Pharmacological properties Trilipix 135 mg:
Trilipix lipid-lowering agent of fibric acid derivatives (fibrates). Fenofibrate lowers serum total cholesterol by 20-25%, LDL and VLDL, TG – by 40-50% and raises HDL by 30-40%, with a decrease ratio of total cholesterol / HDL-C increased in atherogenic hyperlipidemia.
A variety of positive effects of fenofibrate on lipid profile due to the impact on the process of regulation of expression of key genes involved in lipid metabolism, through receptors such as RRAR. Activation of the receptor RRAR fenofibrate reduces the production of apo-CIII, which changes the ratio apo-SII/apo-SIII and leads to increased activity of the enzyme lipoprotein lipase and VLDL catabolism. Fenofibrate helps transform into large VLDL, apo-CIII-depleted, cholesterol, which are easy to communicate with the cellular LDL receptors and are derived from blood, and then subjected catabolism.
Effect of fenofibrate on the receptors leads to activation of RRAR enzymes involved in mitochondrial β-oxidation and subsequent increase in fatty acid oxidation and decreased production of triglycerides. On the fenofibrate is an increase in the level of apo-AI and apo-reducing BI, which in turn helps to improve relations apo-AI/apo-VI, which is an indicator of atherogenic risk, and the reduction of lp (a) – an independent risk factor for atherosclerosis .
Fenofibrate reduces the risk of cardiovascular disease, because there is a direct link between hyperlipidemia and atherosclerosis. During prolonged therapy significantly reduced extravascular cholesterol deposits (xanthoma tendinosum et tuberosum) until the complete involution.
Fenofibrate has a positive effect on the number of nelipidnyh parameters, often disturbed by hyperlipidemia. Fenofibrate exhibits antiplatelet activity by inhibiting platelet aggregation induced by ADP, arachidonic acid and epinephrine, decreases the level of fibrinogen in the blood, improves blood rheology, and also has uricosuric effect, lowering uric acid levels by 25%.
Fenofibrate unchanged in the blood plasma is not defined. The main metabolite is fenofibrinovaya acid. The maximum plasma concentration observed after an average of 5 hours after administration of fenofibrate. Average plasma concentrations when administered a dose of 200 mg is 15 mg / ml. The equilibrium concentration is maintained throughout the treatment period. Fenofibrinovaya acid has a high degree of binding to albumin of blood plasma, which can lead to the exclusion of indirect anikoagulyantov from the binding sites and increase their effect. The half-life fenofibrinovoy acid from plasma is about 20 h.
Fenofibrate is mainly excreted in the urine up to 70% within 24 hours, up to 88% within 6 days after removal of up to 93% (with urine and feces). Fenofibrate is largely excreted as fenofibrinovoy acid and its conjugate with glucuronic acid. Propafenone cumulation in the body is not observed. Fenofibrinovaya acid does not appear in hemodialysis.
Application in the form of micronized fenofibrate significantly increases the bioavailability.
INDICATIONS Trilipix 135 mg:
hypercholesterolemia (Type IIa classification Frideriksona), endogenous hypertriglyceridemia (type IV), as well as their combination (types IIb and III) with lack of effectiveness diet and / or the presence of associated risk factors.
USE Trilipix 135 mg:
100 mg by mouth 3 times daily, when used in micronized form of drug – 200 mg 1 time a day.
Fenofibrate therapy is carried out in combination with diet. Fenofibrate is used for a long time.
Contraindications: severe hepatic and renal failure, children’s age, concomitant treatment with drugs that provide hepatotoxic action (pergeksilina maleate, MAO inhibitors, etc.).
SIDE EFFECTS Trilipix 135 mg:
very rare (less than 2-4%), mild dyspeptic symptoms, skin allergic reactions, elevated transaminases in serum, myalgia. Long-term clinical follow-up (6 years) found no cases of gallstone disease in patients receiving fenofibrate. However, taking into account the existence of such a side effect from taking other lipid-lowering drugs of fibrates (clofibrate), we can not completely exclude the possibility of such pathology in some patients receiving long-term fenofibrate.
SPECIAL NOTES Trilipix 135 mg:
in the absence of the necessary therapeutic effect for 3-6 months of fenofibrate can be assigned to or accompanying an alternative therapy.
Some patients may experience a temporary increase in transaminase activity in serum, and therefore recommended to monitor these indicators every 3 months in the 1st year of therapy. We recommend taking a temporary break in the fenofibrate in a significant increase in ALT activity.
In experimental studies have not revealed teratogenic effects of fenofibrate, however, caution should be exercised when administered to women during pregnancy.
No data on the flow of metabolites of fenofibrate in breast milk, however, assign it to the breast-feeding is not recommended.
INTERACTION:
while oral anticoagulants may potentiate their effects and in the risk of bleeding. In such cases it is recommended to control the level of prothrombin and correct doses of anticoagulants during treatment with fenofibrate, and 8 days after its cancellation.
