Tricor, pills 145mg, 30pcs

Composition

Active ingredient: Fenofibrate (micronized) 145.0 mgm Auxiliary substances: Sucrose 145.0 mg Sodium Lauryl sulfate 10.2 mg Lactose monohydrate 132.0 mg Crospovidone 75.5 mg Microcrystalline cellulose 84.28 mg Silicon dioxide colloidal 1.72 mg Hypromellose 29.0 mg Sodium docusate 2.9 mg Magnesium stearate 0.9 mg

Shell (Opadri ® OY-B-28920): 25.1 mg

Polyvinyl alcohol 11.43 mg

Titanium Dioxide 8.03 mg

Talc 5.02 mg

Soy Lecithin 0.50 mg

Xanthan gum 0.12 mg

Pharmacological action

ATX code: C 10 AB 05 Pharmacological Propertiespharmacodynamicactivating RAPP-alpha (alpha receptors activated by the peroxisome proliferator), fenofibrate enhances lipolysis and elimination of atherogenic lipoproteins with a high content of triglycerides from plasma by activating lipoprotein lipase and reducing the synthesis of apoprotein SH. Activation of RAPP-alpha also leads to increased synthesis of apoproteins AI and AN. Fenofibrate is a derivative of fibroic acid, whose ability to change the lipid content in the human body is mediated by activation of RAPP-alpha. The effects of fenofibrate on lipoproteins described above lead to a decrease in the low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) fractions, which include apoprotein B, and an increase in the high-density lipoprotein (HDL) fractions, which include apoproteins AI and AN. In addition, by correcting violations of VLDL synthesis and catabolism, fenofibrate increases LDL clearance and reduces the content of dense and small LDL particles, an increase in which is observed in patients with an atherogenic lipid phenotype, a frequent violation in patients at risk of coronary heart disease. In clinical studies, it was noted that the use of fenofibrate reduces the level of total cholesterol by 20-25% and triglycerides by 40-55%, while increasing the level of HDL cholesterol by 10-30%. In patients with hypercholesterolemia, in whom the level of LDL cholesterol decreases by 20-35%, the use of fenofibrate led to a decrease in the ratios: “total cholesterol/HDL-cholesterol”, “LDL – cholesterol/HDL-cholesterol” and “Apo B/Apo AI”, which are markers of atherogenic risk. Taking into account the effect of fenofibrate on the level of LDL cholesterol and triglycerides, the drug is effective in patients with hypercholesterolemia, both accompanied and not accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, for example, in type 2 diabetes mellitus. During treatment with fenofibrate, extravascular cholesterol deposits (tendon and tuberous xanthomas) can significantly decrease and even completely disappear. Patients with elevated fibrinogen levels treated with fenofibrate showed a significant decrease in this indicator, as well as in patients with elevated lipoprotein levels. Other markers of inflammation, such as C-reactive protein, are also reduced by treatment with fenofibrate. For patients with dyslipidemia and hyperuricemia, an additional benefit is the uricosuric effect of fenofibrate, which leads to a decrease in uric acid concentration by approximately 25%. In clinical studies and animal experiments, fenofibrate has been shown to reduce platelet aggregation caused by adenosine diphosphate, arachidonic acid, and epinephrine. Pharmacokineticatraycor 145 mg film-coated tablets contain 145 mg of micronized fenofibrate in the form of nanoparticles. The initial fenofibrate is not detected in plasma. The main plasma metabolite is fenofibroic acid. Absorption: the maximum concentration in blood plasma (Cmax) is reached 2-4 hours after oral use. With prolonged use, the concentration of the drug in plasma remains stable, regardless of the individual characteristics of the patient. Unlike the previous dosage forms of fenofibrate, the maximum concentration in blood plasma and the overall effect of fenofibrate in the form of nanoparticles does not depend on food intake. Therefore, Tricor 145 mg can be taken at any time, regardless of food intake. Distribution: fenofibroic acid binds strongly to plasma albumin (more than 99%). Half-life: the half-life of fenofibroic acid (T1/2) is about 20 hours. Metabolism and elimination: after oral use, fenofibrate is rapidly hydrolyzed by esterases. Only the main active metabolite of fenofibrate, fenofibroic acid, is detected in plasma. Fenofibrate is not a substrate for CYP 3A4. It does not participate in microsomal metabolism. It is mainly excreted in the urine in the form of fenofibroic acid and glucuronide conjugate. Within 6 days, fenofibrate is almost completely eliminated. The total clearance of fenofibroic acid determined in elderly patients does not change. The drug does not accumulate after a single dose and with prolonged use. It is not excreted during hemodialysis.

