Atorvastatin-TEVA (atorvastatin)coated tablets 20 mg. №30

active ingredient : atorvastatin;

1 film-coated tablet contains 10 mg or 20 mg, 40 mg, or 80 mg of atorvastatin (as atorvastatin calcium)

Excipients:

core: microcrystalline cellulose, sodium carbonate, maltose, croscarmellose sodium, magnesium stearate

shell: hypromellose (E 464), hydroxypropyl cellulose, triethyl citrate (E 1505), polysorbate 80, titanium dioxide (E 171).

Film-coated tablets.

Basic physical and chemical properties: 20 mg: white or almost white, elliptical, biconvex, smooth tablets, approximately
12.5 mm × 6.6 mm in size.

Drugs that lower the level of cholesterol and triglycerides in the blood serum. HMG-CoA reductase inhibitors. Code ATX C10A A05.

Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase, an enzyme that regulates 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.

Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting hepatic HMG-CoA reductase and cholesterol synthesis and by increasing the number of hepatic LDL receptors on cell surfaces to enhance LDL uptake and catabolism; atorvastatin also reduces the production of LDL and the number of these particles. Atorvastatin lowers LDL cholesterol levels in some patients with homozygous familial hypercholesterolemia, a group of people who rarely respond to treatment with other lipid-lowering drugs.

Numerous clinical studies have shown that 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 – a by A) 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 HDL-C, 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.