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Lipitor 80, 40, 20, 10, 5 mg
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Active Ingredient: Atorvastatin

Lipitor - lipolipidemic drug III generation of the group of statins. Reduces plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase, cholesterol synthesis in the liver and increasing the number of “hepatic” LDL receptors on the cell surface, which leads to increased uptake and catabolism of LDL. Reduces the level of LDL in patients with homozygous familial hypercholesterolemia, which usually does not respond to therapy with lipid-lowering drugs.

Pharmacodynamics of Atorvastatin

Atorvastatin is a selective competitive inhibitor of HMG-CoA reductase-enzyme, which determines the maximum rate of cholesterol biosynthesis, responsible for the conversion of 3-hydroxy-3-methyl-glutaril-coenzyme A into mevalonate, the precursor of sterols, including cholesterol. In the liver, triglycerides and cholesterol are included in very low density lipoproteins (VLDL), enter the blood plasma and are transported to peripheral tissues. Low density lipoproteins (LDL) are formed from VLDL, which are catabolized primarily through interaction with high affinity LDL receptors.

Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver, as well as by increasing the number of “hepatic” LDL receptors on the cell surface, which increases the uptake and LDL catabolism.

Atorvastatin reduces the production of LDL and the amount of LDL particles. Atorvastatin causes a pronounced and persistent increase in the activity of LDL receptors in combination with favorable changes in the quality of circulating LDL particles.

Dose-dependently reduces the level of LDL in patients with homozygous hereditary hypercholesterolemia resistant to treatment with other lipid-lowering drugs.

Studies of the dose / effect ratio showed that atorvastatin reduces the level of total cholesterol (by 30-46%), LDL cholesterol (by 41-61%), apolipoprotein B (by 34-50%) and triglycerides (by 14-33%), simultaneously causing, in varying degrees, an increase in levels of HDL cholesterol and apolipoprotein A. These results were similar in patients with heterozygous familial hypercholesterolemia, nonfamily forms of hypercholesterolemia and mixed hyperlipidemia, including patients with insulin-dependent diabetes mellitus.

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Due to a decrease in total cholesterol, LDL cholesterol and apolipoprotein B, the risk of cardiovascular diseases decreases and, consequently, the risk of death decreases. Studies on the effect of atorvastatin on cardiovascular morbidity and mortality have not yet been completed.

When using the drug in elderly patients, there were no differences in safety, efficacy, or achievement of lipid-lowering therapy goals in comparison with the general population.

Prevention of cardiovascular complications

In the Anglo-Scandinavian study of cardiovascular complications (lipid-lowering branch (ASCOT-LLA) of the effect of atorvastatin on the death and non-fatal outcomes of coronary heart disease (CHD), the effect of atorvastatin at a dose of 10 mg was significantly higher than the effect of placebo, therefore it was decided to terminate the study early after 3.3 years instead of the expected 5 years.


A joint study of the effect of atorvastatin on fatal and non-fatal outcomes of cardiovascular diseases in type 2 diabetes mellitus (CARDS) showed that atorvastatin therapy reduced the risk of developing the following cardiovascular complications regardless of gender, age of the patient or baseline Xc-LDL.


In the study of the reverse development of coronary atherosclerosis with intensive lipid-lowering therapy (REVERSAL) with atorvastatin at a dose of 80 mg in patients with IHD, it was found that the average decrease in the total volume of atheroma (primary efficacy criterion) since the beginning of the study was 0.4%.

Recurrent stroke

In the intensive cholesterol-lowering (SPARCL) program, it was found that atorvastatin at a dose of 80 mg per day reduced the risk of recurring fatal or nonfatal stroke in patients who had a stroke or transient ischemic attack (TIA) without CHD history by 15% compared with placebo . At the same time, the risk of major cardiovascular complications and revascularization procedures was significantly reduced. A reduction in the risk of cardiovascular disorders in therapy with atorvastatin was observed in all groups except for the one that included patients with primary or recurrent hemorrhagic stroke (7 in the atorvastatin group versus 2 in the placebo group).

Hemorrhagic stroke

In patients receiving atorvastatin therapy at a dose of 80 mg, the incidence of hemorrhagic or ischemic stroke (265 vs. 311) or IHD (123 vs. 204) was less than in the control group.

Secondary prevention of cardiovascular complications

In the treatment of the New Purpose Study (TNT), the effect of atorvastatin at doses of 80 mg / day and 10 mg / day was compared with the risk of developing cardiovascular complications in patients with clinically confirmed coronary artery disease.

Pharmacokinetics of Atorvastatin


After oral administration, atorvastatin is rapidly absorbed into the blood. The maximum concentration (C max) in the blood plasma is reached within 1-2 hours, C max for women is 20% higher, the area along the concentration-time curve (AUC) is 10% lower; Cmax in patients with alcoholic cirrhosis of the liver increases by 16 times, AUC - by I. Food intake somewhat reduces the rate and duration of absorption of the drug (by 25% and 9%, respectively), but lowering cholesterol is similar to that when taking atorvastatin without food. Absolute bioavailability of atorvastatin is approximately 12%, systemic bioavailability, which determines the inhibitory activity against HMG-CoA reductase, is 30%. Low systemic bioavailability is caused by presystemic metabolism in the mucous membrane of the gastrointestinal tract and during the "first pass" through the liver.


The average distribution of atorvastatin is approximately 381 liters. Communication with proteins of blood plasma -98%.


