Page last updated: 2024-10-27

fenofibrate and Disease Exacerbation

fenofibrate has been researched along with Disease Exacerbation in 46 studies

Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE

Research Excerpts

ExcerptRelevanceReference
"Experimental studies suggest that fenofibrate prevents abdominal aortic aneurysm (AAA) development by lowering aortic osteopontin (OPN) concentration and reducing the number of macrophages infiltrating the aortic wall."9.34A Randomised Controlled Trial Assessing the Effects of Peri-operative Fenofibrate Administration on Abdominal Aortic Aneurysm Pathology: Outcomes From the FAME Trial. ( Cavaye, D; Golledge, J; Jaeggi, R; Jenkins, JS; Lazzaroni, SM; Moran, CS; Morton, SK; Moxon, JV; Pinchbeck, JL; Quigley, F; Reid, CM; Rowbotham, SE, 2020)
"The purpose of this study is to study the benefit of addition of oral fenofibrate to the current regimen of diabetic macular edema (DME) management and quantify its effect on macular thickness and visual function in DME."9.27Efficiency of fenofibrate in facilitating the reduction of central macular thickness in diabetic macular edema. ( Hande, P; Murali, S; Shetty, J; Srinivasan, S, 2018)
"The combination of antihypertensive agents with micronized fenofibrate can effectively prevent the progression of carotid atherosclerosis and reduce the incidence of stroke in patients with essential hypertension."9.12Inhibitory effects of micronized fenofibrate on carotid atherosclerosis in patients with essential hypertension. ( Meng, QH; Su, G; Zhu, S, 2006)
"Improvement in lipid profiles with fenofibrate in patients with type 2 diabetes was associated with reduced progression from normal albumin excretion to microalbuminuria."9.11Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS). ( Ansquer, JC; Foucher, C; Rattier, S; Steiner, G; Taskinen, MR, 2005)
"The drug fenofibrate has received major attention as a novel medical treatment for diabetic retinopathy (DR) and other diabetes-induced microvascular complications."8.89An update on the molecular actions of fenofibrate and its clinical effects on diabetic retinopathy and other microvascular end points in patients with diabetes. ( Jenkins, AJ; Keech, AC; Lamoureux, EL; Ma, JX; Noonan, JE; Wang, JJ, 2013)
"To review clinical and experimental data for fenofibrate as a possible systemic treatment for diabetic retinopathy."8.88Fenofibrate - a potential systemic treatment for diabetic retinopathy? ( Mitchell, P; Simó, R; Wong, TY, 2012)
"Numerous studies have reported the efficacy of fenofibrate for patients with diabetic retinopathy (DRP)."7.91Efficacy of fenofibrate for diabetic retinopathy: A systematic review protocol. ( Han, L; Liu, HW; Qi, YX; Su, XJ, 2019)
"Diabetic retinopathy is a significant cause of vision impairment, especially affecting those of working age."6.52The use of fenofibrate in the management of patients with diabetic retinopathy: an evidence-based review. ( Newman, D; Ong, J; Ooi, JL; Sharma, N, 2015)
"Fenofibrate also has a favorable impact on a number of nonlipid residual risk factors associated with type 2 diabetes and metabolic syndrome, mediated by peroxisome proliferator-activated receptor-alpha."6.44Fenofibrate for cardiovascular disease prevention in metabolic syndrome and type 2 diabetes mellitus. ( Steiner, G, 2008)
"Experimental studies suggest that fenofibrate prevents abdominal aortic aneurysm (AAA) development by lowering aortic osteopontin (OPN) concentration and reducing the number of macrophages infiltrating the aortic wall."5.34A Randomised Controlled Trial Assessing the Effects of Peri-operative Fenofibrate Administration on Abdominal Aortic Aneurysm Pathology: Outcomes From the FAME Trial. ( Cavaye, D; Golledge, J; Jaeggi, R; Jenkins, JS; Lazzaroni, SM; Moran, CS; Morton, SK; Moxon, JV; Pinchbeck, JL; Quigley, F; Reid, CM; Rowbotham, SE, 2020)
"The purpose of this study is to study the benefit of addition of oral fenofibrate to the current regimen of diabetic macular edema (DME) management and quantify its effect on macular thickness and visual function in DME."5.27Efficiency of fenofibrate in facilitating the reduction of central macular thickness in diabetic macular edema. ( Hande, P; Murali, S; Shetty, J; Srinivasan, S, 2018)
"9%, respectively) and also for dyslipidemia (160 mg daily of fenofibrate plus simvastatin or placebo plus simvastatin) or for systolic blood-pressure control (target, <120 or <140 mm Hg)."5.14Effects of medical therapies on retinopathy progression in type 2 diabetes. ( Ambrosius, WT; Chew, EY; Cushman, WC; Danis, RP; Davis, MD; Elam, MB; Esser, BA; Fine, LJ; Gangaputra, S; Genuth, S; Gerstein, HC; Ginsberg, HN; Goff, DC; Greven, CM; Hubbard, L; Lovato, JF; Perdue, LH; Schubart, U, 2010)
"The combination of antihypertensive agents with micronized fenofibrate can effectively prevent the progression of carotid atherosclerosis and reduce the incidence of stroke in patients with essential hypertension."5.12Inhibitory effects of micronized fenofibrate on carotid atherosclerosis in patients with essential hypertension. ( Meng, QH; Su, G; Zhu, S, 2006)