Indications

Hypercholesterolemia and hypertriglyceridemia isolated or mixed (dyslipidemia type IIa, IIb, III, IV, V) in patients for whom diet or other non-drug treatment measures (for example, weight loss or increased physical activity) have been ineffective, especially in the presence of dyslipidemia-related risk factors such as hypertension and smoking. For the treatment of secondary hyperlipoproteinemia, the drug is used in cases where hyperlipoproteinemia persists despite effective treatment of the underlying disease (for example, dyslipidemia in diabetes mellitus).

Contraindications

The drug is strictly contraindicated in the following cases: :

• hypersensitivity to fenofibrate or other components of the drug,
• liver disease (including cirrhosis),
• severe renal insufficiency (creatinine clearance under 18 years (effectiveness and safety not established),
• a history of photosensitivity or phototoxicity during treatment with fibrates or Ketoprofen,
• gallbladder disease,
• the breast-feeding period,
• congenital galactosemia, lactase deficiency, malabsorption of glucose and galactose (product contains lactose),
• congenital phenylketonuria, the sucrase-isomaltase (the preparation contains sucrose),
• an allergic reaction to peanuts, peanut oil, soybean lecithin or related products in history (due to the risk of hypersensitivity reactions).

With caution in patients with hepatic and / or renal insufficiency, hypothyroidism; in patients who abuse alcohol, the elderly, with a burdened history of hereditary muscle diseases; while taking oral anticoagulants, HMG-CoA reductase inhibitors (see the section “Interaction with other drugs”).

Side effects

From the gastrointestinal tract: >1/100, >>1/1000, From the liver: >1/100, >>1/1000, Musculoskeletal and connective tissue disorders: >>>1/10000, Vascular disorders: >1/1000, Circulatory and lymphatic system disorders: >1/10000, Nervous system disorders: >>1/10000, Respiratory system disorders: Skin and subcutaneous fat disorders: >1/1000, >>1/10000, Laboratory tests:  >1/1000, overdose cases are not described. The specific antidote is unknown. If an overdose is suspected, symptomatic and, if necessary, supportive treatment should be prescribed. Hemodialysis is ineffective.

Interaction

Oral anticoagulants Fenofibrate enhances the effect of oral anticoagulants and may increase the risk of bleeding, which is associated with the displacement of the anticoagulant from the sites of binding to plasma proteins. At the beginning of treatment with fenofibrate, it is recommended to reduce the dose of anticoagulants by approximately one third, followed by a gradual dose adjustment. Dose selection is recommended to be carried out under the control of the level of MHO (international normalized ratio). Cyclosporine Several severe cases of reversible renal impairment have been reported during concomitant treatment with fenofibrate and cyclosporine. Therefore, it is necessary to monitor the state of renal function in such patients and discontinue fenofibrate in the event of a serious change in laboratory parameters. HMG-CoA reductase inhibitors and other fibrates Taking fenofibrate concomitantly with HMG-CoA reductase inhibitors or other fibrates increases the risk of serious toxic effects on muscle fibers (see section “Special instructions”). Cytochrome P450 enzymes: In vitro studies of human liver microsomes have shown that fenofibrate and fenofibroic acid are not inhibitors of the following cytochrome P450 isoenzymes (CYP3A4, CYP2D6, CYP2E1, or CYP1A2). At therapeutic concentrations, these compounds are weak inhibitors of the CYP2C19 and CYP2A6 isoenzymes and weak or moderate inhibitors of CYP2C9.

