Activating receptors PPARa (alpha receptors, peroxisome proliferator-activated), fenofibrate increases lipolysis and clearance from plasma atherogenic lipoprotein with a high content of triglycerides by reducing the activation of lipoprotein lipase anadrol vs dbol synthesis and apoprotein CIII. .Aktivatsiya PPAR-α also leads to increased synthesis of apoprotein AI and AIL. Fenofibrate is fibreboard acid derivative, wherein the ability to alter lipids in humans is mediated by activation of PPARα. The above-described effects of fenofibrate on lipoproteins lead to a reduction in the fraction of low lipoprotein cholesterol content (LDL) and very low density (VLDL), which include apoprotein B and an increase in the fraction of high density lipoprotein (HDL), which include apoproteins AI and AN . Furthermore, by correcting the synthesis disorders and catabolism of VLDL, fenofibrate increases the LDL clearance and reduces the dense and small LDL particles, increase which occurs in patients with the risk of coronary heart disease. In clinical trials, it was noted that the use of fenofibrate reduces total cholesterol by 20 – 25% and triglycerides by 40 – 55% increase in HDL-cholesterol by 10 – 30%. In patients with hypercholesterolemia, in which the LDL-cholesterol level is reduced by 20 – 35% using fenofibrate reduction ratio “total cholesterol / HDL-cholesterol”, “LDL-cholesterol / HDL-cholesterol” and “Apo B / Apo A1” which are markers of atherogenic risk.Given the significant effect on LDL-cholesterol and triglycerides, effective use of fenofibrate in patients with hypercholesterolemia. whether unaccompanied or accompanied by hypertriglyceridemia, including secondary hyperlipoproteinemia, such as type 2 diabetes. Currently, there are no results of long-term controlled clinical trials have demonstrated the efficacy of fenofibrate as a means for the primary or secondary prevention of atherosclerotic complications. During treatment with fenofibrate can significantly decrease or even disappear entirely extravascular deposits of cholesterol (tendinous and tuberous xanthoma). Patients with elevated levels of fibrinogen that received treatment with fenofibrate, a marked decrease in this figure, as well as in patients with elevated levels of Lp (a). Other markers of inflammation such as C-reactive protein, are also reduced with fenofibrate for the treatment. For patients with dyslipidemia and hyperuricemia additional advantage is the uricosuric effect of fenofibrate leading to reduction in plasma uric acid concentrations by approximately 25%. During clinical studies and animal experiments have shown that fenofibrate reduces platelet aggregation induced by adenosine diphosphate, arachidonic acid and epinephrine. The pharmacokinetics source fenofibrate is not detected in the plasma. The major plasma metabolite is fenofibric acid. Suction: maximum plasma concentration (C max ) is reached after 4-5 hours after ingestion. With prolonged use of the drug concentration in the plasma remains stable. The absorption of fenofibrate is enhanced when taken with food. Distribution: fenofibric acid binds strongly to atbuminom blood plasma (99%). The half-life:half-life of fenofibric acid – about 20 hours. Metabolism and excretion: only major metabolite of fenofibrate is detected in plasma – fenofibric acid. Displayed mainly kidneys in the form of fenofibric acid and the glucuronide conjugate. During the 6 days of fenofibrate appears almost completely. The total clearance of fenofibric acid, determined not altered in elderly patients. The drug is not cumulated after a single dose and long-term use. When hemodialysis is not deduced.
Hypercholesterolemia and hypertriglyceridemia isolated or mixed (dyslipidemia, type IIa, IIb, III, IV) in patients for whom diet and other non-drug therapeutic measures (eg weight reduction or increased physical activity) have been ineffective, especially when associated with dyslipidemia risk factors.
Patients should adhere to a diet, which they complied with before treatment.
