The Experts below are selected from a list of 14253 Experts worldwide ranked by ideXlab platform
S Dejager - One of the best experts on this subject based on the ideXlab platform.
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effect of combined fluvastatin Fenofibrate therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia
American Journal of Cardiology, 2000Co-Authors: Michel Farnier, S DejagerAbstract:This double-blind study was designed to assess the efficacy and safety of fluvastatin-Fenofibrate combination therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia (low-density lipoprotein [LDL] cholesterol > or =190 mg/dl [4.9 mmol/L], triglycerides < or =350mg/dl [3.9 mmol/l]). After a 10-week placebo and dietary baseline period, 102 patients were randomized to receive micronized Fenofibrate 200 mg, fluvastatin 20 mg plus micronized Fenofibrate 200 mg, or fluvastatin 40 mg plus micronized Fenofibrate 200 mg. At week 16, Fenofibrate 200 mg alone lowered LDL cholesterol from baseline by 21% compared with 32% for fluvastatin 20 mg plus Fenofibrate 200 mg and 41% for fluvastatin 40 mg plus Fenofibrate 200 mg (p <0.001). Triglycerides decreased by 29% with Fenofibrate 200 mg alone, 39% with fluvastatin 20 mg plus Fenofibrate 200 mg, and 40% with fluvastatin 40 mg plus Fenofibrate 200 mg (p <0.05). Safety was assessed by recording adverse events and measuring clinical laboratory parameters. The adverse event profile was similar for the 3 treatment groups. One patient withdrew due to an increase in transaminase levels. No significant increase in creatine phosphokinase levels was observed with combination therapy. In conclusion, the addition of fluvastatin to micronized Fenofibrate results in substantial improvement in atherogenic plasma lipids and is well tolerated.
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Effect of combined fluvastatin-Fenofibrate therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia
The American journal of cardiology, 2000Co-Authors: Michel Farnier, S DejagerAbstract:This double-blind study was designed to assess the efficacy and safety of fluvastatin-Fenofibrate combination therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia (low-density lipoprotein [LDL] cholesterol > or =190 mg/dl [4.9 mmol/L], triglycerides < or =350mg/dl [3.9 mmol/l]). After a 10-week placebo and dietary baseline period, 102 patients were randomized to receive micronized Fenofibrate 200 mg, fluvastatin 20 mg plus micronized Fenofibrate 200 mg, or fluvastatin 40 mg plus micronized Fenofibrate 200 mg. At week 16, Fenofibrate 200 mg alone lowered LDL cholesterol from baseline by 21% compared with 32% for fluvastatin 20 mg plus Fenofibrate 200 mg and 41% for fluvastatin 40 mg plus Fenofibrate 200 mg (p
James D. Best - One of the best experts on this subject based on the ideXlab platform.
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effect of Fenofibrate on uric acid and gout in type 2 diabetes a post hoc analysis of the randomised controlled field study
The Lancet Diabetes & Endocrinology, 2018Co-Authors: Boris Waldman, Timothy M. E. Davis, James D. Best, David R. Sullivan, Alicia J. Jenkins, Jeanclaude Ansquer, Neil Mcgill, Luke BuizenAbstract:Summary Background Gout is a painful disorder and is common in type 2 diabetes. Fenofibrate lowers uric acid and reduces gout attacks in small, short-term studies. Whether Fenofibrate produces sustained reductions in uric acid and gout attacks is unknown. Methods In the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial, participants aged 50–75 years with type 2 diabetes were randomly assigned to receive either co-micronised Fenofibrate 200 mg once per day or matching placebo for a median of 5 years follow-up. We did a post-hoc analysis of recorded on-study gout attacks and plasma uric acid concentrations according to treatment allocation. The outcomes of this analysis were change in uric acid concentrations and risk of on-study gout attacks. The FIELD study is registered with ISRCTN, number ISRCTN64783481. Findings Between Feb 23, 1998, and Nov 3, 2000, 9795 patients were randomly assigned to Fenofibrate (n=4895) or placebo (n=4900) in the FIELD study. Uric acid concentrations fell by 20·2% (95% CI 19·9–20·5) during the 6-week active Fenofibrate run-in period immediately pre-randomisation (a reduction of 0·06 mmol/L or 1 mg/dL) and remained −20·1% (18·5–21·7, p Interpretation Fenofibrate lowered uric acid concentrations by 20%, and almost halved first on-study gout events over 5 years of treatment. Fenofibrate could be a useful adjunct for preventing gout in diabetes. Funding None.
