Buy Generic Tricor (Fenofibrate) 160, 200 mg online

Last Updated on February 19, 2017 by Dr.Derek Fhisher

Most popular brand: Tricor
Active ingredient: Fenofibrate
Available dosage forms: 160, 200 mg

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Fenofibrate general information

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Fenofibrate *

Description of the active ingredient fenofibrate / Fenofibratum.

Formula: C20H21ClO4, chemical name: 2 – [4 – (4 – chlorobenzoyl) phenoxy] – 2 – methylpropanoic acid 1 – methyl ethyl ether
Pharmacological group: Metaboliki / lipid-lowering agents / fibrates
Mode of action:. hypolipidemic, antiagregatine, uricosuric.

Pharmacological Properties

Fenofibrate is a fibric acid derivative. The metabolism of fenofibrate formed fenofibric acid (active metabolite), which activates receptors PPAR – alpha (alpha – receptors that activate peroxisome proliferator) and enhances lipolysis and clearance from serum of atherogenic lipoproteins rich in triglycerides by reducing the formation of apolipoprotein CIII and activation lipoprotein lipase. Also, when you activate PPAR – alpha enhanced production of apolipoproteins AI and AII. These reactions resulted in a decrease in the level of low density lipoprotein fraction and very low density lipoproteins, which include apolipoprotein B, and increasing high density lipoprotein fraction, which include apolipoproteins AI and AII. Correcting violations formation and catabolism of very low density lipoproteins, fenofibrate increases the clearance of LDL and lowers the concentration of small and dense particles of LDL, an increase that is observed in patients with atherogenic phenotype of lipids (in patients with coronary heart disease risk that is part of a violation) .
In clinical trials indicated that the use of fenofibrate reduces triglyceride concentration by 40 – 55% and total cholesterol by 20 – 25% increase in the cholesterol content of high density lipoproteins at 10 – 30%. In patients with hypercholesterolemia, in which the low-density cholesterol concentration of lipoproteins was decreased by 20 – 35%, the use of fenofibrate reduction ratios: cholesterol low density lipoprotein / cholesterol of high density lipoproteins, total cholesterol / cholesterol high-density lipoproteins, apolipoprotein B / apolipoprotein AI, which are indicative of the atherogenic risk.
Considering the effect on the concentration of triglycerides and low density lipoprotein cholesterol, efficient use of fenofibrate in patients with hypercholesterolemia is accompanied not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, including secondary hyperlipoproteinemia with diabetes mellitus type . Fenofibrate also reduces uric acid concentration increased (approximately 25%) and fibrinogen in the blood serum. When fenofibrate treatment decreases and other markers of inflammation, such as C – reactive protein. In long-term treatment of fenofibrate reduces extravascular deposits of cholesterol (tendinous and tuberous xanthoma). In animal and clinical studies during the studies have shown that fenofibrate reduces platelet aggregation, which is caused by arachidonic acid, adenosine diphosphate, epinephrine
two different forms of fenofibrate compared in clinical studies -. Nemikronizirovannuyu and micronized. When comparing blood samples of healthy humans by ingestion of these two forms it found that 67 mg of micronized fenofibrate form is bioequivalent to 100 mg of fenofibrate nemikronizirovannoy form.
When administered fenofibrate is rapidly hydrolyzed by esterases. The serum is determined only fenofibric acid, which is the main active metabolite of fenofibrate. The maximum concentration of fenofibric acid is achieved within 2 – 5 hours (depending on the dosage form). The absorption of fenofibrate is enhanced when taken with food (maximum concentration in serum and the total effect of fenofibrate nanoparticle independent of meals). With plasma proteins (albumin) of fenofibric acid binds approximately 99%. The equilibrium concentration is reached within 7 days. With prolonged use, the serum concentration of the drug remains stable regardless of the individual characteristics of the patient. The metabolism of fenofibrate and fenofibric acid are not involved cytochrome P450. The half-life of fenofibric acid is approximately 20 hours. The drug is excreted as fenofibric acid and its glucuronide mainly kidneys and intestines. During the 6 days of fenofibrate appears almost completely. Fenofibrate is not accumulates. The drug does not appear in hemodialysis. Clearance fenofibric acid with single dose of fenofibrate inside does not change significantly depending on the age of the patients, and 77 – 87 years of 1.2 l / h, in young patients – 1.1 l / h. In patients with severe renal insufficiency (with creatinine clearance less than 30 ml / min) exposure of fenofibric acid increases by 2.7 times, and in multiple dose accumulation is observed. In case of violation of renal function mild to moderate severity (with creatinine clearance 30 – 80 ml / min) increases the half-life of fenofibric acid.