The drug is strictly contraindicated in the following cases:
- Hypersensitivity to the fenofibrate or the other components of the drug
- liver failure (including cirrhosis),
- renal insufficiency (creatinine clearance less than 20ml / MIN)
- age of 18 years (effectiveness and safety have been established),
- a history of photosensitivity or phototoxicity during treatment with fibrates or ketoprofen,
- gallbladder disease,
- congenital galactosemia, lactase deficiency, malabsorption of glucose and galactose (a drug contains lactose).
When hypothyroidism; patients who abuse alcohol: elderly patients; patients with a history burdened by hereditary muscular diseases; while receiving oral anticoagulants, HMG-CoA reductase inhibitors.
Pregnancy and lactation Pregnancy There are limited data on the use of fenofibrate in pregnant women. In animal experiments, a teratogenic effect of fenofibrate was observed. Embryotoxicity was observed when administered during preclinical trials doses toxic to the mother’s body. The potential risk for humans is unknown. Therefore, during pregnancy Lipantil Capsules ® 200M can be used only after careful evaluation of the risk-benefit ratio when benefit to the mother outweighs the potential risk to the fetus. Lactation period Due to the lack of use of safety data, the drug is contraindicated during breast-feeding. If you need to use Lipantil ® 200M during breast-feeding, breast-feeding should be discontinued.
Should take 1 capsule per day during the main meal.
Duration of therapy is determined by a doctor.
The drug should be taken for a long time, while continuing to follow a diet that is adhered to the patient prior to treatment. In the absence of a therapeutic effect after several months of therapy (usually after 3 months -x) should consider the advisability of appointing a concomitant or alternative therapy.
The incidence of side effects is distributed as follows: very frequently (more than 10% of cases), often (in 1% – 10% of cases); infrequently (gg 0.1 – 1%); rare (0.01% – 0.1% of cases); very rarely (less than 0.01% of the cases), including isolated reports of side effects. On the part of the digestive tract. Common: abdominal pain, nausea, vomiting, diarrhea and flatulence moderate in severity. Uncommon: . Cases of pancreatitis, gallstones occurrence is very rare : episodes of hepatitis. If you have symptoms of hepatitis (jaundice, pruritus) should be carried out laboratory tests and, if confirmed hepatitis cancel fenofibrate. Skin and subcutaneous adipose tissue. Uncommon: skin rash, pruritus, urticaria. Rare: alopecia. Very rare: photosensitivity, accompanied by erythema, blistering or nodules on the skin areas exposed to sunlight or artificial UV light anadrol vs dbol (eg quartz lamp), in some cases, the reaction can occur after long-term use of the drug without any complications. On the part of the musculoskeletal system. rarely: . diffuse myalgia, myositis, muscular cramps and weakness Very rare: rhabdomyolysis ( acute necrosis of striated muscle tissue). On the part of the cardiovascular system. Uncommon:venous thromboembolism (pulmonary embolism, deep vein thrombosis). On the part of the central nervous system. rare: sexual dysfunction, headache. respiratory system: Very rare: interstitial pneumopathy.indicators of laboratory studies: Common: mild increase in activity of “liver” transaminases. Uncommon: increased creatinine and urea in serum. rare: increase in the concentration of hemoglobin and white blood cells.
Cases of overdose have not been described. A specific antidote is not known. If you suspect an overdose, symptomatic and should be appointed, if necessary, under the supports treatment. Hemodialysis is ineffective.Interaction with other medicinal products Oral anticoagulants Fenofibrate enhances oral anticoagulant effect and may increase the risk of bleeding, which is associated with competition in binding to plasma proteins. At the beginning of the treatment with fenofibrate it is recommended to reduce the dose of anticoagulants by about a third, followed by gradual dose selection. Selection of the dose recommended for the control of MHO level (international normalized ratio). Cyclosporine is described more severe cases of reversible decrease in renal function during simultaneous treatment with fenofibrate and cyclosporin. Therefore, regular monitoring of renal function in these patients, and, in the case of major changes in laboratory parameters of the drug should be abolished. Inhibitors of HMG-CoA reductase inhibitors (statins) and other fibrates When receiving fenofibrate together with inhibitors of HMG-CoA reductase inhibitors or other fibrates increased risk severe toxic effects on muscle fibers (. see <a “Special instructions” ). The enzymes of the cytochrome P450: Studies microsomes from in vitro human liver have shown that fenofibrate and fenofibric acid are not inhibitors of these cytochrome P450 isoenzymes (CYP3A4, CYP2D6, CYP2E1, or of CYP1A2) . At therapeutic concentrations of these compounds are weak inhibitors of CYP2C19 isozyme, and CYP2A6 and weak or moderate inhibitors of CYP2C9.