"Improvement in lipid profiles with fenofibrate in patients with type 2 diabetes was associated with reduced progression from normal albumin excretion to microalbuminuria."5.11Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS). ( Ansquer, JC; Foucher, C; Rattier, S; Steiner, G; Taskinen, MR, 2005)
" Fenofibrate significantly slowed the progression of early diabetic retinopathy by 30 to 40% within 4 to 5 years in patients with type 2 diabetes mellitus and pre-existing retinopathy at baseline."4.93Effect of micronized fenofibrate on microvascular complications of type 2 diabetes: a systematic review. ( Czupryniak, L; Gogtay, JA; Joshi, SR; Lopez, M, 2016)
"The drug fenofibrate has received major attention as a novel medical treatment for diabetic retinopathy (DR) and other diabetes-induced microvascular complications."4.89An update on the molecular actions of fenofibrate and its clinical effects on diabetic retinopathy and other microvascular end points in patients with diabetes. ( Jenkins, AJ; Keech, AC; Lamoureux, EL; Ma, JX; Noonan, JE; Wang, JJ, 2013)
"To review clinical and experimental data for fenofibrate as a possible systemic treatment for diabetic retinopathy."4.88Fenofibrate - a potential systemic treatment for diabetic retinopathy? ( Mitchell, P; Simó, R; Wong, TY, 2012)
"Numerous studies have reported the efficacy of fenofibrate for patients with diabetic retinopathy (DRP)."3.91Efficacy of fenofibrate for diabetic retinopathy: A systematic review protocol. ( Han, L; Liu, HW; Qi, YX; Su, XJ, 2019)
"Treatment with fenofibrate did reduce all cardiovascular disease (CVD) events, the secondary end point (by 11%, p = 0."2.73After the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study: implications for fenofibrate. ( Sacks, FM, 2008)
"Eighteen patients with hyperlipidemia and type 2 diabetes mellitus."2.72Effects of fenofibrate therapy on plasma ubiquinol-10 and ubiquinone-10 levels in Japanese patients with hyperlipidemia and type 2 diabetes mellitus. ( Asano, A; Inazu, A; Kawashiri, MA; Kobayashi, J; Mabuchi, H; Murase, Y; Nohara, A; Shimizu, M, 2006)
"A total of 418 subjects with type 2 diabetes were randomly assigned to 200 mg micronized fenofibrate daily or placebo."2.71Relationships between low-density lipoprotein particle size, plasma lipoproteins, and progression of coronary artery disease: the Diabetes Atherosclerosis Intervention Study (DAIS). ( Ansquer, JC; Aubin, F; Foucher, C; Hamsten, A; Rattier, S; Steiner, G; Taskinen, MR; Vakkilainen, J, 2003)
"Disease progression is associated with variation in AAT, and low AAT levels promote atherogenesis."2.71Progression of atherosclerosis is associated with variation in the alpha1-antitrypsin gene. ( Flavell, DM; Frick, MH; Humphries, SE; Jackson, R; Kesäniemi, YA; Martin, S; Nagl, S; Nieminen, MS; Pasternack, A; Steiner, G; Syvänne, M; Talmud, PJ; Taskinen, MR; Whitehouse, DB, 2003)
"Diabetic retinopathy is a significant cause of vision impairment, especially affecting those of working age."2.52The use of fenofibrate in the management of patients with diabetic retinopathy: an evidence-based review. ( Newman, D; Ong, J; Ooi, JL; Sharma, N, 2015)
"Especially diabetic nephropathy is a leading cause of morbidity and mortality, and its prevalence is increasing."2.48Fibrates: therapeutic potential for diabetic nephropathy? ( Kouroumichakis, I; Liakopoulos, V; Maltezos, E; Mikhailidis, DP; Papanas, N; Zarogoulidis, P, 2012)
"Microalbuminuria is an early marker of diabetic nephropathy and an independent risk factor for cardiovascular disease."2.44Microvascular complications of diabetes mellitus: renal protection accompanies cardiovascular protection. ( Brown, WV, 2008)
"Fenofibrate also has a favorable impact on a number of nonlipid residual risk factors associated with type 2 diabetes and metabolic syndrome, mediated by peroxisome proliferator-activated receptor-alpha."2.44Fenofibrate for cardiovascular disease prevention in metabolic syndrome and type 2 diabetes mellitus. ( Steiner, G, 2008)
"Multifactorial diseases such as type 2 diabetes mellitus (T2DM), are driven by a complex network of interconnected mechanisms that translate to a diverse range of complications at the physiological level."1.40Network signatures link hepatic effects of anti-diabetic interventions with systemic disease parameters. ( Kelder, T; Radonjic, M; van Gool, AJ; van Ommen, B; Verschuren, L, 2014)
"The development of diabetic nephropathy was assessed biochemically and histologically."1.36The low dose combination of fenofibrate and rosiglitazone halts the progression of diabetes-induced experimental nephropathy. ( Arora, MK; Balakumar, P; Reddy, K, 2010)
"Fenofibrate treatment decreased hepatic macrophage accumulation and abolished steatosis."1.33Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates. ( Buffat, L; Gijbels, MJ; Hofker, MH; Maeda, N; Noel, B; Shiri-Sverdlov, R; Staels, B; van Bilsen, M; van Gorp, PJ; Wouters, K, 2006)

