$51.00
Manufacturer: Poland
Atorvastatin reduces the risk of cardiovascular disease in adults with various risk factors, including diabetes and symptomatic coronary artery disease. It also lowers cholesterol levels in both adults and children, making it a versatile treatment option.
Description
Ingredients
active ingredient : atorvastatin;
1 coated tablet contains 41.44 mg of atorvastatin calcium, which corresponds to 40 mg of atorvastatin, respectively;
excipients: mannitol (E 421), microcrystalline cellulose, calcium carbonate, povidone, sodium croscarmellose, sodium lauryl sulfate, colloidal silicon dioxide, magnesium stearate, hypromellose, titanium dioxide (E 171), macrogol 6000, talc.
Dosage form
Film-coated tablets.
Basic physical and chemical properties:
40 mg film-coated tablets, white, oval biconvex, 8.2 x 17 mm.
Pharmacotherapeutic group
Drugs that lower the level of cholesterol and triglycerides in the blood serum. HMG-CoA reductase inhibitors. ATX code C10A A05.
Pharmacodynamics
Atorvastatin is a synthetic lipid-lowering drug. Atorvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early step in cholesterol biosynthesis that limits the rate of its formation.
Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase, an enzyme that determines the rate of conversion of 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream in combination with lipoproteins. These complexes are separated by ultracentrifugation into HDL (high density lipoprotein), LDLP (intermediate density lipoprotein), LDL (low density lipoprotein) and VLDL (very low density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the blood plasma for transport to peripheral tissues. LDL is formed by VLDL and catabolized by interaction with high-affinity LDL receptors.
Elevated levels of total cholesterol, LDL cholesterol and apo B (membrane complex for LDL cholesterol) provoke the development of atherosclerosis. Similarly, reduced levels of HDL cholesterol (and its transport complex, apo B) are associated with the development of atherosclerosis.
Epidemiological studies have established that cardiovascular morbidity and mortality vary in direct proportion to the level of total cholesterol and LDL cholesterol and inversely with the level of HDL cholesterol.
Atorvastatin reduces total cholesterol, LDL cholesterol and apo B in patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemia. Atorvastatin also lowers VLDL and TG cholesterol levels, and also causes an unsustainable increase in HDL cholesterol and apolipoprotein A-1. Atorvastatin lowers total cholesterol, LDL cholesterol, VLDL cholesterol, apo B, triglycerides, and non-HDL cholesterol, and increases HDL cholesterol in patients with isolated hypertriglyceridemia. Atorvastatin reduces LDL-C in patients with dysbetalipoproteinemia.
Like LDL, lipoproteins rich in cholesterol and triglycerides, including VLDL, LDLP, and residues, may also contribute to the development of atherosclerosis. Elevated plasma triglyceride levels are often found in the triad of low HDL cholesterol and small LDL lobules, as well as in combination with non-lipid metabolic risk factors for coronary heart disease. Total plasma triglycerides per se have not been consistently shown to be an independent risk factor for coronary artery disease. In addition, an increase in HDL or a decrease in triglycerides has been found to have an independent effect on the risk of coronary and cardiovascular morbidity and mortality.
Atorvastatin, like some of its metabolites, is pharmacologically active in humans. The main site of action of atorvastatin is the liver, which plays a major role in cholesterol synthesis and LDL clearance. The dose of the drug, in contrast to the systemic concentration of the drug, better correlates with a decrease in LDL cholesterol. Individual dose selection should be carried out depending on the therapeutic response.
Indications
Preventing cardiovascular disease in adults
For adult patients without symptomatic coronary heart disease, but with several risk factors for coronary heart disease, such as age, smoking, hypertension, low HDL, or a family history of early coronary heart disease, Atorvasterol (atorvastatin) is indicated for:
- reducing the risk of myocardial infarction;
- reducing the risk of stroke;
- reducing the risk of revascularization procedures and angina pectoris.
For adult patients with type II diabetes mellitus and without clinically significant coronary heart disease, but with several risk factors for coronary heart disease, such as retinopathy, albuminuria, smoking or arterial hypertension, Atorvasterol is indicated for:
- reducing the risk of myocardial infarction;
- reducing the risk of stroke.
