Torvacard pills 20 mg 90 pcs
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Active ingredients
Atorvastatin
Release form
Pills
Composition
Active ingredient: Atorvastatin (Atorvastatin) Concentration of the active substance (mg): 20
Pharmacological effect
Lipid-lowering drug from the group of statins. a selective competitive inhibitor of GMG-coa-reductase - an enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme and into mevalonic acid, which is a precursor of steroids, including cholesterol. in the liver, triglycerides and cholesterol are included in the composition of lopps, enter the blood plasma and are transported to peripheral tissues. of lopps, lpnp is formed during interaction with the receptor for lpnp. atorvastatin reduces cholesterol (xc) and plasma lipoproteins by inhibiting GMC-co-reductase, cholesterol synthesis in the liver and increasing the number of LPNP receptors in the liver on the cell surface, which leads to increased seizure and catabolism. LPP. curvastatin reduces the formation of LPP, causes a pronounced and persistent increase in the activity of lpnp receptors. atorvastatin reduces the level of lpnp in patients with homozygous familial hypercholesterolemia, which usually does not respond to therapy with other hypolipidemic agents. decreases the level of total xc by 30-46%, lpnp - by 41-61%, apolipoprotein in - by 34-50% and triglycerides - by 14-33%; causes an increase in the concentration of cs-apvp and apolipoprotein a. dose-dependently reduces the level of lpnp in patients with homozygous hereditary hypercholesterolemia resistant to treatment with other lipid-lowering drugs.
Pharmacokinetics
Absorption is high. Cmax is achieved in 1-2 hours. Cmax in women above the norm by 20%, AUC - below the norm by 10%; Cmax in patients with alcoholic cirrhosis of the liver is 16 times higher than normal, AUC - 11 times higher than normal. Food somewhat reduces the rate and duration of absorption of the drug (by 25% and 9%, respectively), but lowering LDL cholesterol is similar to that when using atorvastatin without food. Atorvastatin concentration when applied in the evening is lower than in the morning (approximately 30%). A linear relationship was found between the degree of absorption and the dose of the drug. The bioavailability is 12%, the systemic bioavailability of the inhibitory activity against HMG-CoA reductase is 30%. Low systemic bioavailability is caused by presystemic metabolism in the mucous membrane of the gastrointestinal tract and during the first passage through the liver. DistributionMedium Vd is 381 l.Plasma protein binding is 98%. Metabolism Metabolized mainly in the liver under the action of CYP3A4, CYP3A5 and CYP3A7 isoenzymes with the formation of pharmacologically active metabolites (ortho and parahydroxylated derivatives, beta-oxidation products). In vitro ortho- and para-hydroxylated metabolites have an inhibitory effect on HMG-CoA reductase, comparable to that of atorvastatin. The inhibitory effect of the drug in relation to HMG-CoA reductase is approximately 70% determined by the activity of circulating metabolites. or extrahepatic metabolism (not subjected to severe enterohepatic recirculation). T1 / 2 - 14 h. The inhibitory activity on HMG-CoA reductase remains about 20-30 h due to the presence of active metabolites. Less than 2% of the ingested dose of the drug is determined in the urine. It is not displayed during hemodialysis.
Indications
In combination with a diet to reduce elevated total cholesterol concentrations, cholesterol / LDL, apolipoprotein B and triglyceride levels and increasing concentrations of HDL cholesterol in patients with primary hypercholesterolemia, heterozygous familial and non-familial hypercholesterolemia and combined (mixed) hyperlipidemia (Types IIa and IIb by Frederickson); In combination with a diet for the treatment of patients with elevated serum concentrations of triglycerides (familial endogenous hypertriglyceridemia type IV by Frederickson) and patients with dysbetali poproteinemia (type III by Frederickson), in which diet therapy does not give an adequate effect; To reduce the concentration of total cholesterol and cholesterol / LDL in patients with homozygous familial hypercholesterolemia, when diet therapy and other non-pharmacological treatments are not effective enough (as a supplement to lipid-lowering therapy, including autohemotransfusions of blood purified from LDL) Cardiovascular diseases (in patients with elevated risk factors for CHD, an elderly person older than 55 years, smoking, hypertension, diabetes mellitus, peripheral vascular disease, previous stroke, left ventricular hypertrophy, protein- / albuminuria, coronary heart disease in close relatives), including:on the background of dyslipidemia - secondary prevention in order to reduce the overall risk of death, myocardial infarction, stroke, re-hospitalization for angina and the need for a revascularization procedure.
Contraindications
Hypersensitivity to the components of the drug; Active liver disease or increased serum activity of “liver” transaminases (more than 3 times compared with the upper limit of the norm) of unclear genesis, liver failure (severity A and B on the Child-Pugh scale); Hereditary diseases , such as lactose intolerance, lactase deficiency or glucose-galactose malabsorption (due to the presence of lactose in the composition); Pregnancy, lactation period; Women of reproductive age who do not use adequate and methods of contraception; Age up to 18 years (efficacy and safety have not been established).