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Effects of Fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study
Diabetologia, 2010Co-Authors: Timothy M. E. Davis, Ru Ting, James D. Best, Mark Donoghoe, Paul L. Drury, David R. Sullivan, Alicia J. Jenkins, Rachel O'connell, Malcolm J. Whiting, Paul GlasziouAbstract:Aims/hypothesis Fenofibrate caused an acute, sustained plasma creatinine increase in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies. We assessed Fenofibrate’s renal effects overall and in a FIELD washout sub-study. Methods Type 2 diabetic patients (n=9,795) aged 50 to 75 years were randomly assigned to Fenofibrate (n=4,895) or placebo (n=4,900) for 5 years, after 6 weeks Fenofibrate
Philip Mathew - One of the best experts on this subject based on the ideXlab platform.
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Effect of Colesevelam HCl on Single-Dose Fenofibrate Pharmacokinetics
Clinical Pharmacokinetics, 2004Co-Authors: Michael R. Jones, Brian A. Baker, Philip MathewAbstract:Objective The primary aim of this study was to determine whether there is an effect of colesevelam HCl (WelChol®; Sankyo Pharma Inc., Parsippany, NJ, USA) on fenofibric acid (active metabolite of Fenofibrate, TriCor®, Abbott Laboratories, North Chicago, IL, USA) pharmacokinetics following single-dose Fenofibrate when colesevelam HCl and Fenofibrate are administered concomitantly, or when colesevelam HCl is administered 4 hours following Fenofibrate therapy. Methods Thirty healthy volunteers were enrolled in a randomised, open-label, three-way crossover, drug interaction study. Subjects received one of three treatments at each of three dose administration periods: (i) treatment A -Fenofibrate 160mg plus colesevelam HCl 3750mg (6 × 625mg tablets) administered with breakfast; (ii) treatment B - Fenofibrate 160mg administered with breakfast, followed 4 hours later by colesevelam HC1 3750mg (6 × 625mg tablets) administered with lunch; or (iii) treatment C - Fenofibrate 160mg administered with breakfast. Treatments were separated by a 10-day washout period. Blood samples were collected at predetermined time intervals, both before and after drug administration. Plasma concentrations of Fenofibrate and fenofibric acid were measured using a validated liquid chromatography/mass spectroscopy/mass spectroscopy method. Results Area under the concentration-time curve (AUC) from time zero to the timepoint of the lowest quantifiable concentration (AUCt), AUC from time zero to infinity (AUC_∞) and maximum plasma concentration (C_max) for fenofibric acid were 92.1%, 93.9% and 79.8%, respectively, of control values when colesevelam HC1 and Fenofibrate were coadministered with breakfast; and 91.9%, 93.9% and 99.1%, respectively, when Fenofibrate was administered followed 4 hours later by administration of colesevelam HC1. The 90% confidence intervals for the ratios of geometric means for AUC_t, AUC_∞ and C_max comparing the three treatments were contained within the 80–125% equivalence range, with the exception of C_max for treatment A. Coadministration of Fenofibrate with colesevelam HCl resulted in an approximate 20% reduction in C_max of the active metabolite (fenofibric acid). There were no significant differences in the time to C_max, elimination rate constant or elimination half-life between any of the treatment groups. Conclusions Colesevelam HCl had no significant effect on Fenofibrate bioavailability when administered either concomitantly with Fenofibrate or 4 hours after Fenofibrate.