For adult patients with symptomatic coronary artery disease, Atorvasterol is indicated for:
- reducing the risk of non-lethal myocardial infarction;
- reducing the risk of fatal and non-fatal stroke;
- reducing the risk of revascularization procedures;
- reduced risk of hospitalization due to congestive heart failure;
- reducing the risk of angina pectoris.
Hyperlipidemia
In adult patients
- As an adjunct to diet to reduce elevated levels of total cholesterol, LDL cholesterol, apolipoprotein B and triglycerides, and to increase HDL cholesterol levels in patients with primary hypercholesterolemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson type IIa and IIb) .
- As an adjunct to diet for the treatment of patients with elevated serum triglyceride levels (Fredrickson type IV).
- For the treatment of patients with primary dysbetalipoproteinemia (Fredrickson type III) in cases where dietary compliance is not effective enough.
- To reduce total and LDL cholesterol in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (eg, LDL apheresis) or when such treatments are not available.
In children
- As an adjunct to a diet to reduce total cholesterol, LDL cholesterol, and apolipoprotein B in children aged 10 to 17 years with heterozygous familial hypercholesterolemia, if, after appropriate dietary therapy, test results are:
a) LDL cholesterol remains ³ 190 mg/dl (4.91 mmol/l) or
b) LDL cholesterol ³ 160 mg / dl (4.14 mmol / l) and:
- family history of early cardiovascular disease or
- two or more other risk factors for cardiovascular disease are present in a pediatric patient.
Contraindications
- Active liver disease, which may include a persistent increase in liver transaminases of unknown etiology.
- hypersensitivity to any of the components of Atorvasterol (atorvastatin).
- Pregnancy.
- Lactation.
Dosage and administration
Hyperlipidemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson type IIa and IIb)
The recommended starting dose of Atorvasterol (atorvastatin) is 10 or 20 mg once daily. For patients who require a significant reduction in LDL cholesterol (greater than 45%), therapy can be initiated with doses of 40 mg once daily. Dosing range of the drug is in the range from 10 to 80 mg 1 time per day. The drug can be taken as a single dose at any time, regardless of the meal. Initial and maintenance doses of the drug should be selected individually depending on the purpose of treatment and response. After initiation of treatment and after titration of the dose of atorvastatin, lipid levels should be analyzed over a period of 2 to 4 weeks and the dose adjusted accordingly.
Heterozygous familial hypercholesterolemia in pediatric patients (10-17 years old)
The recommended starting dose is 10 mg/day; the maximum recommended dose is 20 mg/day (doses exceeding 20 mg have not been studied in this group of patients). Doses of the drug should be selected individually in accordance with the recommended goal of treatment. Dose adjustments should be made at intervals of 4 weeks or more.
Homozygous familial hypercholesterolemia
The dose of Atorvasterol (atorvastatin) for patients with homozygous familial hypercholesterolemia is from 10 to 80 mg per day. Atorvastatin should be used as an adjunct to other lipid-lowering therapies (eg, LDL apheresis) or as primary therapy if lipid-lowering therapies are not available.
Simultaneous lipid-lowering therapy
Atorvasterol (atorvastatin) can be used with bile acid sequestrants. The combination of HMG-CoA reductase inhibitors (statins) and fibrates should generally be used with caution.
Dosing for patients with impaired renal function
Kidney disease does not affect either plasma concentrations or LDL-C lowering with atorvastatin; therefore, dose adjustment of the drug for patients with impaired renal function is not required.
Dosing for patients taking ciclosporin, clarithromycin, itraconazole, letermovir, or certain protease inhibitors
Treatment with Atorvasterol (atorvastatin) should be avoided in patients taking cyclosporine, HIV protease inhibitors (tipranavir + ritonavir), or an inhibitor of hepatitis C protease (telaprevir). Atorvastatin should be used with caution in HIV patients taking lopinavir + ritonavir and used at the most appropriate dose. For patients taking clarithromycin, itraconazole, and for patients with HIV taking saquinavir + ritonavir, darunavir + ritonavir, fosamprenavir, or fosamprenavir + ritonavir in combination, the therapeutic dose of atorvastatin should be limited to 20 mg, and appropriate clinical evaluations to determine the lowest required dose of atorvastatin. For patients taking the HIV protease inhibitor nelfinavir or the hepatitis C protease inhibitor boceprevir.
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