lipoprotein-increasing effect of bezafibrate was more marked (+20% vs. +14%), triglycerides and very low density lipoprotein cholesterol were lowered by bezafibrate (-22% and -27%, respectively) and tended to increase with colestyramine (+11% and +10%, respectively). In the light of results of a multicenter primary prevention trial bezafibrate also should have a protective effect on coronary heart disease. This, however, has to be proven in longterm prospective trials.

Bezafibrate↗
PubMed1979

[A comparison of bezafibrate and clofibrate in type II B and type IV hyperlipoproteinemia].

In 36 patients with primary hyperlipoproteinemia of type II B or IV the effect of bezafibrate, a new derivate of clofibrate, has been compared with the effect of clofibrate. In an open cross-over-study the effect of 1.5 g clofibrate p.d. has been compared with that of 450 mg bezafibrate p.d. for several months. The effect of bezafibrate on plasma triglyceride concentration and plasma cholesterol concentration was more pronounced than that of clofibrate. This difference was statistically significantly only in the concentration of plasma triglycerides of type IV patients. It is obvious that the difference between bezafibrate and clofibrate would have been more pronounced if the dose of bezafibrate had been in the optimal range. Serious side-effects caused by bezafibrate could not be observed.

Adult↗
PubMedDate not supplied

Lovastatin versus bezafibrate for hyperlipemia treatment after heart transplantation.

BACKGROUND: Elevation in total and low-density lipoprotein cholesterol levels and a decrease in high-density lipoprotein cholesterol plasma concentrations are common in heart transplant recipients. The pathogenesis of this hyperlipemia after heart transplantation is complex. Currently available antilipemic agents are difficult to use because their adverse effects are potentiated by immunosuppressor treatment. The present investigation was carried out to test the safety and efficacy of lovastatin and bezafibrate in 18 patients with hyperlipemia after heart transplantation. METHODS: In this crossover study, after 3 months of dietary recommendations, the subjects were randomly assigned to an 8-week period of lovastatin treatment (10 mg/day) followed by an additional 8-week period of treatment with bezafibrate (400 mg/day) or vice versa. The two treatments were separated by an 8-week washout period. RESULTS: Both drugs reduced total and low-density lipoprotein cholesterol and apoprotein B concentrations. High-density lipoprotein cholesterol was only increased with bezafibrate. The total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratios were decreased under both treatments, but these changes were greater with bezafibrate. Apo AI levels increased with lovastatin. Bezafibrate produced a rise in high-density lipoprotein cholesterol and reduced total and very low-density lipoprotein triglycerides and very low-density lipoprotein cholesterol. Both drugs decreased intermediate density lipoprotein cholesterol and triglyceride levels, but the effect of bezafibrate on intermediate-density lipoprotein triglycerides was significantly greater. The two drugs were well tolerated and liver enzymes, creatine kinase, and renal function remained stable.

Adult↗