Buy Torvakard tablets 20 mg number 30
  • Buy Torvakard tablets 20 mg number 30

Torvacard pills 20 mg №30

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Dosage form

Coated Tablets

Composition

1 tab. contains Atorvastatin (in the form of Calcium salt) 20 mg

Packing

30 pieces

Mechanism of action

Torvacardum is a lipid-lowering drug. Selective competitive inhibitor of HMG-CoA reductase - the main enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A into mevalonic acid - the precursor of steroids, including cholesterol. In the liver, triglycerides and cholesterol are included in the composition of VLDL, enter the blood plasma and are transported to peripheral tissues. LDLs produce LDLs that are catabolized when interacting with high affinity LDL receptors. Atorvastatin reduces cholesterol (Xc) and plasma lipoproteins by inhibiting HMG-CoA reductase in the liver and increasing the number of LDL receptors in the liver on the cell surface, which leads to increased capture and catabolism of Xc-LDL.
Atorvastatin reduces the formation of Xc-LDL and the number of LDL particles. The drug causes a pronounced and persistent increase in the activity of LDL receptors, and also has a beneficial effect on the quality of circulating LDL. Atorvastatin effectively reduces the level of LDL-LDL in patients with homozygous hypercholesterolemia, which usually cannot be treated with other lipid-lowering drugs.
In the study of the dose-dependence effect of atorvastatin, it was shown that the drug (at a dose of 10-80 mg) reduced the level of total Xc (by 30-46%), Xc-LDL (by 41-61%), apolipoprotein B (by 34-50%) and triglycerides (14-33%). The results of treatment were similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia (including in patients with non-insulin dependent diabetes mellitus). Atorvastatin reduces the levels of total Xc, Xc-LDL, Xc-VLDL, apolipoprotein B, triglycerides and Xc, which is not part of HDL, and increases the level of Xc-HDL in patients with isolated hypertriglyceridemia. Atorvastatin reduces the level of intermediate-density lipoprotein cholesterol (Xc-Lpp) in patients with dysbetalipoproteinemia. Like LDL, lipoproteins containing triglycerides (including VLDL, LPPP and their residues) also accelerate the development of atherosclerosis. Increased plasma triglycerides are often found in combination with a decrease in HD-C HDL and the presence of small LDL particles, as well as in combination with non-lipid metabolic risk factors for CHD. It has not yet been proven that an increase in total plasma triglyceride levels is an independent risk factor for CHD. It is also not proven that an increase in HD-C HDL or a decrease in triglyceride levels in itself affects the risk of coronary and other cardiovascular complications and mortality of patients.
Atorvastatin and some of its metabolites are pharmacologically active.The primary target organ of the action of atorvastatin is the liver, where cholesterol synthesis and LDL clearance is performed.
Dynamics of the level of Xc-LDL correlates better with the dose of atorvastatin than with its concentration in the blood plasma. The dose of the drug should be selected based on the therapeutic effect.

Indications and usage

- in combination with a diet to reduce elevated levels of total Xc, Xc-LDL, apolipoprotein B and triglycerides and increase the level of Xc-LDL in patients with primary hypercholesterolemia, heterozygous familial and non-familial hypercholesterolemia, and combined (mixed) hyperlipidemia (type II and i) and i and i) and i and i) and i and i and i and i and i and i and i and i and i will not have imitation of idiophobicidemia. );
- in combination with a diet for the treatment of patients with elevated serum levels of triglycerides (type IV according to Fredrickson) and patients with dysbetalipoproteinemia (type III according to Fredrickson), in whom diet therapy does not give an adequate effect;
- to reduce the levels of total Xc and Xc-LDL in patients with homozygous familial hypercholesterolemia, when diet therapy and other non-pharmacological treatment methods are not sufficiently effective.

Contraindications

- active liver disease or increased serum transaminase activity (more than 3 times compared with the upper limit of the norm) of unclear genesis;
- pregnancy;
- lactation period;
- children's and teenage age up to 18 years (efficiency and safety are not established);
- Hypersensitivity to the components of the drug Torvacard.
Carefully should be used for chronic alcoholism, liver disease history, severe electrolyte imbalance, endocrine and metabolic disorders, arterial hypotension, severe acute infections (sepsis), uncontrolled epilepsy, with extensive surgical interventions, injuries of skeletal muscles.

Pregnancy and Breastfeeding

Atorvastatin is contraindicated for use during pregnancy and lactation (breastfeeding).
It is not known whether atorvastatin is excreted in breast milk. Given the possibility of adverse events in infants, if necessary, use of the drug during lactation should decide on the termination of breastfeeding. Women of reproductive age during treatment should use adequate methods of contraception. Atorvastatin can be prescribed to women of reproductive age only if the probability of pregnancy is very low and the patient is informed about the possible risk of treatment for the fetus.

Dosage and administration

Before prescribing Torvacard, the patient should be advised to recommend a standard lipid-lowering diet, which he must continue to follow throughout the entire period of therapy.
The initial dose is an average of 10 mg 1 time / day. The dose varies from 10 to 80 mg 1 time / day. The drug can be taken at any time of the day with food or regardless of meal times.The dose is selected based on the initial levels of LDL-C, the goal of therapy and the individual effect. At the beginning of treatment and / or during the dose increase of Torvacard, it is necessary to monitor plasma lipid levels every 2-4 weeks and correct the dose accordingly.
Atprimary hypercholesterolemia and mixed hyperlipidemia in most cases, it is enough to give a dose of 10 mg of the drug Torvacard 1 time / 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.

