TRILIPIX SUMMARY
Trilipix (fenofibric acid) is a lipid regulating agent available as delayed release capsules for oral administration. Each delayed release capsule contains choline fenofibrate, equivalent to 45 mg or 135 mg of fenofibric acid.
Co-administration Therapy with Statins for the Treatment of Mixed Dyslipidemia
Trilipix is indicated as an adjunct to diet in combination with a statin to reduce TG and increase HDL-C in patients with mixed dyslipidemia and CHD or a CHD risk equivalent who are on optimal statin therapy to achieve their LDL-C goal.
CHD risk equivalents comprise:
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Other clinical forms of atherosclerotic disease (peripheral arterial disease, abdominal aortic aneurysm, and symptomatic carotid artery disease);
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Diabetes;
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Multiple risk factors that confer a 10-year risk for CHD > 20%
Treatment of Severe Hypertriglyceridemia
Trilipix is indicated as adjunctive therapy to diet to reduce TG in patients with severe hypertriglyceridemia. Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacological intervention. Markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dL) may increase the risk of developing pancreatitis. The effect of Trilipix therapy on reducing this risk has not been adequately studied.
Treatment of Primary Hyperlipidemia or Mixed Dyslipidemia
Trilipix is indicated as adjunctive therapy to diet to reduce elevated LDL-C, Total-C, TG, and Apo B, and to increase HDL-C in patients with primary hyperlipidemia or mixed dyslipidemia.
Important Limitations of Use
No incremental benefit of Trilipix on cardiovascular morbidity and mortality over and above that demonstrated for statin monotherapy has been established.
General Considerations for Treatment
Fenofibrate at a dose equivalent to 135 mg of Trilipix was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus.
Laboratory studies should be performed to establish that lipid levels are abnormal before instituting Trilipix therapy.
Every reasonable attempt should be made to control serum lipids with non-drug methods including appropriate diet, exercise, weight loss in obese patients, and control of any medical problems such as diabetes mellitus and hypothyroidism that may be contributing to the lipid abnormalities. Medications known to exacerbate hypertriglyceridemia (beta-blockers, thiazides, estrogens) should be discontinued or changed if possible, and excessive alcohol intake should be addressed before triglyceride-lowering drug therapy is considered. If the decision is made to use lipid-altering drugs, the patient should be instructed that this does not reduce the importance of adhering to diet.
Drug therapy is not indicated for patients who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of VLDL.
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NEWS HIGHLIGHTSMedia Articles Related to Trilipix (Fenofibrate)
FDA OKs New Cholesterol Drug Trilipix
Source: MedicineNet gemfibrozil Specialty [2008.12.16]
Title: FDA OKs New Cholesterol Drug Trilipix
Category: Health News
Created: 12/16/2008
Last Editorial Review: 12/16/2008
Published Studies Related to Trilipix (Fenofibrate)
Correlation of non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol with apolipoprotein B during simvastatin + fenofibrate therapy in patients with combined hyperlipidemia (a subanalysis of the SAFARI trial). [2009.08.15]
Guidelines have recommended non-high-density lipoprotein (non-HDL) cholesterol as a secondary target for therapy after the low-density lipoprotein (LDL) cholesterol goals have been met in patients with hypertriglyceridemia; non-HDL cholesterol is viewed as a surrogate for apolipoprotein (Apo)B, an alternate end point of treatment.
Relationships of HDL cholesterol, ApoA-I, and ApoA-II with homocysteine and creatinine in patients with type 2 diabetes treated with fenofibrate. [2009.06]
CONCLUSIONS: PPAR alpha agonists that have a more robust effect on HDL-C and apoA-I would be desirable.
Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial. [2009.05.23]
BACKGROUND: Amputations in people with type 2 diabetes mellitus substantially impair their quality of life and impose high costs on health-care systems. Our aim was to assess the effect of fenofibrate on amputation events in a large cohort of patients with type 2 diabetes... INTERPRETATION: Classic markers of macrovascular and microvascular risk were associated with lower extremity amputations in patients with type 2 diabetes. Treatment with fenofibrate was associated with a lower risk of amputations, particularly minor amputations without known large-vessel disease, probably through non-lipid mechanisms. These findings could lead to a change in standard treatment for the prevention of diabetes-related lower-limb amputations. FUNDING: Laboratoires Fournier SA (now part of Solvay Pharmaceuticals) and National Health and Medical Research Council of Australia.
Effect of fenofibrate on adiponectin and inflammatory biomarkers in metabolic syndrome patients. [2009.03]
Adiponectin is an adipose-secreted hormone with anti-inflammatory properties mediated by inhibition of nuclear factor-kappaB (NF-kappaB) signaling. This study investigates whether fenofibrate alters adiponectin levels in patients with hypertriglyceridemia and the metabolic syndrome, and examines the association of adiponectin with circulating inflammatory markers and whole blood cytokine production.