Research

Studies (46)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's1 (2.17)18.2507
2000's14 (30.43)29.6817
2010's26 (56.52)24.3611
2020's5 (10.87)2.80

Authors

AuthorsStudies
Okabayashi, Y1
Nagasaka, S1
Kanzaki, G1
Tsuboi, N1
Yokoo, T1
Shimizu, A1
Lefere, S1
Puengel, T1
Hundertmark, J1
Penners, C1
Frank, AK1
Guillot, A1
de Muynck, K1
Heymann, F1
Adarbes, V1
Defrêne, E1
Estivalet, C1
Geerts, A1
Devisscher, L1
Wettstein, G1
Tacke, F1
Moxon, JV2
Rowbotham, SE1
Pinchbeck, JL1
Lazzaroni, SM1
Morton, SK1
Moran, CS1
Quigley, F1
Jenkins, JS1
Reid, CM1
Cavaye, D1
Jaeggi, R1
Golledge, J2
Yen, CL1
Fan, PC1
Lin, MS1
Lee, CC1
Tu, KH1
Chen, CY1
Hsiao, CC1
Hsu, HH1
Tian, YC1
Chang, CH1
Chekaoui, A1
Ertl, HCJ1
Srinivasan, S1
Hande, P1
Shetty, J1
Murali, S1
Maas, R1
Mieth, M1
Titze, SI1
Hübner, S1
Fromm, MF1
Kielstein, JT1
Schmid, M1
Köttgen, A1
Kronenberg, F1
Krane, V1
Hausknecht, B1
Eckardt, KU1
Schneider, MP1
Su, XJ1
Han, L1
Qi, YX1
Liu, HW1
Simó, R2
Roy, S1
Behar-Cohen, F1
Keech, A1
Mitchell, P4
Wong, TY3
Hu, Z1
Huang, S1
Wu, Y1
Liu, Y1
Liu, X1
Su, D1
Tao, Y1
Fu, P1
Zhang, X1
Peng, Z1
Zhang, S1
Yang, Y1
Noonan, JE1
Jenkins, AJ2
Ma, JX1
Keech, AC2
Wang, JJ2
Lamoureux, EL1
Waldman, B1
Davis, TM1
Taskinen, MR4
Scott, R1
O'Connell, RL1
Gebski, VJ1
Ng, MK1
Chew, EY2
Davis, MD2
Danis, RP2
Lovato, JF2
Perdue, LH2
Greven, C1
Genuth, S2
Goff, DC2
Leiter, LA1
Ismail-Beigi, F1
Ambrosius, WT2
Kelder, T1
Verschuren, L1
van Ommen, B1
van Gool, AJ1
Radonjic, M1
Sharma, N1
Ooi, JL1
Ong, J1
Newman, D1
Esmaeili, MA1
Yadav, S1
Gupta, RK1
Waggoner, GR1
Deloach, A1
Calingasan, NY1
Beal, MF1
Kiaei, M1
Czupryniak, L1
Joshi, SR1
Gogtay, JA1
Lopez, M1
Robinson, JG1
Brown, WV1
Steiner, G5
Sacks, FM1
Tsimihodimos, V1
Liberopoulos, E1
Elisaf, M1
Arora, MK1
Reddy, K1
Balakumar, P1
Foucher, C3
Brugère, L1
Ansquer, JC3
Klein, BE1
Gangaputra, S1
Greven, CM1
Hubbard, L1
Esser, BA1
Cushman, WC1
Ginsberg, HN1
Elam, MB1
Gerstein, HC1
Schubart, U1
Fine, LJ1
Lim, LS1
Liew, G2
Cheung, N1
Giral, P1
Rosenbaum, D1
Baum, SJ1
Egan, A1
Byrne, M1
Moustafa, T1
Fickert, P1
Magnes, C1
Guelly, C1
Thueringer, A1
Frank, S1
Kratky, D1
Sattler, W1
Reicher, H1
Sinner, F1
Gumhold, J1
Silbert, D1
Fauler, G1
Höfler, G1
Lass, A1
Zechner, R1
Trauner, M1
Kouroumichakis, I1
Papanas, N1
Zarogoulidis, P1
Liakopoulos, V1
Maltezos, E1
Mikhailidis, DP1
Davidson, M1
Rosenson, RS1
Maki, KC1
Nicholls, SJ1
Ballantyne, CM1
Setze, C1
Carlson, DM1
Stolzenbach, J1
Krishna, SM1
Seto, SW1
Rush, C1
Walker, PJ1
Norman, PE1
Vakkilainen, J1
Aubin, F1
Rattier, S2
Hamsten, A1
Talmud, PJ1
Martin, S1
Flavell, DM1
Whitehouse, DB1
Nagl, S1
Jackson, R1
Frick, MH1
Nieminen, MS1
Kesäniemi, YA2
Pasternack, A1
Humphries, SE1
Syvänne, M1
Jokinen, V1
Ukkola, O1
Airaksinen, KE1
Koistinen, JM1
Ikäheimo, MJ1
Huikuri, HV1
Shiri-Sverdlov, R1
Wouters, K1
van Gorp, PJ1
Gijbels, MJ1
Noel, B1
Buffat, L1
Staels, B1
Maeda, N1
van Bilsen, M1
Hofker, MH1
Asano, A1
Kobayashi, J1
Murase, Y1
Nohara, A1
Kawashiri, MA1
Inazu, A1
Shimizu, M1
Mabuchi, H1
Zhu, S1
Su, G1
Meng, QH1
McLaughlin, PR1
Gladstone, P1
Forster, T1

