Buy Atorvastatin tablets 20mg №60
  • Buy Atorvastatin tablets 20mg №60

Atorvastatin pills 20mg №60

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Composition

1 tablet, film coated, contains:

active substance: atorvastatin Calcium in terms of atorvastatin - 20 mg

excipients (core): lactose monohydrate (milk sugar) - 124.0 mg; calcium carbonate - 66.0 mg; Povidone K 30 (medium molecular weight polyvinylpyrrolidone) - 12.0 mg; croscarmellose sodium (primelloza) - 13.5 mg; sodium fumarate - 3.0 mg; colloidal silicon dioxide (Aerosil) - 1.5 mg; microcrystalline cellulose - 60.0 mg;

excipients (shell):

Opadry II (polyvinyl alcohol, partially hydrolyzed - 3.96 mg; macrogol (polyethylene glycol) 3350 - 1.1115 mg; talc - 1.8 mg; titanium dioxide E 171 - 1.7253 mg; soy lecithin E 322 - 0.315 mg; indigo carmine dye-based aluminum lacquer - 0.0054 mg; dye-based aluminum lacquer azorubine - 0.0459 mg; aluminum dye-based crimson lacquer [Ponzo 4R] - 0.0369 mg).

Mechanism of action


Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase, the key enzyme that converts 3-hydroxy-3-methylglutaryl-CoA into mevalonate, the precursor of steroids, including cholesterol; synthetic lipid-lowering agent.

In patients with homozygous and heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed dyslipidemia, atorvastatin decreases plasma cholesterol (CH) concentration,Low-density lipoprotein cholesterol (LDL-LDL) and apolipoprotein B (apo-B), as well as very low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG), causes an unstable increase in the concentration of high-density lipoprotein cholesterol (LDL-C).

Atorvastatin reduces the concentration of cholesterol and lipoproteins in the blood plasma by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and increasing the number of “liver” LDL receptors on the cell surface, which leads to increased capture and catabolism of LDL-C.

Atorvastatin reduces the production of LDL-C and the number of LDL particles, causes a pronounced and persistent increase in the activity of LDL-receptors in combination with favorable qualitative changes in LDL-particles, and also reduces the concentration of LDL-C in patients with homozygous familial familial hypercholesterolemia resistant to other hypolipids. means.

Atorvastatin in doses from 10 mg to 80 mg reduces the concentration of cholesterol by 30% - 46%, LDL-C - by 41% - 61%, apolipoprotein-B - by 34% - 50% and TG - by 14% - 33%. The results of therapy are similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia, including in patients with type 2 diabetes.

In patients with isolated hypertriglyceridemia, atorvastatin reduces the concentration of cholesterol, LDL-C, LDL-C, VLDL, apo-B and TG and increases the concentration of HDL-C.In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate density lipoprotein cholesterol.

In patients with type IIa and IIb hyperlipoproteinemia, according to Fredrickson's classification, the mean value of an increase in the concentration of HDL-C HDL with treatment with atorvastatin (10-80 mg) compared to the baseline is 5.1.% - 8.7% and does not depend on the dose. There is a significant dose-dependent decrease in the ratio: total cholesterol / cholesterol-HDL and cholesterol-LDL / cholesterol-HDL by 29% - 44% and 37% - 55%, respectively. The anti-sclerotic effect of atorvastatin is a consequence of its effect on the walls of blood vessels and blood components. Atorvastatin inhibits the synthesis of isoprenoids, which are growth factors for the cells of the inner lining of blood vessels. Under the influence of atorvastatin, the endothelium-dependent dilation of blood vessels is improved, the concentration of cholesterol-LDL, apolipoprotein B, TG is reduced, the concentration of cholesterol cholesterol-HDL and apolipoprotein A.

Atorvastatin reduces the viscosity of blood plasma and the activity of some coagulation factors and platelet aggregation. Due to this, it improves hemodynamics and normalizes the state of the coagulation system. HMG-CoA reductase inhibitors also have an effect on the metabolism of macrophages, block their activation and prevent the rupture of an atherosclerotic plaque.

Atorvastatin-SZ at a dose of 80 mg reliably reduces the risk of developing ischemic complications and the death rate by 16% after a 16-week course, and the risk of re-hospitalization for angina, accompanied by signs of myocardial ischemia, at 26%. In patients with different baseline concentrations of LDL-C, atorvastatin-SZ causes a reduction in the risk of ischemic complications and mortality (in patients with myocardial infarction without Q wave and unstable angina, as in men and women, and in patients younger than 65 years old).