Indications

Hypertriglyceridemia and

isolated hypercholesterolemia or mixed (dyslipidemia type IIa, IIb, III, IV, V) in patients for whom diet or other non-drug treatment activities (increase in physical activity, reduced body weight and others) have been ineffective, especially in there is associated with dyslipidemia risk factors such as smoking and hypertension; secondary hyperlipoproteinemia, hyperlipoproteinemia when preserved under effective therapy of the underlying disease (dyslipidemia in diabetes and others).

How to use a dose of fenofibrate and

fenofibrate ingested simultaneously with food intake (micronized form can be taken independently of meal times), 200 – 400 mg per day in 3 divided doses, micronized form – 145 – 200 mg 1 time per day
. Before you begin to fenofibrate therapy is necessary to appropriate treatment to eliminate the cause of secondary hypercholesterolemia, for example, in diseases such as hypothyroidism, uncontrolled diabetes of the second type, dysproteinemia, nephrotic syndrome, obstructive liver disease, alcoholism, the effects of drug treatment.
When receiving fenofibrate may increase the activity of liver transaminases. Basically, this increase was slight, temporary and asymptomatic. During treatment with fenofibrate is necessary to monitor the activity of hepatic transaminases every 3 months during the first year of treatment and periodically during the course of further treatment; with an increase in alanine aminotransferase and aspartate aminotransferase in 2 or more times the upper limit of normal fenofibrate overturned. If you have symptoms of hepatitis (pruritus, jaundice) you must carry out laboratory tests and, upon confirmation of the diagnosis of hepatitis, cancel fenofibrate.
When receiving fenofibrate reported pancreatitis development. In these cases, the possible causes of pancreatitis are the direct effects of the drug, the lack of efficacy in patients with severe hypertriglyceridemia, secondary phenomena that are associated with the formation of a precipitate or the presence of stones in the bile ducts, which are accompanied by obstruction of the common bile duct.
In the first 3 months therapy should determine the level of creatinine, and periodically during the course of further treatment; with an increase in serum creatinine of more than 50% above the upper limit of normal, therapy should be suspended.
When receiving fenofibrate reported on the development of toxic effects on muscle with or without renal impairment, including rhabdomyolysis. The frequency of such disorders increases with a history of renal insufficiency and hypoalbuminemia. The toxic effect on the muscles can be suspected based on the patient’s complaints of diffuse myalgia, weakness, myositis, muscle cramps or spasms and / or a marked increase in the activity of creatinine phosphokinase (more than 5 times the upper limit of normal). In these cases, treatment with fenofibrate should be stopped. The risk of rhabdomyolysis may be increased in patients with a predisposition to myopathy and / or rhabdomyolysis, including history burdened by hereditary muscle disease, age older than 70 years, hypothyroidism, kidney failure, alcohol abuse. Such patients should be prescribed fenofibrate only when the expected benefit of treatment over the potential risk of rhabdomyolysis.
Therapy should be held for a long time, along with hypolipidemic diet and under medical supervision. Efficacy of treatment should be evaluated by the content of lipids (triglycerides, total cholesterol, low density lipoprotein) in the blood plasma. If no effect after 3 – 6 months of therapy is necessary to consider the appointment of a concomitant or alternative treatment
Patients with hyperlipidemia who take estrogen or hormonal contraceptives, which contain estrogen, you should find out whether hyperlipidemia primary or secondary nature. as the increased concentration of lipids may be caused by estrogen
When fenofibrate together with inhibitors of HMG -. CoA – reductase inhibitors or fibrates other increases the risk of serious toxic effects on muscles, particularly if the patient had prior to treatment of muscle disease. Such a joint application is possible only if the high cardiovascular risk of the patient and the heavy mixed dyslipidemia, in the absence of muscle disease and a history under scrutiny, which is aimed at identifying signs of toxic effects on muscles.
With careful use of fenofibrate in the performance activities related to the high concentration of attention and speed of mental and motor responses (including the management of vehicles and mechanisms to work with).

Contraindications

Hypersensitivity, biliary cirrhosis, hepatic failure, persistent dysfunction of the liver of unknown origin, severe renal insufficiency (creatinine clearance less than 30 ml / min), photosensitivity or phototoxicity in the treatment with fibrates or ketoprofen history, pathology of the gallbladder (including in the anamnesis ), acute or chronic pancreatitis (except in cases of acute pancreatitis, which is caused by severe hypertriglyceridemia), age 18 years (safety and efficiency have not been established), the period of breastfeeding.