Precautionary measures
The drug should be kept out of the reach of children.
Use during pregnancy and lactation
Atorvastatin is contraindicated for use during pregnancy and lactation (breastfeeding). Since cholesterol and substances synthesized from cholesterol are important for fetal development, the potential risk of inhibition of HMG-CoA reductase exceeds the benefits of using the drug during pregnancy. When using Lovastatin (an HMG-CoA reductase inhibitor) with dextroamphetamine in the first trimester of pregnancy, there have been cases of births of children with deformities of the bones, tracheoesophageal fistula, and anus atresia. If pregnancy is diagnosed during treatment with Torvacard, the drug should be immediately discontinued, and patients warned of the potential risk to the fetus. If you need to use the drug during lactation, taking into account the possibility of undesirable effects in infants, you should decide whether to stop breastfeeding. Use in women of reproductive age is possible only in the case of using reliable methods of contraception. The patient should be informed of the possible risk of treatment for the fetus.
Dosage and administration
Before prescribing TORVACARD, the patient should be advised to recommend a standard cholesterol-lowering diet, which he must continue to follow during the entire period of therapy.The drug is taken orally at any time of the day, regardless of the meal time. The initial dose is an average of 10 mg 1 time / day. The dose varies from 10 to 80 mg 1 time / day. The dose is selected based on the initial concentrations of cholesterol / LDL, the goal of therapy and individual effect. At the beginning of treatment and / or during the dose increase of the drug Torvacard it is necessary every 2-4 weeks to monitor plasma lipid concentrations and adjust the dose accordingly. The maximum daily dose is 80 mg in 1 reception. Primary hypercholesterolemia and mixed hyperlipidemia. In most cases, it is enough to give a dose of 10 mg of TORVACARD® 1 time per day. A significant therapeutic effect is observed after 2 weeks, as a rule, and the maximum therapeutic effect is usually observed after 4 weeks. With long-term treatment, this effect persists. When determining the goal of treatment, you can use the following recommendations.
Side effects
The frequency of adverse reactions listed below was determined according to the following (classification of the World Health Organization): very often - more than 1/10, often - from more than 1/100 to less than 1/10, infrequently - from more than 1/1000 to less than 1/100 , rarely - from more than 1/10000 to less than 1/1000, very rarely - from less than 1/10000, including individual messages. From the side of the central nervous system: often - headache, asthenia, insomnia; infrequently, dizziness, drowsiness, nightmares, amnesia, depression, peripheral neuropathy, ataxia, hypoesthesia, paresthesia. On the part of the digestive system: often - nausea, vomiting, constipation or diarrhea, flatulence, gastralgia, abdominal pain; infrequently - anorexia or increased appetite, hepatitis, pancreatitis, cholestatic jaundice. From the musculoskeletal system: very often - myalgia; arthralgia; infrequently - myopathy; rarely - myositis, rhabdomyolysis, back pain, cramps of the calf muscles of the legs. Allergic reactions: often - pruritus, rash; infrequently - urticaria; very rarely - angioedema, anaphylactic shock, bullous eruptions, polyformal exudative erythema, incl. Stevens-Johnson syndrome, toxic epidermal necrolysis (Lyell's syndrome). Laboratory indicators: infrequently - hyperglycemia, hypoglycemia, increased activity of serum creatine phosphokinase (CPK), increased activity of aspartate aminotransferase (ACT) and alanine aminotransferase (ALT).Other: often - chest pain, peripheral edema; infrequently - impotence, alopecia, tinnitus, weight gain, malaise, weakness, thrombocytopenia, secondary renal failure.
Overdose
Treatment: symptomatic treatment. There is no specific antidote. Hemodialysis is ineffective.