: Before you begin, there should be an appropriate treatment to eliminate the cause of secondary hypercholesterolemia, for example, in diseases such as uncontrolled type 2 diabetes mellitus, hypothyroidism, nephrotic syndrome, Dysproteinemia, obstructive liver disease, the effects of drug therapy, alcoholism.
The effectiveness of therapy should be evaluated on lipid content (total cholesterol, LDL cholesterol, triglyceride) in the blood serum. In the absence of a therapeutic effect after a few months of therapy (usually after 3 months -x) to consider whether the use of alternative or concomitant therapy. The effectiveness of drug treatment should be periodically evaluated by a physician.
Increasing lipid levels may be caused by intake of estrogen. Patients with hyperlipidemia, taking estrogen or hormonal contraceptives containing estrogens, it is necessary to find out anadrol vs dbol whether hyperlipidemia primary or secondary nature. Liver function: When you receive Lipantil ® 200M and other drugs that reduce the concentration of lipids in some patients described increased activity of “liver” transaminases. In most cases, this increase in activity was temporary, minor and asymptomatic. During the first 12 months of treatment is recommended to control the activity of transaminases every 3 months. Patients with treatment increased the activity of enzymes, need attention, and for an increase in ALT concentrations (alanine aminotransferase) and ACT (aspartate aminotransferase) greater than 3 times the upper limit of the norm taking the drug discontinued. Pancreatitis: Cases of pancreatitis have been described during drug treatment. Possible causes of pancreatitis in these cases were: lack of efficacy in patients with severe hypertriglyceridemia, a direct effect of the drug, as well as secondary phenomena associated with the presence of calculous cholecystitis accompanied by obstruction of the common bile duct.Muscles: When receiving Lipantil ® 200M and other drugs that reduce lipid concentrations, cases of toxic effects are described in the muscle tissue, including the very rare cases of rhabdomyolysis. The frequency of such disorders is increased in case of renal insufficiency and hypoalbuminemia history. The possibility of this complication increases in cases of hypoalbuminaemia and renal failure. The toxic effect on muscle tissue can be suspected based on the patient’s complaints of weakness, diffuse myalgia, myositis, muscle spasms and cramps, and / or expressed increasing creatinine phosphokinase (CPK) (more than 5 fold compared with the upper limit of normal). In these cases, treatment Lipantil ® 200M should be discontinued. The risk of rhabdomyolysis may be increased in patients with a predisposition to myopathy and / or rhabdomyolysis, including age above 70 years, weighed down by history for a hereditary muscular disease, renal failure, hypothyroidism, alcohol abuse. Such patients should be prescribed only if the expected benefits outweigh the potential risk of rhabdomyolysis. When receiving Lipantil ® 200M simultaneously with inhibitors of HMG-CoA reductase inhibitors or other fibrates increases the risk of serious toxic effects on muscle fibers, especially if the patient prior to treatment suffered muscle disease. Therefore, co-administration Lipantil ® 200M and statins is permissible only if the patient has severe mixed dyslipidemia and high cardiovascular risk, in the absence of muscle disease in history and in a regular control, aimed at identifying signs of toxic effects on muscle tissue . Renal function: in the case of kreatinsha increase plasma concentrations of more than 50% above the upper limit of normal, treatment should be suspended. In the first three months of treatment is recommended to determine kreatinta plasma concentrations. dragon pharma labs