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effect of colesevelam hcl on single dose Fenofibrate pharmacokinetics
Clinical Pharmacokinectics, 2004Co-Authors: Michael R. Jones, Brian A. Baker, Philip MathewAbstract:The primary aim of this study was to determine whether there is an effect of colesevelam HCl (WelChol®; Sankyo Pharma Inc., Parsippany, NJ, USA) on fenofibric acid (active metabolite of Fenofibrate, TriCor®, Abbott Laboratories, North Chicago, IL, USA) pharmacokinetics following single-dose Fenofibrate when colesevelam HCl and Fenofibrate are administered concomitantly, or when colesevelam HCl is administered 4 hours following Fenofibrate therapy. Thirty healthy volunteers were enrolled in a randomised, open-label, three-way crossover, drug interaction study. Subjects received one of three treatments at each of three dose administration periods: (i) treatment A -Fenofibrate 160mg plus colesevelam HCl 3750mg (6 × 625mg tablets) administered with breakfast; (ii) treatment B - Fenofibrate 160mg administered with breakfast, followed 4 hours later by colesevelam HC1 3750mg (6 × 625mg tablets) administered with lunch; or (iii) treatment C - Fenofibrate 160mg administered with breakfast. Treatments were separated by a 10-day washout period. Blood samples were collected at predetermined time intervals, both before and after drug administration. Plasma concentrations of Fenofibrate and fenofibric acid were measured using a validated liquid chromatography/mass spectroscopy/mass spectroscopy method. Area under the concentration-time curve (AUC) from time zero to the timepoint of the lowest quantifiable concentration (AUCt), AUC from time zero to infinity (AUC∞) and maximum plasma concentration (Cmax) for fenofibric acid were 92.1%, 93.9% and 79.8%, respectively, of control values when colesevelam HC1 and Fenofibrate were coadministered with breakfast; and 91.9%, 93.9% and 99.1%, respectively, when Fenofibrate was administered followed 4 hours later by administration of colesevelam HC1. The 90% confidence intervals for the ratios of geometric means for AUCt, AUC∞ and Cmax comparing the three treatments were contained within the 80–125% equivalence range, with the exception of Cmax for treatment A. Coadministration of Fenofibrate with colesevelam HCl resulted in an approximate 20% reduction in Cmax of the active metabolite (fenofibric acid). There were no significant differences in the time to Cmax, elimination rate constant or elimination half-life between any of the treatment groups. Colesevelam HCl had no significant effect on Fenofibrate bioavailability when administered either concomitantly with Fenofibrate or 4 hours after Fenofibrate.
Michel Farnier - One of the best experts on this subject based on the ideXlab platform.
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effect of combined fluvastatin Fenofibrate therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia
American Journal of Cardiology, 2000Co-Authors: Michel Farnier, S DejagerAbstract:This double-blind study was designed to assess the efficacy and safety of fluvastatin-Fenofibrate combination therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia (low-density lipoprotein [LDL] cholesterol > or =190 mg/dl [4.9 mmol/L], triglycerides < or =350mg/dl [3.9 mmol/l]). After a 10-week placebo and dietary baseline period, 102 patients were randomized to receive micronized Fenofibrate 200 mg, fluvastatin 20 mg plus micronized Fenofibrate 200 mg, or fluvastatin 40 mg plus micronized Fenofibrate 200 mg. At week 16, Fenofibrate 200 mg alone lowered LDL cholesterol from baseline by 21% compared with 32% for fluvastatin 20 mg plus Fenofibrate 200 mg and 41% for fluvastatin 40 mg plus Fenofibrate 200 mg (p <0.001). Triglycerides decreased by 29% with Fenofibrate 200 mg alone, 39% with fluvastatin 20 mg plus Fenofibrate 200 mg, and 40% with fluvastatin 40 mg plus Fenofibrate 200 mg (p <0.05). Safety was assessed by recording adverse events and measuring clinical laboratory parameters. The adverse event profile was similar for the 3 treatment groups. One patient withdrew due to an increase in transaminase levels. No significant increase in creatine phosphokinase levels was observed with combination therapy. In conclusion, the addition of fluvastatin to micronized Fenofibrate results in substantial improvement in atherogenic plasma lipids and is well tolerated.
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Effect of combined fluvastatin-Fenofibrate therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia
The American journal of cardiology, 2000Co-Authors: Michel Farnier, S DejagerAbstract:This double-blind study was designed to assess the efficacy and safety of fluvastatin-Fenofibrate combination therapy compared with Fenofibrate monotherapy in severe primary hypercholesterolemia (low-density lipoprotein [LDL] cholesterol > or =190 mg/dl [4.9 mmol/L], triglycerides < or =350mg/dl [3.9 mmol/l]). After a 10-week placebo and dietary baseline period, 102 patients were randomized to receive micronized Fenofibrate 200 mg, fluvastatin 20 mg plus micronized Fenofibrate 200 mg, or fluvastatin 40 mg plus micronized Fenofibrate 200 mg. At week 16, Fenofibrate 200 mg alone lowered LDL cholesterol from baseline by 21% compared with 32% for fluvastatin 20 mg plus Fenofibrate 200 mg and 41% for fluvastatin 40 mg plus Fenofibrate 200 mg (p
David R. Sullivan - One of the best experts on this subject based on the ideXlab platform.