Special notes

Before starting treatment with Torvacard, the patient should be prescribed a standard hypocholesterol diet, which he must follow during the entire period of treatment.
The use of HMG-CoA reductase inhibitors to reduce the level of lipids in the blood can lead to changes in biochemical parameters reflecting the function of the liver. Liver function should be monitored before starting therapy, 6 weeks, 12 weeks after starting to take 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. Patients with increased transaminase levels should be monitored until the level of enzymes returns to normal.In the event that the ALT or AST values ​​are more than 3 times higher than the upper limit of normal (VGN) level, it is recommended to reduce the dose of Torvacard or discontinue treatment.
Torvacard should be used with caution in patients who abuse alcohol and / or have liver disease. Active liver disease or a persistent increase in the activity of aminotransferases of unclear genesis serve as contraindications to the administration of Torvacard.
Treatment with Torvacard can cause myopathy. In patients with common myalgia, muscle soreness or weakness and / or a pronounced increase in CPK activity, one should bear in mind the possibility of developing myopathy (pain and weakness in muscles combined with an increase in CPK activity more than 10 times as compared with VGN). Patients should be warned that they should immediately inform the doctor about the appearance of unexplained pain or weakness in the muscles, if they are accompanied by indisposition or fever. Therapy with Torvacard should be discontinued in the case of a pronounced increase in the activity of CPK or in the presence of a confirmed or suspected myopathy. The risk of myopathy in the treatment of other drugs of this class increased with the simultaneous use of cyclosporine, fibrates, Erythromycin , nicotinic acid or azole antifungal agents. Many of these drugs inhibit the metabolism mediated by the CYP3A4 isoenzyme and / or the transport of drugs. Atorvastatin is biotransformed by CYP3A4.When prescribing atorvastatin in combination with fibrates, erythromycin, immunosuppressive drugs, azole antifungal drugs or nicotinic acid in lipid-lowering doses, the expected benefit and risk of treatment should be carefully weighed and regularly monitored by patients to identify pain or weakness in muscles, especially during the first months of treatment and during periods of increasing the dose of any drug. In such situations, periodic determination of CPK activity can be recommended, although such monitoring does not prevent the development of severe myopathy.
When using atorvastatin, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria are described. 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 disturbances and uncontrolled seizures). Before starting treatment with 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. Patients should be warned thatthat they should immediately see a doctor if they develop unexplained pains or weakness in the muscles, especially if they are accompanied by indisposition or fever.
Influence on ability of driving and work with mechanisms
No adverse effect of Torvacard on the ability to drive and work with mechanisms was reported.

The risk of myopathy during treatment with other drugs of this class is increased with simultaneous use of cyclosporine, fibrates, erythromycin, antifungal drugs related to azoles, and niacin.
With simultaneous ingestion of atorvastatin and a suspension containing Magnesium and aluminum hydroxide, plasma concentrations of atorvastatin decreased by approximately 35%, however, the degree of decrease in LDL-C levels did not change.
With simultaneous use of atorvastatin does not affect the pharmacokinetics of antipyrine, therefore, interactions with other drugs metabolized by the same cytochrome isoenzymes are not expected.
With simultaneous use of colestipol, the concentration of atorvastatin in the blood plasma decreased by approximately 25%. However, the lipid-lowering effect of the combination of atorvastatin and colestipol was superior to that of each drug separately.
When repeated administration of Digoxin and atorvastatin at a dose of 10 mg, the equilibrium concentration of digoxin in the 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 monitoring.
With simultaneous use of atorvastatin and erythromycin (500 mg 4 times / day) or Clarithromycin (500 mg 2 times / day), which inhibit the CYP3A4 isoenzyme, an increase in the concentration of atorvastatin in the blood plasma was observed.
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 did not change.
Atorvastatin did not have a clinically significant effect on the concentration of terfenadine in plasma, which is metabolized mainly with the participation of CYP3A4; therefore, it seems unlikely that atorvastatin can significantly affect the pharmacokinetic parameters of other CYP3A4 substrates.
With simultaneous use of atorvastatin and oral contraceptive containing norethindrone and ethinyl estradiol, there was a significant increase in the AUC of norethindrone and ethinyl estradiol by about 30% and 20%, respectively. This effect should be considered when choosing an oral contraceptive for a woman receiving atorvastatin.
When studying the interaction of atorvastatin with Warfarin and cimetidine signs of a clinically significant interaction was not found.
With simultaneous use of atorvastatin 80 mg and Amlodipine 10 mg, the pharmacokinetics of atorvastatin in an equilibrium state did not change.
The simultaneous use of atorvastatin with protease inhibitors, known as inhibitors of the CYP3A4 isoenzyme, was accompanied by an increase in plasma atorvastatin concentrations.
No clinically significant undesirable interaction of atorvastatin and antihypertensive drugs, as well as with estrogens. Studies of the interaction with all specific drugs were not conducted.
Pharmaceutical incompatibility is unknown.

Symptoms: possible hypotension.
Treatment: conducting symptomatic therapy. There is no specific antidote. Hemodialysis is ineffective.

The drug should be stored out of the reach of children at a temperature of 10 ° to 30 ° C.

2 years.