Torvacard, 20 mg 90 pcs
€30.57 €26.50
Torvacard is a hypolipidemic.
Pharmacodynamics
Hypolipidemic drug from the group of statins. Selective competitive inhibitor of HMG-CoA reductase – an enzyme which converts 3-hydroxy-3-methylglutaryl coenzyme A into mevalonic acid, which is a precursor of sterols, including cholesterol (CH). Triglycerides (TG) and CH in the liver are incorporated into LDL, enter the blood plasma, and are transported to peripheral tissues. LDL are formed from LDLNP during interaction with LDL receptors.
Atorvastatin reduces plasma concentrations of CH and lipoproteins due to inhibition of HMG-CoA reductase, CH synthesis in the liver and increasing the number of hepatic LDL receptors on the cell surface, which leads to increased capture and catabolism of LDL. Reduces LDL formation, causes a pronounced and persistent increase in LDL receptor activity. Reduces LDL concentration in patients with homozygous familial hypercholesterolemia, which usually does not respond to therapy with hypolipidemic agents. Reduces the concentration of total cholesterol by 30-46%, LDL by 41-61%, apolipoprotein B by 34-50% and TG by 14-33%; causes an increase in concentration of HDL-C and apolipoprotein A.
Dose-dependently reduces LDL concentration in patients with homozygous hereditary hypercholesterolemia resistant to therapy with other hypolipidemic agents.
Pharmacokinetics
Absorption is high. Cmax in plasma is reached after 1-2 h, Cmax is 20% higher in women, AUC is 10% lower; Cmax in patients with alcoholic liver cirrhosis is 16 times higher than normal, AUC is 11 times higher.
Food slightly reduces rate and duration of drug absorption (by 25% and 9%, respectively), but decrease of LDL-C is similar to that with atorvastatin without food. Concentration of atorvastatin when administered in the evening is lower than in the morning (approximately by 30%). A linear relationship between the degree of absorption and the drug dose was found.
Bioavailability is 12%, systemic bioavailability of HMG-CoA reductase inhibitory activity is 30%. Low systemic bioavailability is due to presystemic metabolism in the gastrointestinal mucosa and during first passage through the liver.
The average Vd is 381 l, the binding to plasma proteins is 98%. It is metabolized mainly in liver under the action of CYP3A4, CYP3A5 and CYP3A7 isoenzymes with formation of pharmacological active metabolites (ortho- and parahydroxylated derivatives, β-oxidation products). In vitro, ortho- and parahydroxylated metabolites have an inhibitory effect on HMG-CoA reductase that is comparable to that of atorvastatin. The inhibitory effect of the drug against HMG-CoA reductase is approximately 70% determined by the activity of circulating metabolites.
Extracted through the intestine with bile after hepatic and/or extrahepatic metabolism (not subject to marked intestinal-hepatic recirculation).
T1/2 – 14 h. Inhibitory activity against HMG-CoA reductase persists for about 20-30 h due to the presence of active metabolites. Less than 2% of the oral dose is detected in the urine. It is not excreted during hemodialysis.
Indications
Active ingredient
Composition
1 tablet contains:
The active ingredient:
atorvastatin (in the form of calcium salt) 20 mg;
Associates:
Magnesium oxide heavy,
microcrystalline cellulose,
lactose monohydrate,
Croscarmellose sodium,
Hydroxypropylcellulose low substituted LH21,
Colloid silicon dioxide,
Magnesium stearate.
Composition of the shell:
Hypromellose 2910/5,
Macrogol 6000,
Titanium dioxide,
Talk.
How to take, the dosage
Before prescribing Torvacard, the patient should be recommended a standard hypolipidemic diet, which he should continue to follow for the duration of therapy.
The initial dose is on average 10 mg once daily. The dose varies from 10 to 80 mg once daily. The drug may be taken at any time of the day with food or regardless of the time of meals. The dose is selected taking into account the initial levels of LDL-C, the purpose of therapy and individual effect. At the beginning of treatment and/or during dose increase of Torvacard it is necessary to monitor plasma lipid levels every 2-4 weeks and adjust the dose accordingly.