Efficacy and safety of coadministration of fenofibrate and ezetimibe compared with each as monotherapy in patients with type IIb dyslipidemia and features of the metabolic syndrome: a prospective, randomized, double-blind, three-parallel arm, multicenter, comparative study. [2009]
BACKGROUND: Patients with type IIb, or mixed, dyslipidemia have high levels of low-density lipoprotein cholesterol (LDL-C) with predominance of small dense LDL particles, high levels of triglycerides (TG), and low levels of high-density lipoprotein cholesterol (HDL-C). Fenofibrate significantly reduces TG and, more moderately, LDL-C, increases HDL-C and produces a shift from small to large LDL particle size; the main effect of ezetimibe is a reduction in LDL-C levels. Combined treatment with fenofibrate and ezetimibe may correct all the abnormalities of type IIb dyslipidemia. OBJECTIVE: To assess the efficacy and safety of coadministration of fenofibrate (NanoCrystal(R)) and ezetimibe in patients with type IIb dyslipidemia and the metabolic syndrome compared with administration of fenofibrate and ezetimibe alone (ClinicalTrials.gov Identifier: NCT00349284; Study ID: CLF178P 04 01)... CONCLUSION: In patients with type IIb dyslipidemia and features of the metabolic syndrome, coadministration of fenofibrate 145 mg and ezetimibe 10 mg daily was more effective than either monotherapy in reducing LDL-C, non-HDL-C, apolipoprotein B, and cardiovascular risk ratios, and was as effective as fenofibrate 145 mg alone in reducing TG and in increasing HDL-C in patients with low baseline HDL-C levels.
Clinical Trials Related to Trilipix (Fenofibrate)
Rosiglitazone And Fenofibrate Additive Effects on Lipids (RAFAEL) [Recruiting]
The design of the study will be randomized, double blind trial, which will examine the
effects of Rosiglitazone on the fasting triglycerides (TG), high-density lipoprotein (HDL),
HDL particle size, low-density lipoprotein (LDL), LDL particle size, and plasma
concentrations of apolipoproteins A-I, A-II, and C-III, function compared to Fenofibrate and
placebo. This study will also assess the synergistic effect of Rosiglitazone and Fenofibrate
on the same parameters. Data from this study will help clarify whether Rosiglitazone
favorably impacts plasma lipid and lipoprotein concentrations through improving insulin
sensitivity and glycemic control, or by directly influencing the synthesis of the
apolipoproteins that are responsible for very-low-density lipoprotein (VLDL) and HDL
metabolism.
Use of Fenofibrate for Primary Biliary Cirrhosis [Recruiting]
This is a pilot study to evaluate the safety and efficacy of fenofibrate on patients with
primary biliary cirrhosis who have an incomplete response to ursodeoxycholic acid.
Effect of Fenofibrate on Endothelial Function and High-Density Lipoproteins (HDL) Physicochemical and Functional Characteristics in Patients With Coronary Heart Disease [Recruiting]
Fenofibrate is a drug that acts on the PPAR alpha receptors, increasing HDL-cholesterol and
decreasing triglyceride levels. The interaction with these receptors has antiatherogenic
actions by regulating the expression con key proteins that participate in vascular
inflammation, plaque stability and thrombosis.
Fenofibrate reduces triglycerides and increases HDL-C in plasma. It also decreases small,
dense LDL particles. The use of this drug has resulted in improvement of vascular function
measured by endothelial function. Our hypotheses state that fenofibrate will improve:
endothelial function, improve HDL antioxidant capacity and size distribution towards a
predominance of small HDL particles.
Fenofibrate and Pharmacogenetic Impact in Dyslipidemia [Recruiting]
The purpose of the study is to learn whether genetics plays a role in predicting response to
a commonly used and FDA (Food and Drug Administration) approved medication for lowering
triglycerides and cholesterol. Our hypothesis: The pharmacogenetics of genes which affect
drug metabolism (how the body handles the drug) and drug targets (how the drug acts on the
body) influences how a person responds to the lipid lowering medication- fenofibrate.
The Effect of a Peroxisome Proliferator-Activated Receptor (PPAR) Alpha Agonist on Cytochrome P450 (CYP) Monooxygenase Activity in Humans [Not yet recruiting]
The hypothesis is to test to see if the drug fenofibrate will increase important chemicals
in the body and specifically in the kidney, help to rid the body of salt by the kidneys,
decrease blood pressure and improve insulin sensitivity during high-salt intake in
individuals with hypertension.
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Page last updated: 2009-10-20
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