Linked Life Data

Triglide (Tablet)

Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/1553

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Triglide (Tablet)
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Patients should be placed on an appropriate lipid-lowering diet before receiving TRIGLIDE and should continue on this diet during treatment with TRIGLIDE. TRIGLIDE may be administered with or without food. For the treatment of adult patients with primary hypercholesterolemia or mixed hyperlipidemia, the initial dose of TRIGLIDE is 160 mg per day. For adult patients with hypertriglyceridemia, the initial dose is 50 mg to 160 mg once daily. Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. The maximum dose is 160 mg per day. Treatment with TRIGLIDE should be initiated at a dose of 50 mg/day in patients with impaired renal function, and increased only after evaluation of the effects on renal function and lipid levels at this dose. In the elderly, the initial dose should likewise be limited to 50 mg/day. Lipid levels should be monitored periodically and consideration should be given to reducing the dosage of TRIGLIDE if lipid levels fall significantly below the targeted range.
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A variety of clinical studies have demonstrated that elevated levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and apolipoprotein B (apo B), an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of high-density lipoprotein cholesterol (HDL-C) and its transport complex, apolipoprotein A (apo A-I and apo A-II) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of TC, LDL-C, and triglycerides (TG), and inversely with the level of HDL-C. The independent effect of raising HDL-C or lowering TG on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treatedpatients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apo AI and apo AII. The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor��(PPAR��). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity). The resulting fall in TG produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPAR��also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.<br/>Pharmacokinetics: AbsorptionThe absolute bioavailability of fenofibrate cannot be determined as the compound is virtually insoluble in aqueous media suitable for injection. However, after fenofibrate is dissolved, fenofibrate is well absorbed from the gastrointestinal tract. Peak plasma levels of fenofibric acid occur an average of 3 hours after administration. TRIGLIDE 160 mg tablet exhibits a similar extent of absorption but 32% higher rate of absorption compared to the 200 mg micronized fenofibrate capsule under low-fat fed conditions. Effect of Food on AbsorptionFenofibrate is insoluble in water and its bioavailability is optimized when taken with meals. The extent of absorption of TRIGLIDE(AUC) is comparable between fed and fasted conditions. Food increases the rate of absorption of TRIGLIDE approximately 55%. DistributionIn healthy volunteers administered nonmicronized formulation of fenofibrate, steady-state plasma levels of fenofibric acid were shown to be achieved within 5 days of daily dosing with single oral doses and did not demonstrate accumulation across time following multiple dose administration. Serum protein binding was approximately 99% bound to plasma proteins in normal and hyperlipidemic subjects. MetabolismFollowing oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite, fenofibric acid; no unchanged fenofibrate is detected in plasma of healthy subjects following fenofibrate administration. Fenofibric acid is primarily conjugated with glucuronic acid and then excreted in urine. A small amount of fenofibric acid is reduced at the carbonyl moiety to a benzhydrol metabolite which is, in turn, conjugated with glucuronic acid and excreted in urine. In vivo metabolism data indicate that neither fenofibrate nor fenofibric acid undergo oxidative metabolism (e.g., cytochrome P450) to a significant extent. ExcretionAfter absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide. After administration of radiolabeled fenofibrate, approximately 60% of the dose appeared in the urine and 25% was excreted in the feces. Fenofibric acid is eliminated with a half-life of approximately 16 hours, allowing once daily administration in a clinical setting.<br/>Pharmacokinetics in Special Populations: GeriatricsTRIGLIDE has not been investigated in adequate and well-controlled trials in geriatric patients. However, a previous study using nonmicronized formulation show that the oral clearance of fenofibric acid is similar to that of young adults. This indicates that a similar dosage regimen can be used in the elderly, without increasing accumulation of the drug or metabolites. PediatricsTRIGLIDE has not been investigated in adequate and well-controlled trials in pediatric patients. GenderNo pharmacokinetic difference between males and females has been observed for fenofibrate. RaceThe influence of race on the pharmacokinetics of fenofibrate has not been studied, however fenofibrate is not metabolized by enzymes known for exhibiting inter-ethnic variability. Therefore, inter-ethnic pharmacokinetic differences are very unlikely. Renal insufficiencyTRIGLIDE has not been investigated in patients with renal impairment. In a study using nonmicronized formulation in patients with severe renal impairment (creatinine clearance<50 mL/min), the rate of clearance of fenofibric acid was greatly reduced, and the compound accumulated during chronic dosage. However, in patients having moderate renal impairment (creatinine clearance of 50 to 90 mL/min), the oral clearance and the oral volume of distribution of fenofibric acid are increased compared to healthy adults. Therefore, the dosage of TRIGLIDE should be minimized in patients who have severe renal impairment, while no modification of dosage is required in patients having moderate renal impairment. Hepatic InsufficiencyNo pharmacokinetic studies have been conducted in patients with hepatic insufficiency. Drug-Drug InteractionsIn vitro studies using human liver microsomes indicate that fenofibrate and fenofibric acid are not inhibitors of cytochrome P450 (CYP) isoforms CYP3A4, CYP2D6, CYP2E1, or CYP1A2. They are weak inhibitors of CYP2C19 and CYP2A6, and mild-to-moderate inhibitors of CYP2C9 at therapeutic concentrations. Potentiation of coumarin-type anticoagulants has been observed with prolongation of the prothrombin time/INR. Bile acid sequestrants have been shown to bind other drugs given concurrently. Therefore, fenofibrate should be taken at least 1 hour before or 4-6 hours after a bile acid binding resin to avoid impeding its absorption. .