How to take it, course of use and dosage

Trikor 145 mg tablets should be swallowed whole, without chewing, with water. Tricor 145 mg can be taken at any time of the day, regardless of food intake. Adults. One tablet of Trikor 145 mg once a day. Patients taking one capsule of fenofibrate 200 mg or one tablet of fenofibrate 160 mg per day can switch to taking 1 tablet of Trikor 145 mg without additional dose adjustment. Elderly patients. It is recommended to take the standard adult dose (one tablet of Trikor 145 mg once a day). Patients with liver diseases. The use of the drug in patients with liver diseases has not been studied. The drug should be taken for a long time, while continuing to follow the diet that the patient followed before starting treatment with Trikor 145 mg.

Special instructions

Before starting treatment with Trikor 145 mg, appropriate treatment should be carried out to eliminate the cause of secondary hypercholesterolemia, for example, in diseases such as uncontrolled type 2 diabetes, hypothyroidism, nephrotic syndrome, dysproteinemia, obstructive liver diseases, consequences of drug therapy, alcoholism. The effectiveness of therapy should be evaluated by the content of lipids (total cholesterol, LDL, triglycerides) in the blood serum. In the absence of a therapeutic effect after several months of therapy (usually after 3 months), the expediency of prescribing concomitant or alternative therapy should be considered. In patients with hyperlipidemia who are taking estrogens or hormonal contraceptives containing estrogens, it is necessary to determine whether the hyperlipidemia is of a primary or secondary nature. In such cases, an increase in lipid levels may be caused by taking estrogens Liver function: When taking Trikor 145 mg and other drugs that reduce lipid concentrations, an increase in the level of “hepatic” transaminases has been described in some patients. In most cases, this increase was temporary, insignificant, and asymptomatic. During the first 12 months of treatment, it is recommended to monitor the level of transaminases (ALT, ACT) every 3 months. Patients who have increased transaminase concentrations during treatment require attention, and in case of an increase in ALT and ACT concentrations by more than 3 times compared to the upper limit of normal, the drug is discontinued. Pancreatitis: Cases of pancreatitis have been reported during treatment with Trikor 145 mg. Possible causes of pancreatitis in these cases were: insufficient efficacy of the drug in patients with severe hypertriglyceridemia, direct exposure to the drug, as well as secondary phenomena associated with the presence of stones or sediment formation in the gallbladder, accompanied by obstruction of the common bile duct. Muscle: When taking Trikor 145 mg and other lipid-lowering medications, cases of toxic effects on muscle tissue have been reported, including very rare cases of rhabdomyolysis. The frequency of this disorder increases in the case of hypoalbuminemia and a history of renal failure. Toxic effects on muscle tissue may be suspected based on patient complaints of weakness, diffuse myalgia, myositis, muscle spasms and convulsions, and / or a marked increase in creatinine phosphokinase (CPK) (more than 5 times the upper limit of normal). In these cases, treatment with Trikor 145 mg should be discontinued. The risk of developing rhabdomyolysis may be increased in patients with a predisposition to myopathy and/or rhabdomyolysis, including those over 70 years of age, a history of hereditary muscle diseases, impaired renal function, hypothyroidism, and alcohol abuse. Such patients should be prescribed the drug only if the expected benefit exceeds the possible risk of developing rhabdomyolysis. When taking Trikor 145 mg concomitantly with HMG-CoA reductase inhibitors or other fibrates, the risk of serious toxic effects on muscle fibers increases, especially if the patient suffered from muscle disease before starting treatment. In this regard, the combined use of Trikor 145 mg and statin is permissible only if the patient has severe mixed dyslipidemia and a high cardiovascular risk, in the absence of a history of muscle disease and in conditions of close monitoring aimed at detecting signs of toxic effects on muscle tissue. Renal function: If the creatinine concentration increases by more than 50% above the upper limit of normal, treatment should be suspended. In the first three months of treatment, it is recommended to determine creatinine concentrations. Effect on the ability to drive a car and other mechanisms When using the drug, there was no effect on the ability to drive a car and manage mechanisms.

Active ingredient

Fenofibrate

Conditions of release from pharmacies

By prescription

Dosage form

Tablets