Clinical Trials (6)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Effects of Oral Fenofibrate on Retinal Thickness and Macular Volume: Assessments on Retinal Endothelial Vascular Dysfunction, Inflammation, and Angiogenesis in Diabetic Retinopathy With Dyslipidemia[NCT04885153]36 participants (Actual)Interventional2016-11-01Completed
Action to Control Cardiovascular Risk in Diabetes (ACCORD)[NCT00000620]Phase 310,251 participants (Actual)Interventional1999-09-30Completed
Action to Control Cardiovascular Risk in Diabetes (ACCORD) Eye Study[NCT00542178]Phase 33,472 participants (Actual)Interventional2003-10-31Completed
Clinical Study to Evaluate the Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients[NCT06155331]Phase 444 participants (Anticipated)Interventional2023-12-31Recruiting
Evaluation of Choline Fenofibrate (ABT-335) on Carotid Intima-Media Thickness (cIMT) in Subjects With Type IIb Dyslipidemia With Residual Risk in Addition to Atorvastatin Therapy (FIRST) Trial[NCT00616772]Phase 3682 participants (Actual)Interventional2008-02-29Completed
Effects of Fenofibrate Administration in Patients With Diabetic Nephropathy[NCT03869931]Phase 3300 participants (Anticipated)Interventional2019-03-08Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Death From Any Cause in the Glycemia Trial.

"Time to death from any cause. Secondary measure for Glycemia Trial.~A finding of higher mortality in the intensive-therapy group led to an early discontinuation of therapy after a mean of 3.5 years of follow-up. Intensive arm participants were transitioned to standard arm strategy over a period of 0.2 year and followed for an additional 1.2 years to the planned end of the Glycemia Trial while participating in one of the other sub-trials (BP or Lipid)." (NCT00000620)
Timeframe: 4.9 years

Interventionparticipants (Number)
Glycemia Trial: Intensive Control391
Glycemia Trial: Standard Control327

First Occurrence of a Major Cardiovascular Event (MCE); Specifically Nonfatal Heart Attack, Nonfatal Stroke, or Cardiovascular Death (Measured Throughout the Study) in the Glycemia Trial.

"Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. This was the primary outcome measure in all three trials: Glycemia (all participants), Blood Pressure (subgroup of participants not in Lipid Trial), and Lipid (subgroup of participants not in Blood Pressure Trial).~In the Glycemia Trial, a finding of higher mortality in the intensive arm group led to an early discontinuation of therapy after a mean of 3.5 years of follow-up. Intensive arm participants were transitioned to standard arm strategy over a period of 0.2 year and followed for an additional 1.2 years to the planned end of the Glycemia Trial while participating in one of the other sub-trials (BP or Lipid) to their planned completion." (NCT00000620)
Timeframe: 4.9 years

Interventionparticipants (Number)
Glycemia Trial: Intensive Control503
Glycemia Trial: Standard Control543

First Occurrence of Major Cardiovascular Event (MCE) in the Blood Pressure Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. Primary outcome for Blood Pressure Trial. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
BP Trial: Intensive Control208
BP Trial: Standard Control237

First Occurrence of Major Cardiovascular Event (MCE) in the Lipid Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death in Lipid Trial participants. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
Lipid Trial: Fenofibrate291
Lipid Trial: Placebo310

First Occurrence of MCE or Revascularization or Hospitalization for Congestive Heart Failure (CHF) in Lipid Trial.