The decrease in plasma concentration of cholesterol-LDL correlates better with the dose of the drug than with its concentration in the blood plasma. The dose is selected based on the therapeutic effect (see the section "Dosage and administration"). The therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum after 4 weeks and lasts for the entire period of therapy.

Indications

  • Primary hypercholesterolemia (heterozygous familial and non-familial hypercholesterolemia (Fredrickson type IIa);
  • Combined (mixed) hyperlipidemia (IIa and IIb types according to Fredrickson's classification);
  • Disbetalipoproteinemia (type III according to Fredrickson's classification) (as a supplement to the diet);
  • Familial endogenous hypertriglyceridemia (type IV according to Fredrickson's classification), resistant to diet;
  • Homozygous familial hypercholesterolemia with insufficient effectiveness of diet therapy and other non-pharmacological treatment methods;
  • Prevention of cardiovascular diseases:
  • Primary prevention of cardiovascular complications in patients without clinical signs of coronary heart disease (CHD), but having several risk factors for its development: age over 55 years, nicotine dependence, arterial hypertension, diabetes mellitus, genetic predisposition, including against the background of dyslipidemia;
  • Secondary prevention of cardiovascular complications in patients with coronary artery disease in order to reduce the total mortality rate, myocardial infarction, stroke, re-hospitalization for angina and the need for revascularization.

Contraindications

Hypersensitivity to any component of the drug.

Active liver disease or increased activity of liver transaminases in plasma of unknown origin is more than 3 times compared with the upper limit of normal.

Age up to 18 years (not enough clinical data on the efficacy and safety of the drug in this age group).

Lactose intolerance, lactase deficiency, glucose-galactose malabsorption.

Hypersensitivity to soy and peanuts.

Pregnancy and breastfeeding period.

Use in women planning pregnancy and not using reliable methods of contraception.

With caution:

Alcohol abuse, liver disease in history, muscular system diseases (in history from the use of other members of the HMG-CoA reductase inhibitor group),severe violations of water electrolyte balance, endocrine (hyperthyroidism) and metabolic disorders, severe acute infections (sepsis), arterial hypotension, diabetes mellitus, uncontrolled epilepsy, extensive surgical interventions, injuries.

Side effects

Classification of the incidence of side effects of the World Health Organization (WHO): very often (≥1 / 10), often (from ≥1 / 100 to <1/10), infrequently (from ≥1 / 1000 to <1/100), rarely (from ≥1 / 10 000 to <1/1000), very rarely (from <1/10 000, including individual messages), frequency unknown - unwanted reactions with unknown frequency (cannot be calculated from the available data).

The nervous system: often - headache, insomnia, dizziness, paresthesia, asthenic syndrome; infrequently - peripheral neuropathy, amnesia, hypoesthesia, nightmares.

On the part of the organ of hearing: infrequently - tinnitus.

Since the cardiovascular system: palpitations, symptoms of vasodilation, migraine, postural hypotension, increased blood pressure, phlebitis, arrhythmia.

From the hemopoietic system: infrequently - thrombopitopia.

On the part of the respiratory system: rarely - nasopharyngitis, epistaxis.

On the part of the digestive system: often - constipation, dyspepsia , nausea, diarrhea, flatulence (abdominal distension), abdominal pain; infrequently - a violation of taste perception, vomiting, pancreatitis, belching; rarely - hepatitis, cholestatic jaundice; very rarely - liver failure.

On the part of the urinary system: often - urinary tract infections; infrequently - secondary renal failure.

From the reproductive system and the mammary gland: infrequently - a decrease in potency.

On the part of the musculoskeletal system: often - myalgia, arthralgia, swelling of the joints; infrequently - myopathy, muscle cramps; rarely - myositis, rhabdomyolysis, tendinopathy (in some cases with tendon rupture).

From the skin of the subcutaneous tissues: often - skin rash, pruritus; infrequently - alopecia.

Allergic reactions: infrequently - urticaria; very rarely - angioedema, bullous rash, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, anaphylaxis;

From the laboratory parameters: infrequently - increased activity of ACT, ALT, increased activity of serum CPK, leukocyturia; very rarely - hyperglycemia, hypoglycemia.

Other: often - peripheral edema, chest pain, back pain; infrequently - weakness, fatigue, fever, anorexia, weight gain, the appearance of "veil" before the eyes.

In the post-marketing use of statins, the following undesirable effects were reported: memory loss or decrease, depression, sexual dysfunction, gynecomastia, increased glycosylated hemoglobin concentration, isolated cases of interstitial lung disease (especially with prolonged use), cases of immune-mediated necrotic myopathy.

The causal relationship of some undesirable effects with the use of the drug Atorvastatin-SZ, which is regarded as "very rare", has not been established.