In primary hypercholesterolemia and mixed hyperlipidemia, a dose of 10 mg of Torvacard once daily is sufficient in most cases. Significant therapeutic effect is usually observed after 2 weeks, and the maximum therapeutic effect is usually observed after 4 weeks. This effect persists with long-term treatment.
Interaction
The risk of myopathy during treatment with other drugs of this class is increased with concomitant use of cyclosporine, fibrates, erythromycin, azole antifungals, and niacin.
Concomitant oral administration of atorvastatin and suspension containing magnesium and aluminum hydroxide decreased plasma concentrations of atorvastatin by approximately 35%, but the degree of decrease in HDL-C levels did not change.
In concomitant use atorvastatin does not affect pharmacokinetics of antipyrine, so no interaction with other drugs metabolized by the same cytochrome isoenzymes is expected.
Concomitant use of colestipol decreased plasma concentrations of atorvastatin by approximately 25%. However, hypolipidemic effect of combination of atorvastatin and colestipol was superior to that of each drug individually.
When digoxin and atorvastatin were administered repeatedly in dose of 10 mg, equilibrium plasma concentrations of digoxin were not changed. However, when using digoxin in combination with atorvastatin at a dose of 80 mg/day, digoxin concentrations increased by approximately 20%. Patients receiving digoxin in combination with atorvastatin require monitoring.
In concomitant use of atorvastatin and erythromycin (500 mg 4 times/day) or clarithromycin (500 mg 2 times/day), which inhibit CYP3A4 isoenzyme, increased plasma concentration of atorvastatin was observed.
When concomitant use of atorvastatin (10 mg once daily) and azithromycin (500 mg once daily) the plasma concentration of atorvastatin was not changed.
Atorvastatin had no clinically significant effect on plasma concentrations of terfenadine, which is metabolized primarily with CYP3A4; in this regard, it seems unlikely that atorvastatin can significantly affect pharmacokinetic parameters of other CYP3A4 substrates.
In concomitant use of atorvastatin and oral contraceptives containing norethindrone and ethinylestradiol, there was a significant increase in AUC of norethindrone and ethinylestradiol by approximately 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 no signs of clinically significant interaction were found.
When concomitant use of atorvastatin 80 mg and amlodipine 10 mg pharmacokinetics of atorvastatin were not changed in equilibrium.
The concomitant use of atorvastatin with protease inhibitors, known as CYP3A4 isoenzyme inhibitors, was accompanied by an increase in plasma concentration of atorvastatin.
No clinically significant adverse interactions of atorvastatin and antihypertensive agents and with estrogens have been observed. Studies of interaction with all specific drugs have not been conducted.
Pharmaceutical incompatibility is unknown.
Special Instructions
Before starting therapy with Torvacard, the patient should be prescribed a standard hypocholesterolemic diet, which must be followed during the entire period of treatment.
The use of HMG-CoA reductase inhibitors to reduce blood lipid levels may lead to changes in biochemical parameters reflecting liver function. Liver function should be monitored before therapy, at 6 weeks, 12 weeks after the start of Torvacard and after each dose increase, as well as periodically (e.g., every 6 months). Elevated serum liver enzyme activity may be observed during therapy with Torvacard. Patients with elevated transaminase levels should be monitored until enzyme levels return to normal. If ALT or AST values are more than 3 times the upper limit of normal (ULN), 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 persistent elevation of aminotransferase activity of unclear genesis are contraindications to the prescription of Torvacard.
Treatment with Torvacard may cause myopathy. In patients with widespread myalgia, muscle soreness or weakness and/or a marked increase in CPK activity, the possibility of myopathy (muscle pain and weakness combined with an increase in CPK activity of more than 10 times that of IGN) should be kept in mind. Patients should be warned that they should immediately inform the doctor about unexplained muscle pain or weakness if accompanied by malaise or fever. Torvacard therapy should be discontinued if there is a marked increase in CPK activity or if there is confirmed or suspected myopathy.