Time to first occurrence of nonfatal myocardial infarction, nonfatal stroke, cardiovascular death, revascularization procedure or hospitalization for CHF in Lipid Trial participants. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
Lipid Trial: Fenofibrate641
Lipid Trial: Placebo667

Stroke in the Blood Pressure Trial.

Time to first occurrence of nonfatal or fatal stroke among participants in the BP Trial. (NCT00000620)
Timeframe: 4.7 years

Interventionparticipants (Number)
BP Trial: Intensive Control36
BP Trial: Standard Control62

Cataract Extraction

(NCT00542178)
Timeframe: Measured at Year 4

InterventionParticipants (Count of Participants)
Intensive Glycemia Control547
Standard Glycemia Control623
Intensive Blood Pressure Control266
Standard Blood Pressure Control300
Fenofibrate + Simvastatin Therapy305
Placebo + Simvastatin Therapy299

Development or Progression of Macular Edema

(NCT00542178)
Timeframe: Measured at Year 4

InterventionParticipants (Count of Participants)
Intensive Glycemia Control44
Standard Glycemia Control40
Intensive Blood Pressure Control18
Standard Blood Pressure Control20
Fenofibrate + Simvastatin Therapy24
Placebo + Simvastatin Therapy22

Loss of Visual Acuity

(NCT00542178)
Timeframe: Measured at Year 4

InterventionParticipants (Count of Participants)
Intensive Glycemia Control744
Standard Glycemia Control752
Intensive Blood Pressure Control367
Standard Blood Pressure Control382
Fenofibrate + Simvastatin Therapy354
Placebo + Simvastatin Therapy393

Number of Participants With Progression of Diabetic Retinopathy of at Least 3 Stages on the Early Treatment Diabetic Retinopathy Study (ETDRS) Scale, or Development of Proliferative Diabetic Retinopathy Necessitating Photocoagulation Therapy or Vitrectomy

Diabetic retinopathy status was defined according to the eye with the highest level on the ETDRS Final Severity Scale for Persons, as follows: no diabetic retinopathy, a level of less than 20; mild diabetic retinopathy, a level of 20; moderate nonproliferative diabetic retinopathy (NPDR), a level above 20 but less than 53; severe diabetic retinopathy, a level of 53 but less than 60; and proliferative diabetic retinopathy (PDR), a level of 60 or higher. (NCT00542178)
Timeframe: Measured at Year 4

Interventionparticipants (Number)
Intensive Glycemia Control104
Standard Glycemia Control149
Intensive Blood Pressure Control67
Standard Blood Pressure Control54
Fenofibrate + Simvastatin Therapy52
Placebo + Simvastatin Therapy80

Rate of Change in Composite of Mean of Maximal Posterior-wall and Anterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of maximal posterior-wall and anterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.003
Placebo + Atorvastatin-0.019

Rate of Change in Composite of Mean of Maximal Posterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of maximal posterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.014
Placebo + Atorvastatin-0.008

Rate of Change in Composite of Mean of the Mean Posterior-wall Intima-media Thickness (IMT)

Rate of change (mm/year) from baseline in composite of mean of the mean posterior-wall intima-media thickness (IMT) of the left and right common carotid artery, internal carotid artery, and carotid bifurcation. The statistical model used change from baseline as the dependent variable, with time of IMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. IMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.010
Placebo + Atorvastatin-0.004

Rate of Change in Mean of Maximal Posterior-wall Carotid Intima-media Thickness (cIMT)

Rate of change (mm/year) from baseline in mean of maximal posterior-wall carotid intima-media thickness (cIMT) of the left and right common carotid artery. The statistical model used change from baseline as the dependent variable, with time of cIMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. cIMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.005
Placebo + Atorvastatin-0.003

Rate of Change in Mean Posterior-wall Carotid Intima-media Thickness (cIMT)

Rate of change (mm/year) from baseline in mean of posterior-wall carotid intima-media thickness (cIMT) of the left and right common carotid artery. The statistical model used change from baseline as the dependent variable, with time of cIMT assessment (in years) as one of the factors in the model. The between-group difference in the rate of change was based on the parameter coefficient for the time-by-treatment interaction. The within-group rate of change was obtained from estimate statements within the repeated measures analysis. cIMT was measured using non-invasive ultrasound. (NCT00616772)
Timeframe: Baseline, 6 months, 12 months, 18 months, and 24 months

Interventionmm/year (Mean)
ABT-335 + Atorvastatin-0.006
Placebo + Atorvastatin0.000

Reviews

12 reviews available for fenofibrate and Disease Exacerbation

ArticleYear
Fenofibrate: a new treatment for diabetic retinopathy. Molecular mechanisms and future perspectives.
    Current medicinal chemistry, 2013, Volume: 20, Issue:26

    Topics: Animals; Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans;

2013
An update on the molecular actions of fenofibrate and its clinical effects on diabetic retinopathy and other microvascular end points in patients with diabetes.
    Diabetes, 2013, Volume: 62, Issue:12

    Topics: Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypolipidemic Agents; Microvessels;