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TRIGLIDE (fenofibrate) tablets, are available as a tablet in two strengths: 50 mg round off-white tablets debossed with���FH 50���are availablein bottles of 90 tablets (NDC 59630-480-90).in bottles of 30 tablets (NDC 59630-480-30). 160 mg round off-white tablets debossed with���FH 160���are availablein bottles of 90 tablets (NDC 59630-485-90).in bottles of 30 tablets (NDC 59630-485-30). Storage: Store at 20-25��C (68-77��F); excursions permitted between 15-30��C (59-86��F).[See USP Controlled Room Temperature]. Protect from light and moisture. Manufactured for: First Horizon Pharmaceutical Corporation by SkyePharma Production SAS, France. Made in France
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fenofibrate
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Triglide (Tablet)
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Adverse events reported by 2% or more of patients treated with fenofibrate during the double-blind, placebo-controlled trials, regardless of causality, are listed in the table below. Adverse events led to discontinuation of treatment in 5.0% of patients treated with fenofibrate and in 3.0% treated with placebo. Increases in liver function tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double-blind trials. Additional adverse events reported by three or more patients in placebo-controlled trials or reported in other controlled or open trials, regardless of causality are listed below. BODY AS A WHOLE: Chest pain, pain (unspecified), infection, malaise, allergic reaction, cyst, hernia, fever, photosensitivity reaction, and accidental injury. CARDIOVASCULAR SYSTEM: Angina pectoris, hypertension, vasodilatation, coronary artery disorder, electrocardiogram abnormal, ventricular extrasystoles, myocardial infarct, peripheral vascular disorder, migraine, varicose vein, cardiovascular disorder, hypotension, palpitation, vascular disorder, arrhythmia, phlebitis, tachycardia, extrasystoles, and atrial fibrillation. DIGESTIVE SYSTEM: Dyspepsia, flatulence, nausea, increased appetite, gastroenteritis, cholelithiasis, rectal disorder, esophagitis, gastritis, colitis, tooth disorder, vomiting, anorexia, gastrointestinal disorder, duodenal ulcer, nausea and vomiting, peptic ulcer, rectal hemorrhage, liver fatty deposit, cholecystitis, eructation, gamma glutamyl transpeptidase, and diarrhea. ENDOCRINE SYSTEM: Diabetes mellitus HEMIC AND LYMPHATIC SYSTEM: Anemia, leukopenia, ecchymosis, eosinophilia, lymphadenopathy, and thrombocytopenia. METABOLIC AND NUTRITIONAL DISORDERS: Creatinine increased, weight gain, hypoglycemia, gout, weight loss, edema, hyperuricemia, and peripheral edema. MUSCULOSKELETAL SYSTEM: Myositis, myalgia, arthralgia, arthritis, tenosynovitis, joint disorder, arthrosis, leg cramps, bursitis, and myasthenia. NERVOUS SYSTEM: Dizziness, insomnia, depression, vertigo, libido decreased, anxiety, paresthesia, dry mouth, hypertonia, nervousness, neuralgia, and somnolence. RESPIRATORY SYSTEM: Pharyngitis, bronchitis, cough increased, dyspnea, asthma, pneumonia, laryngitis, and sinusitis. SKIN AND APPENDAGES: Rash, pruritus, eczema, herpes zoster, urticaria, acne, sweating, fungal dermatitis, skin disorder, alopecia, contact dermatitis, herpes simplex, maculopapular rash, nail disorder, and skin ulcer. SPECIAL SENSES: Conjunctivitis, eye disorder, amblyopia, ear pain, otitis media, abnormal vision, cataract specified, and refraction disorder. UROGENITAL SYSTEM: Urinary frequency, prostatic disorder, dysuria, kidney function abnormal, urolithiasis, gynecomastia, unintended pregnancy, vaginal moniliasis, and cystitis.<br/>Laboratory Tests/Altered Laboratory Findings:: In patients treated with fenofibrate, the following has been reported:
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Treatment of Hypercholesterolemia: Triglide is indicated as adjunctive therapy to diet for the reduction of LDL-C, Total-C, Triglycerides and Apo B in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Frederickson Types IIa and IIb). Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and non-pharmacological interventions alone has been inadequate (see National Cholesterol Education Program [NCEP] Treatment Guidelines, below).<br/>Treatment of Hypertriglyceridemia: TRIGLIDE is indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. Markedly elevated levels of serum triglycerides (e.g.>2,000 mg/dL) may increase the risk of developing pancreatitis. The effect of TRIGLIDE therapy on reducing this risk has not been studied. Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of very low-density lipoprotein (VLDL). Inspection of plasma refrigerated for 14 hours is helpful in distinguishing Types I, IV and V hyperlipoproteinemia (Nikkila, 1983). The initial treatment for dyslipidemia is dietary therapy specific for the type of lipoprotein abnormality. Excess body weight and excess alcohol intake may be important factors in hypertriglyceridemia and should be addressed prior to any drug therapy. Physical exercise can be an important ancillary measure. Diseases contributory to hyperlipidemia, such as hypothyroidism or diabetes mellitus should be looked for and adequately treated. Estrogen therapy, like thiazide diuretics and beta-blockers, is sometimes associated with massive rises in plasma triglycerides, especially in subjects with familial hypertriglyceridemia. In such cases, discontinuation of the specific etiologic agent may obviate the need for specific drug therapy of hypertriglyceridemia. The use of drugs should be considered only when reasonable attempts have been made to obtain satisfactory results with non-drug methods. If the decision is made to use drugs, the patient should be instructed that this does not reduce the importance of adhering to diet. .
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Triglide