Restrictions on the use

Kidney failure, alcoholism, hypothyroidism, hereditary muscle diseases in history, advanced age, the presence of factors that predispose to the development of myopathy and / or rhabdomyolysis, concomitant use of oral anticoagulants, HMG inhibitors – CoA – reductase, pregnancy.

Pregnancy and breastfeeding

There are no adequate data on the use of fenofibrate in pregnancy. In animal studies, teratogenic effects of fenofibrate is not revealed. Embryotoxicity was observed at doses toxic to the mother’s body. Possible risk to humans is unknown. The use of fenofibrate in pregnancy is possible if the intended effect of treatment for the mother above the possible risk to the fetus. Fenofibrate is contraindicated during breast-feeding. Insufficient information on the allocation of fenofibrate and its metabolites in breast milk. It is impossible to eliminate the risk to infants. At the time of fenofibrate therapy should stop breastfeeding.

Side effects of fenofibrate

The nervous system and sensory organs: headache, fatigue, dizziness, fatigue
cardio – vascular system and blood (hemostasis, blood formation):. Venous thromboembolism (deep vein thrombosis, pulmonary embolism), leukocytosis, increased hemoglobin levels
Digestive system:. nausea, abdominal pain, vomiting, flatulence, diarrhea, pancreatitis, increased liver transaminases, cholelithiasis, complications of cholelithiasis, cholangitis, cholecystitis, biliary colic, jaundice, hepatitis
Urogenital system: sexual dysfunction, erectile dysfunction, acute renal failure
The supporting – motor apparatus.. : myositis, muscle weakness, myalgia, diffuse myalgia, muscle spasm, muscle damage, increased creatine phosphokinase, rhabdomyolysis
The skin, subcutaneous – adipose tissue, allergic reactions:. photosensitivity, alopecia, pruritus, skin rash, urticaria, hypersensitivity reactions, severe skin reactions (eg, Stevens – Johnson syndrome, erythema multiforme, toxic epidermal necrolysis)
Other: interstitial pneumonia, increase in urea. serum giperkreatinemiya, interstitial lung disease.

fenofibrate Interaction with other substances

Fenofibrate potentiates the effect of oral anticoagulants (acenocoumarol, warfarin, etc.) and may increase the risk of bleeding. This is due to the displacement of fenofibrate anticoagulant from the binding sites to plasma proteins; the sharing of caution. At the beginning of fenofibrate therapy should be to reduce the dose of anticoagulant about 1/3 with further gradual titration controlled by the level of international normalized ratio
When used together, fenofibrate and cyclosporin may decrease renal function.; necessary to monitor renal function in these patients, and to cancel the fenofibrate with a serious change in laboratory parameters. When used together, fenofibrate and potentially nephrotoxic drugs should carefully evaluate the risks and benefits and make use of fenofibrate in the lowest effective dose
When using fenofibrate together with inhibitors of HMG -. CoA – reductase inhibitors (atorvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, fluvastatin, cerivastatin sodium, etc.), or other fibrates increases the risk of myopathy, rhabdomyolysis, acute renal failure; it is not recommended to share
For suspected cholelithiasis in a patient who received ezetimibe and fenofibrate, it is necessary to conduct a study of the gall bladder and appoint another lipid-lowering treatment
bile acid sequestrants (cholestyramine and others) reduce the absorption of fenofibrate..; fenofibrate to be taken every 4 – 6 hours or 1 hour prior to receiving their
In in vitro studies shown that fenofibrate and fenofibric acid does not inhibit isoenzymes CYP2D6, CYP3A4, CYP1A2 and CYP2E1 cytochrome P450.. At therapeutic concentrations, fenofibrate and fenofibric acid are weak inhibitors of the CYP2A6 and CYP2C19 and a weak or moderate inhibitors of CYP2C9. Patients who are taking fenofibrate together with drugs that are metabolised isozymes CYP2A6, CYP2C19 and CYP2C9 in particular with a narrow therapeutic index should be carefully monitored and, if necessary, adjust the recommended dose of drugs.
Any message paradoxical reduction in plasma level of high density lipoprotein amid joint application glitazones (rosiglitazone and others) and fenofibrate. Reducing the level of HDL is a risk factor for serious diseases of the circulatory system, including stroke and myocardial infarction. It is necessary to exercise extreme caution and to regularly monitor the condition of the patient during this treatment, and the detection of low concentrations of cholesterol HDL drugs mentioned.

Overdose

fenofibrate overdose cases are not described. Treatment: If you suspect an overdose of fenofibrate must be symptomatic and supportive treatment; Hemodialysis is ineffective; specific antidote is not known.

Trading names of drugs with working substance fenofibrate

Grofibrat® Lipantil 200 M