The risk of myopathy when treated with other drugs in this class was increased with concomitant use of cyclosporine, fibrates, erythromycin, nicotinic acid, or azole antifungals. Many of these drugs inhibit CYP3A4 isoenzyme-mediated metabolism and/or drug transport. Atorvastatin is biotransformed by CYP3A4. Prescribing atorvastatin in combination with fibrates, erythromycin, immunosuppressive agents, azole antifungals or nicotinic acid in hypolipidemic doses, the expected benefits and risks of treatment should be carefully weighed and patients should be regularly observed for muscle pain or weakness, especially during the first months of treatment and during periods of increasing dose of any drug. In such situations, periodic determination of CPK activity may be recommended, although such monitoring does not prevent the development of severe myopathy.
In the use of atorvastatin, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria have been described. Therapy with Torvacard should be temporarily discontinued or completely canceled if there are signs of possible myopathy or a risk factor for renal failure in rhabdomyolysis (eg, severe acute infection, arterial hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders and uncontrolled convulsions). Before starting therapy with Torvacard, an attempt should be made to achieve control of hypercholesterolemia through adequate diet therapy, increased physical activity, weight reduction in obese patients, and treatment of other conditions. Patients should be warned to seek immediate medical attention if they experience unexplained muscle pain or weakness, especially if accompanied by malaise or fever.
Effects on driving and operating machinery
No adverse effects of Torvacard on driving and operating machinery have been reported.
Contraindications
Side effects
Infectious and parasitic diseases: often – nasopharyngitis.
Blood and lymphatic system disorders: rarely – thrombocytopenia.
The immune system: often – allergic reactions; very rare – anaphylaxis.
Metabolism and nutrition: frequently – hyperglycemia; infrequently – hypoglycemia, weight gain, anorexia.
Psychiatric disorders: infrequent – sleep disorders, including insomnia and nightmares.
Nervous system disorders: often – headache; infrequent – dizziness, paraesthesia, hypoesthesia, perversion of taste, loss or reduction of memory; rarely – peripheral neuropathy.
An organ of vision: infrequent – decreased clarity of vision; rarely – visual impairment.
Hearing organ and labyrinth disorders: infrequent – tinnitus; very rare – hearing loss.
Respiratory system, chest and mediastinum: often – pain in the throat and trachea, nasal bleeding.
The digestive system: often – constipation, flatulence, dyspepsia, nausea, diarrhea; infrequently – vomiting, pain in the upper and lower abdomen, belching, pancreatitis.
Hepatic and biliary tract disorders: infrequent – hepatitis; rare – cholestasis; very rare – liver failure.
Skin and subcutaneous tissue: infrequent urticaria, skin rash, pruritus, alopecia; rarely – angioedema, bullous dermatitis, including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis.
Muscular and connective tissue disorders: often – myalgia, arthralgia, pain in extremities, muscle cramps, joint swelling, back pain; infrequently – neck pain, muscle weakness; rarely – myopathy, myositis, rhabdomyolysis, tendinopathy (sometimes complicated by tendon rupture).
General disorders and disorders at the site of administration: infrequent – malaise, asthenia, chest pain, peripheral edema, increased fatigue, fever.
Laboratory and instrumental data: frequently – increased hepatic transaminases activity, increased CPK activity; infrequently – leukocyturia, increased concentration of glycosylated hemoglobin.
Overdose
Symptoms: arterial hypotension is possible.
Treatment: symptomatic therapy.
There is no specific antidote.
Hemodialysis is ineffective.
Pregnancy use
Atorvastatin is contraindicated in pregnancy and during lactation (breastfeeding).
It is unknown whether atorvastatin is excreted with breast milk.
With regard to the possibility of adverse events in breastfed children, if it is necessary to use the drug during lactation, the question of stopping breastfeeding should be considered.
Women of reproductive age should use adequate contraceptive methods during treatment.
Atorvastatin may be administered to women of reproductive age only if the likelihood of pregnancy is very low and the patient is informed about the possible risk of treatment to the fetus.
Similarities
Weight | 0.059 kg |
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Shelf life | 2 years |
Conditions of storage | At 10-30 °C |
Manufacturer | Saneka Pharmaceuticals a.s., Slovakia |
Medication form | pills |
Brand | Saneka Pharmaceuticals a.s. |
Other forms…
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