2013
The use of fenofibrate in the management of patients with diabetic retinopathy: an evidence-based review.
    Australian family physician, 2015, Volume: 44, Issue:6

    Topics: Australia; Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans

2015
Effect of micronized fenofibrate on microvascular complications of type 2 diabetes: a systematic review.
    Expert opinion on pharmacotherapy, 2016, Volume: 17, Issue:11

    Topics: Diabetes Mellitus, Type 2; Diabetic Nephropathies; Diabetic Retinopathy; Disease Progression; Drug C

2016
LDL reduction: how low should we go and is it safe?
    Current cardiology reports, 2008, Volume: 10, Issue:6

    Topics: Allylamine; Anticholesteremic Agents; Azetidines; Cholesterol, LDL; Colesevelam Hydrochloride; Coron

2008
Microvascular complications of diabetes mellitus: renal protection accompanies cardiovascular protection.
    The American journal of cardiology, 2008, Dec-22, Volume: 102, Issue:12A

    Topics: Cardiovascular Diseases; Diabetes Mellitus, Type 2; Diabetic Nephropathies; Disease Progression; Dys

2008
Fenofibrate for cardiovascular disease prevention in metabolic syndrome and type 2 diabetes mellitus.
    The American journal of cardiology, 2008, Dec-22, Volume: 102, Issue:12A

    Topics: Atherosclerosis; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Disease Progression; Fenofibrat

2008
Pleiotropic effects of fenofibrate.
    Current pharmaceutical design, 2009, Volume: 15, Issue:5

    Topics: Animals; Atherosclerosis; Disease Progression; Fenofibrate; Gene Expression Regulation; Humans; Hypo

2009
How can we improve the management of vascular risk in type 2 diabetes: insights from FIELD.
    Cardiovascular drugs and therapy, 2009, Volume: 23, Issue:5

    Topics: Albuminuria; Amputation, Surgical; Cholesterol, HDL; Diabetes Mellitus, Type 2; Diabetic Angiopathie

2009
Fenofibrate, homocysteine and renal function.
    Current vascular pharmacology, 2010, Volume: 8, Issue:5

    Topics: Animals; Biomarkers; Creatinine; Disease Progression; Dyslipidemias; Fenofibrate; Glomerular Filtrat

2010
Fibrates: therapeutic potential for diabetic nephropathy?
    European journal of internal medicine, 2012, Volume: 23, Issue:4

    Topics: Animals; Creatinine; Diabetic Nephropathies; Disease Progression; Fenofibrate; Fibric Acids; Humans;

2012
Fenofibrate - a potential systemic treatment for diabetic retinopathy?
    American journal of ophthalmology, 2012, Volume: 154, Issue:1

    Topics: Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypolipid

2012

Trials

14 trials available for fenofibrate and Disease Exacerbation

ArticleYear
A Randomised Controlled Trial Assessing the Effects of Peri-operative Fenofibrate Administration on Abdominal Aortic Aneurysm Pathology: Outcomes From the FAME Trial.
    European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery, 2020, Volume: 60, Issue:3

    Topics: Aged; Aorta, Abdominal; Aortic Aneurysm, Abdominal; Biomarkers; Disease Progression; Double-Blind Me

2020
Efficiency of fenofibrate in facilitating the reduction of central macular thickness in diabetic macular edema.
    Indian journal of ophthalmology, 2018, Volume: 66, Issue:1

    Topics: Aged; Diabetic Retinopathy; Disease Progression; Dose-Response Relationship, Drug; Female; Fenofibra

2018
HDL-C and HDL-C/ApoA-I predict long-term progression of glycemia in established type 2 diabetes.
    Diabetes care, 2014, Volume: 37, Issue:8

    Topics: Aged; Apolipoprotein A-I; Blood Glucose; Cholesterol, HDL; Cross-Sectional Studies; Diabetes Mellitu

2014
The effects of medical management on the progression of diabetic retinopathy in persons with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Eye Study.
    Ophthalmology, 2014, Volume: 121, Issue:12

    Topics: Aged; Cardiovascular Diseases; Cataract Extraction; Diabetes Mellitus, Type 2; Diabetic Retinopathy;

2014
The effects of medical management on the progression of diabetic retinopathy in persons with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Eye Study.
    Ophthalmology, 2014, Volume: 121, Issue:12

    Topics: Aged; Cardiovascular Diseases; Cataract Extraction; Diabetes Mellitus, Type 2; Diabetic Retinopathy;

2014
The effects of medical management on the progression of diabetic retinopathy in persons with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Eye Study.
    Ophthalmology, 2014, Volume: 121, Issue:12

    Topics: Aged; Cardiovascular Diseases; Cataract Extraction; Diabetes Mellitus, Type 2; Diabetic Retinopathy;

2014
The effects of medical management on the progression of diabetic retinopathy in persons with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Eye Study.
    Ophthalmology, 2014, Volume: 121, Issue:12