If severe adverse effects occur, use of the drug Atorvastatin-SZ should be discontinued.

Interaction

The risk of myopathy during treatment with HMG-CoA reductase is increased while the use of cyclosporine, fibrates, antibiotics (erythromycin, Clarithromycin , quinupristin / dalfopristin), nefazodone, HIV protease inhibitors (indinavir, ritonavir), colchicine, antifungals - azole derivatives, and nicotinic acid in lipid-lowering doses (more than 1 g / day).

Inhibitors of the isoenzyme CYP3A4

Since atorvastatin is metabolized by a CYP3A4 isoenzyme, the combined use of atorvastatin with CYP3A4 isoenzyme inhibitors can lead to an increase in plasma atorvastatin concentrations. The degree of interaction and potentiation effect is determined by the variability of exposure to the CYP3A4 isoenzyme.

Inhibitors of the transport protein OATP1B1

Atorvastatin and its metabolites are substrates of the transport protein OATP1B1. OATR1B1 inhibitors (for example, cyclosporin) can increase the bioavailability of atorvastatin. Thus, the combined use of atorvastatin at a dose of 10 mg and cyclosporine at a dose of 5.2 mg / kg / day leads to an increase in the concentration of atorvastatin in the blood plasma by 7.7 times. If necessary, the simultaneous use of cyclosporine dose of atorvastatin-SZ should not exceed 10 mg / day.

Erythromycin / clarithromycin

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 plasma atorvastatin concentration was observed. Care should be taken to apply the lowest effective dose of atorvastatin while using clarithromycin.

Protease inhibitors

The simultaneous use of atorvastatin with protease inhibitors, known as inhibitors of the CYP3A4 isoenzyme, is accompanied by an increase in plasma atorvastatin concentration (with simultaneous use of atorvastatin with erythromycin Cmax, it increases by 40%).

The combination of protease inhibitors

Patients taking HIV protease inhibitors and hepatitis C inhibitors should use caution and use the lowest effective dose of atorvastatin.

In patients taking telaprevir or a tipranavir / ritonavir combination, the dose of atorvastatin-SZ should not exceed 10 mg / day.

Patients receiving HIV protease inhibitor tipranavir + ritonavir or hepatitis C protease inhibitor telaprevir should avoid taking Atorvastatin-NZ at the same time. Patients taking HIV protease inhibitors lopinavir + ritonavir should be careful when prescribing Atorvastatin-SZ and the lowest required dose should be prescribed. In patients taking HIV protease inhibitors saquinavir + ritonavir, darunavir + ritonavir, fosamprenavir or fosamprenavir + ritonavir, the dose of atorvastatin-SZ should not exceed 20 mg and the drug should be used with caution.In patients taking HIV protease inhibitor nelfinavir or hepatitis C protease inhibitor boceprevir, the dose of atorvastatin-SZ should not exceed 40 mg and careful clinical monitoring is recommended.

Diltiazem

The combined use of atorvastatin at a dose of 40 mg with diltiazem at a dose of 240 mg leads to an increase in plasma atorvastatin concentration.

Ketoconazole, spironolactone and cimetidine

Caution should be exercised with the simultaneous use of atorvastatin with drugs that reduce the concentration of endogenous steroid hormones, such as Ketoconazole , spironolactone and cimetidine.

Itraconazole

The simultaneous use of atorvastatin in doses from 20 mg to 40 mg and itraconazole at a dose of 200 mg resulted in an increase in the AUC value of atorvastatin. Caution should be exercised and apply the lowest effective dose of atorvastatin while using itraconazole.

Grapefruit juice

Since grapefruit juice contains one or more components that inhibit CYP3A4 isoenzyme, its excessive consumption (more than 1.2 liters per day) can cause an increase in plasma atorvastatin concentration.

Inductors of isoenzyme CYP3A4

The combined use of atorvastatin with inducers of the CYP3A4 isoenzyme (for example, efavirenz, phenytoin or rifampicin) can lead to a decrease in plasma atorvastatin concentrations. Due to the dual mechanism of interaction with rifampicin (CYP3A4 isoenzyme inducer and hepatocyte transport inhibitor OATP1B1), simultaneous use of atorvastatin and rifampicin is recommended,since the delayed taking of atorvastatin after taking rifampicin leads to a significant decrease in the concentration of atorvastatin in the blood plasma.

Antacids

Simultaneous ingestion of a suspension containing Magnesium hydroxide and aluminum hydroxide, reduced the concentration of atorvastatin in the blood plasma by about 35%, however, the degree of decrease in the concentration of Xc-LDL did not change.

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