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effect of Fenofibrate on uric acid and gout in type 2 diabetes a post hoc analysis of the randomised controlled field study
The Lancet Diabetes & Endocrinology, 2018Co-Authors: Boris Waldman, Timothy M. E. Davis, James D. Best, David R. Sullivan, Alicia J. Jenkins, Jeanclaude Ansquer, Neil Mcgill, Luke BuizenAbstract:Summary Background Gout is a painful disorder and is common in type 2 diabetes. Fenofibrate lowers uric acid and reduces gout attacks in small, short-term studies. Whether Fenofibrate produces sustained reductions in uric acid and gout attacks is unknown. Methods In the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial, participants aged 50–75 years with type 2 diabetes were randomly assigned to receive either co-micronised Fenofibrate 200 mg once per day or matching placebo for a median of 5 years follow-up. We did a post-hoc analysis of recorded on-study gout attacks and plasma uric acid concentrations according to treatment allocation. The outcomes of this analysis were change in uric acid concentrations and risk of on-study gout attacks. The FIELD study is registered with ISRCTN, number ISRCTN64783481. Findings Between Feb 23, 1998, and Nov 3, 2000, 9795 patients were randomly assigned to Fenofibrate (n=4895) or placebo (n=4900) in the FIELD study. Uric acid concentrations fell by 20·2% (95% CI 19·9–20·5) during the 6-week active Fenofibrate run-in period immediately pre-randomisation (a reduction of 0·06 mmol/L or 1 mg/dL) and remained −20·1% (18·5–21·7, p Interpretation Fenofibrate lowered uric acid concentrations by 20%, and almost halved first on-study gout events over 5 years of treatment. Fenofibrate could be a useful adjunct for preventing gout in diabetes. Funding None.
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Effects of Fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study
Diabetologia, 2010Co-Authors: Timothy M. E. Davis, Ru Ting, James D. Best, Mark Donoghoe, Paul L. Drury, David R. Sullivan, Alicia J. Jenkins, Rachel O'connell, Malcolm J. Whiting, Paul GlasziouAbstract:Aims/hypothesis Fenofibrate caused an acute, sustained plasma creatinine increase in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) and Action to Control Cardiovascular Risk in Diabetes (ACCORD) studies. We assessed Fenofibrate’s renal effects overall and in a FIELD washout sub-study. Methods Type 2 diabetic patients (n=9,795) aged 50 to 75 years were randomly assigned to Fenofibrate (n=4,895) or placebo (n=4,900) for 5 years, after 6 weeks Fenofibrate
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plasma pcsk9 concentrations correlate with ldl and total cholesterol in diabetic patients and are decreased by Fenofibrate treatment
Clinical Chemistry, 2008Co-Authors: David R. Sullivan, Gilles Lambert, Nicolas Ancellin, Francesca Charlton, Daniel Comas, Julia Pilot, Anthony C Keech, Sanjay Patel, Jeffrey S CohnAbstract:Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes the degradation of the LDL receptor (LDLr) in hepatocytes, and its expression in mouse liver has been shown to decrease with Fenofibrate treatment. Methods: We developed a sandwich ELISA using recombinant human PCSK9 protein and 2 affinity-purified polyclonal antibodies directed against human PCSK9. We measured circulating PCSK9 concentrations in 115 diabetic patients from the FIELD (Fenofibrate Intervention and Event Lowering in Diabetes) study before and after Fenofibrate treatment. Results: We found that plasma PCSK9 concentrations correlate with total ( r = 0.45, P = 0.006) and LDL ( r = 0.54, P = 0.001) cholesterol but not with triglycerides or HDL cholesterol concentrations in that cohort. After 6 weeks of treatment with comicronized Fenofibrate (200 mg/day), plasma PCSK9 concentrations decreased by 8.5% ( P = 0.041 vs pretreatment). This decrease correlated with the efficacy of Fenofibrate, as judged by a parallel reduction in plasma triglycerides ( r = 0.31, P = 0.015) and LDL cholesterol concentrations ( r = 0.27, P = 0.048). Conclusions: We conclude that this decrease in PCSK9 explains at least in part the LDL cholesterol–lowering effects of Fenofibrate. Fenofibrate might be of interest to further reduce cardiovascular risk in patients already treated with a statin.