    Topics: Aged; Cardiovascular Diseases; Cataract Extraction; Diabetes Mellitus, Type 2; Diabetic Retinopathy;

2014
After the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study: implications for fenofibrate.
    The American journal of cardiology, 2008, Dec-22, Volume: 102, Issue:12A

    Topics: Anticholesteremic Agents; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Disease Progression; D

2008
Effects of medical therapies on retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, Jul-15, Volume: 363, Issue:3

    Topics: Antihypertensive Agents; Cardiovascular Diseases; Cholesterol, LDL; Diabetes Mellitus, Type 2; Diabe

2010
Effects of medical therapies on retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, Jul-15, Volume: 363, Issue:3

    Topics: Antihypertensive Agents; Cardiovascular Diseases; Cholesterol, LDL; Diabetes Mellitus, Type 2; Diabe

2010
Effects of medical therapies on retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, Jul-15, Volume: 363, Issue:3

    Topics: Antihypertensive Agents; Cardiovascular Diseases; Cholesterol, LDL; Diabetes Mellitus, Type 2; Diabe

2010
Effects of medical therapies on retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, Jul-15, Volume: 363, Issue:3

    Topics: Antihypertensive Agents; Cardiovascular Diseases; Cholesterol, LDL; Diabetes Mellitus, Type 2; Diabe

2010
Study design, rationale, and baseline characteristics: evaluation of fenofibric acid on carotid intima-media thickness in patients with type IIb dyslipidemia with residual risk in addition to atorvastatin therapy (FIRST) trial.
    Cardiovascular drugs and therapy, 2012, Volume: 26, Issue:4

    Topics: Aged; Aged, 80 and over; Anticholesteremic Agents; Atorvastatin; Carotid Arteries; Carotid Intima-Me

2012
Relationships between low-density lipoprotein particle size, plasma lipoproteins, and progression of coronary artery disease: the Diabetes Atherosclerosis Intervention Study (DAIS).
    Circulation, 2003, Apr-08, Volume: 107, Issue:13

    Topics: Adult; Aged; Coronary Angiography; Coronary Artery Disease; Diabetes Mellitus, Type 2; Diabetic Angi

2003
Progression of atherosclerosis is associated with variation in the alpha1-antitrypsin gene.
    Arteriosclerosis, thrombosis, and vascular biology, 2003, Apr-01, Volume: 23, Issue:4

    Topics: 3' Untranslated Regions; Aged; Alleles; alpha 1-Antitrypsin; alpha 1-Antitrypsin Deficiency; Amino A

2003
Temporal changes in cardiovascular autonomic regulation in type II diabetic patients: association with coronary risk variables and progression of coronary artery disease.
    Annals of medicine, 2003, Volume: 35, Issue:3

    Topics: Adult; Aged; Arteriosclerosis; Autonomic Nervous System; Coronary Angiography; Diabetes Mellitus, Ty

2003
Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS).
    American journal of kidney diseases : the official journal of the National Kidney Foundation, 2005, Volume: 45, Issue:3

    Topics: Albuminuria; Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Anti

2005
Effects of fenofibrate therapy on plasma ubiquinol-10 and ubiquinone-10 levels in Japanese patients with hyperlipidemia and type 2 diabetes mellitus.
    Pharmacotherapy, 2006, Volume: 26, Issue:4

    Topics: Coenzymes; Diabetes Mellitus, Type 2; Disease Progression; Female; Fenofibrate; Humans; Hyperlipidem

2006
Inhibitory effects of micronized fenofibrate on carotid atherosclerosis in patients with essential hypertension.
    Clinical chemistry, 2006, Volume: 52, Issue:11

    Topics: Anti-Inflammatory Agents; Antihypertensive Agents; Biomarkers; Carotid Artery Diseases; Demography;

2006
Diabetes Atherosclerosis Intervention Study (DAIS): quantitative coronary angiographic analysis of coronary artery atherosclerosis.
    Catheterization and cardiovascular diagnosis, 1998, Volume: 44, Issue:3

    Topics: Adult; Aged; Coronary Angiography; Coronary Artery Disease; Diabetes Mellitus, Type 2; Diabetic Angi

1998

Other Studies

20 other studies available for fenofibrate and Disease Exacerbation

ArticleYear
Group 1 innate lymphoid cells are involved in the progression of experimental anti-glomerular basement membrane glomerulonephritis and are regulated by peroxisome proliferator-activated receptor α.
    Kidney international, 2019, Volume: 96, Issue:4

    Topics: Animals; Anti-Glomerular Basement Membrane Disease; Biopsy; CD8 Antigens; Cells, Cultured; Chemokine

2019
Differential effects of selective- and pan-PPAR agonists on experimental steatohepatitis and hepatic macrophages
    Journal of hepatology, 2020, Volume: 73, Issue:4

    Topics: Animals; Disease Models, Animal; Disease Progression; Dose-Response Relationship, Drug; Fatty Liver;