Interaction with other drugs
With the simultaneous use of cyclosporine, fibrates, erythromycin, clarithromycin, immunosuppressive and antifungal drugs of the azoles group, nicotinic acid and nicotinamide, drugs inhibiting metabolism, mediated by the isoenzyme 3A4 CYP450, and / or drug transport, concentration of atorvastatin in the blood plasma (the risk of the risk of the risk of treating anesthesia, and the concentration of atorvastatin in the blood plasma (and the risk of the risk of the risk of the risk of atomic plasma, and the concentration of atorvastatin in the blood plasma (A) and the transport of drugs, the concentration of atorvastatin in the blood plasma (AARP), and the concentration of atorvastatin in the blood plasma (A) and the concentration of atorvastatin in the blood plasma) rises. When prescribing these drugs, one should carefully weigh the expected benefit and risk of treatment, regularly monitor patients to identify pain or weakness in muscles, especially during the first months of treatment and during the dose increase period of any drug, periodically determine the activity of CPK, although this control does not allow prevent the development of severe myopathy. Therapy with Torvacard should be discontinued in the event of a pronounced increase in CPK activity or in the presence of confirmed or suspected myopathy. Atorvastatin did not have a clinically significant effect on plasma terfenadine concentration, which is metabolized mainly by the isoenzyme of CYP3A4; therefore, it seems unlikely that atorvastatin can significantly affect the pharmacokinetic parameters of other substrates of the isoenzyme, CYP3A4. With simultaneous use of atorvastatin (10 mg 1 time / day) and azithromycin (500 mg 1 time / day), the concentration of atorvastatin in the blood plasma does not change. When simultaneously taking atorvastatin and drugs containing magnesium and aluminum hydroxides, the concentration of atorvastatin in the plasma blood decreased by approximately 35%, however, the degree of reduction in LDL-C LDL levels did not change. With simultaneous use of colestipol, plasma concentrations of atorvastatin decreased by about 25%. However, the lipid-lowering effect of the combination of atorvastatin and colestipol exceeded that of each drug separately. When used simultaneously, atorvastatin does not affect the pharmacokinetics of phenazone, therefore, interaction with other drugs metabolized by the same isoenzymes of CYR450 is not expected. When studying the interaction of atorvastatin with warfarin, cymethyldine, is not expected.phenazone signs of clinically significant interaction not detected. Simultaneous use with drugs that reduce the concentration of endogenous steroid hormones (including cimetidine, ketoconazole, spironolactone), increases the risk of reducing endogenous steroid hormones (caution should be exercised). There is no clinically significant unwanted atorvastatin interaction with antihypertensives, as well as with estrogens. With simultaneous use of atorvastatin in a dose of 80 mg / day and oral contraceptives, Norethindrone and ethinyl estradiol, there was a significant increase in the concentration of norethindrone and ethinyl estradiol by about 30% and 20%, respectively. This effect should be taken into account when choosing an oral contraceptive for women receiving Torvacard. When atorvastatin is used at a dose of 80 mg and amlodipine at a dose of 10 mg, the pharmacokinetics of atorvastatin in an equilibrium state did not change. When repeated administration of digoxin and atorvastatin at a dose of 10 mg, the equilibrium concentrations of digoxin in blood plasma did not change. However, when using digoxin in combination with atorvastatin at a dose of 80 mg / day, the concentration of digoxin increased by about 20%. Patients receiving digoxin in combination with atorvastatin require observation. Studies of interactions with other drugs have not been conducted.
special instructions
Before starting treatment with drug Torvacard, it is necessary to try to control hypercholesterolemia by adequate diet therapy, increasing physical activity, reducing body weight in patients with obesity and treating other conditions. The use of HMG-CoA reductase inhibitors to reduce blood lipids can lead to changes in biochemical parameters, reflecting liver function. Liver function should be monitored before starting therapy, after 6 weeks, 12 weeks after starting the administration of the drug Torvacard and after each dose increase, as well as periodically (for example, every 6 months). An increase in the activity of liver enzymes in the serum may be observed during therapy with Torvacard (usually during the first 3 months). Patients with increased transaminase levels should be monitored until the level of enzymes returns to normal.If ALT or AST values are more than 3 times higher than VGN, it is recommended to reduce the dose of Torvacard or stop treatment. Treatment with Torvacard can cause myopathy (pain and weakness in muscles combined with an increase in the activity of CPK more than 10 times as compared to with VGN). Torvacard can cause an increase in serum CPK, which should be taken into account in the differential diagnosis of chest pains. Patients should be warned that they should immediately consult a doctor if they develop unexplained pains or weakness in the muscles, especially if they are accompanied by indisposition or fever. Therapy with Torvacard should be temporarily stopped or completely canceled if there are signs of possible myopathy or a risk factor for the development of renal failure in the presence of rhabdomyolysis (for example, severe acute infection, hypotension, serious surgery, trauma, severe metabolic, endocrine and electrolyte disorders and uncontrolled seizures ). Preparations of the class of statins can cause an increase in the concentration of glucose in the blood. In some patients with a high risk of developing diabetes mellitus, such changes can lead to its manifestation, which is an indication for prescribing antidiabetic therapy. However, reducing the risk of vascular diseases during the use of statins exceeds the risk of developing diabetes, therefore this factor should not serve as a basis for discontinuation of treatment with statins. Patients at risk (blood glucose concentration on an empty stomach 5.6-6.9 mmol / l, BMI> 30 kg / m2, hypertriglyceridemia, history of arterial hypertension) should be monitored and regularly monitored biochemical parameters. Effect on ability to drive and work with The mechanisms of the adverse effects of Torvacard on the ability to drive vehicles and engage in other activities requiring concentration of attention and speed of psychomotor reactions were not reported.