2020
Fenofibrate Delays the Need for Dialysis and Reduces Cardiovascular Risk Among Patients With Advanced CKD.
    The Journal of clinical endocrinology and metabolism, 2021, 05-13, Volume: 106, Issue:6

    Topics: Adult; Aged; Cardiovascular Diseases; Cohort Studies; Disease Progression; Female; Fenofibrate; Hear

2021
PPARα Agonist Fenofibrate Enhances Cancer Vaccine Efficacy.
    Cancer research, 2021, 09-01, Volume: 81, Issue:17

    Topics: Animals; Cancer Vaccines; CD8-Positive T-Lymphocytes; Cell Line; Disease Progression; Epitopes; Fema

2021
Drugs linked to plasma homoarginine in chronic kidney disease patients-a cross-sectional analysis of the German Chronic Kidney Disease cohort.
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2020, 07-01, Volume: 35, Issue:7

    Topics: Adolescent; Adult; Aged; Cohort Studies; Cross-Sectional Studies; Disease Progression; Female; Fenof

2020
Efficacy of fenofibrate for diabetic retinopathy: A systematic review protocol.
    Medicine, 2019, Volume: 98, Issue:14

    Topics: Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypolipidemic Agents; Macular Edema;

2019
Hereditary features, treatment, and prognosis of the lipoprotein glomerulopathy in patients with the APOE Kyoto mutation.
    Kidney international, 2014, Volume: 85, Issue:2

    Topics: Adolescent; Adult; Aged; Apolipoprotein E2; Biomarkers; Biopsy; Case-Control Studies; China; Creatin

2014
Network signatures link hepatic effects of anti-diabetic interventions with systemic disease parameters.
    BMC systems biology, 2014, Sep-11, Volume: 8

    Topics: Animals; Diabetes Mellitus, Type 2; Disease Progression; Fenofibrate; Hydrocarbons, Fluorinated; Liv

2014
Preferential PPAR-α activation reduces neuroinflammation, and blocks neurodegeneration in vivo.
    Human molecular genetics, 2016, Jan-15, Volume: 25, Issue:2

    Topics: Amyotrophic Lateral Sclerosis; Animals; Cell Death; Disease Models, Animal; Disease Progression; Fem

2016
The low dose combination of fenofibrate and rosiglitazone halts the progression of diabetes-induced experimental nephropathy.
    European journal of pharmacology, 2010, Jun-25, Volume: 636, Issue:1-3

    Topics: Animals; Blood Glucose; Blood Urea Nitrogen; Creatinine; Diabetic Nephropathies; Disease Models, Ani

2010
Reduction in risk of progression of diabetic retinopathy.
    The New England journal of medicine, 2010, Jul-15, Volume: 363, Issue:3

    Topics: Antihypertensive Agents; Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Drug

2010
Mixed messages on systemic therapies for diabetic retinopathy.
    Lancet (London, England), 2010, Oct-30, Volume: 376, Issue:9751

    Topics: Blood Glucose; Blood Pressure; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypol

2010
Retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, 11-25, Volume: 363, Issue:22

    Topics: 2,3-Diphosphoglycerate; Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofi

2010
Retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, 11-25, Volume: 363, Issue:22

    Topics: Cholesterol, HDL; Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Drug Therapy

2010
Retinopathy progression in type 2 diabetes.
    The New England journal of medicine, 2010, 11-25, Volume: 363, Issue:22

    Topics: Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypertens

2010
Effects of medical therapies on retinopathy progression in type 2 diabetes.
    Irish medical journal, 2011, Volume: 104, Issue:2

    Topics: Diabetes Mellitus, Type 2; Diabetic Retinopathy; Disease Progression; Fenofibrate; Humans; Hypolipid

2011
Alterations in lipid metabolism mediate inflammation, fibrosis, and proliferation in a mouse model of chronic cholestatic liver injury.
    Gastroenterology, 2012, Volume: 142, Issue:1

    Topics: Animals; ATP Binding Cassette Transporter, Subfamily B; ATP-Binding Cassette Sub-Family B Member 4;

2012
Fenofibrate increases high-density lipoprotein and sphingosine 1 phosphate concentrations limiting abdominal aortic aneurysm progression in a mouse model.
    The American journal of pathology, 2012, Volume: 181, Issue:2

    Topics: Angiotensin II; Animals; Aorta; Aorta, Thoracic; Aortic Aneurysm, Abdominal; Apoptosis; Azo Compound

2012
Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates.
    Journal of hepatology, 2006, Volume: 44, Issue:4

    Topics: Animals; Apolipoprotein E2; Apolipoproteins E; ATP-Binding Cassette Transporters; Clofibric Acid; Di

2006
[Milestone in the treatment of diabetic dyslipidemia: the DAIS Study].
    Orvosi hetilap, 2001, Jul-22, Volume: 142, Issue:29

    Topics: Adult; Coronary Angiography; Coronary Artery Disease; Diabetes Mellitus, Type 2; Disease Progression

2001