Atorvastatin is metabolized mainly in the liver with the participation of CYP3A4, CYP3A5 and CYP3A7 cytochrome P450 isoenzymes with the formation of pharmacologically active metabolites (ortho and parahydroxylated derivatives, beta-oxidation products). In vitro, ortho and parahydroxylated metabolites have an inhibitory effect on HMG-CoA reductase, comparable to that of atorvastatin. The inhibitory effect of the drug in relation to HMG-CoA reductase about 70% is determined by the activity of circulating metabolites.


Atorvastatin is excreted mainly with bile after hepatic and / or extrahepatic metabolism (it does not undergo pronounced enterohepatic recirculation).

The half-life is 14 hours. Inhibitory activity against HMG-CoA reductase remains for about 20-30 hours due to the presence of active metabolites. Less than 2% of the ingested dose of the drug is determined in the urine. Not displayed during hemodialysis.

Indications for use

  1. in patients with primary hypercholesterolemia, heterozygous familial and non-familial hypercholesterolemia and combined (mixed) hyperlipidemia (types Pa and lib of Fredryksonu) in combination with a diet to reduce elevated total cholesterol, LDL cholesterol, apolipoprotein B and triglyceride levels and increasing HDL cholesterol
  2. for the treatment of patients with elevated serum levels of triglycerides (type IV according to Fredrikson) and patients with dysbetalipoproteinemia (type III according to Fredrikson), in whom diet therapy does not give an adequate effect
  3. in patients with homozygous familial hypercholesterolemia to reduce levels of total cholesterol and LDL cholesterol, when diet therapy and other non-pharmacological treatment methods are not sufficiently effective;


  • hypersensitivity to the drug;

  • active liver disease or increased activity of “liver” enzymes of unclear genesis (more than 3 times as compared with the upper limit of the norm);
  • liver failure (severity according to the Child-Pugh A and B classification);
  • pregnancy;
  • lactation period;
  • age up to 18 years (efficiency and safety are not established)

With caution: alcohol abuse, a history of liver disease, severe electrolyte imbalance, endocrine and metabolic disorders, arterial hypotension, severe acute infections (sepsis), uncontrolled epilepsy, extensive surgical interventions, injuries, skeletal muscle diseases.

Pregnancy and lactation

Atorvastatin is contraindicated for use during pregnancy and during 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 should use adequate contraceptives during treatment. Atorvastatin can be prescribed to women of reproductive age only if they have a very low probability of pregnancy and the patient is informed about the possible risk of treatment for the fetus.

Dosage and administration

Usually the initial dose is 10 mg once a day. The dose ranges from 10 to 80 mg / day. The drug can be taken at any time of the day once a day, regardless of the meal. Doses should be selected individually, taking into account the initial level of LDL cholesterol, the goal of therapy and the patient's response to treatment. At the beginning and / or during the dose increase of Atorvatatin-Teva, it is necessary every 2-4 weeks to monitor plasma lipid levels and adjust the dose accordingly.

Dose adjustment should be done at intervals of at least 4 weeks. The maximum daily dose is 80 mg.

For patients with established coronary heart disease (CHD) and other patients with a high risk of cardiovascular complications, the following lipid levels correction targets are recommended: LDL cholesterol less than 3.0 mmol / l (or less than 115 mg / dl) and total cholesterol less than 5.0 mmol / L (or less than 190 mg / dL).

Primary hypercholesterolemia and combined (mixed) hyperlipidemia

In most patients, the necessary control of lipid levels is provided by taking 10 mg of Atorvastatin-Teva once a day. A significant therapeutic effect is usually observed after 4 weeks. With long-term treatment, this effect persists.

Heterozygous familial hypercholesterolemia

Treatment of patients should begin with the appointment of 10 mg of Atorvastatin Teva per day. Carrying out individual dose adjustment every 4 weeks, you should bring it up to 40 mg / day. After that, you can increase the dose to a maximum level of 80 mg / day, or use the combined appointment of 40 mg of Atorvastatin-Teva and bile acid sequestrant.

Homozygous familial hypercholesterolemia

Assign a dose of 80 mg 1 time per day. In patients with renal insufficiency.

Kidney disease does not affect the plasma concentration of atorvastatin or the degree of lipid reduction in its use; therefore, no dose adjustment is required in patients with kidney disease.

In patients with hepatic impairment

In liver failure, a dose reduction or drug withdrawal may be required.

Side effect

Most often (1% and more): insomnia, headache, asthenic syndrome; nausea, diarrhea, abdominal pain, dyspepsia, flatulence, constipation; myalgia. Less often (less than 1%):

From the nervous system: malaise, dizziness, amnesia, paresthesia, peripheral neuropathy, hypoesthesia.

On the part of the digestive system: vomiting, anorexia, hepatitis, pancreatitis, cholestatic jaundice.

On the part of the musculoskeletal system: back pain, muscle cramps, myositis, myopathy, myalgia, arthralgia, rhabdomyolysis.

Allergic reactions: urticaria, pruritus, rash, anaphylaxis, bullous rash, polymorphic exudative erythema (including Stevens-Johnson syndrome), Lyell's syndrome, angioedema.

From the side of blood-forming organs: thrombocytopenia.

On the part of the metabolism: hypo-or hyperglycemia, increased activity of serum creatine phosphokinase (CK).

Other: impotence, peripheral edema, weight gain, chest pain, secondary renal failure, alopecia, tinnitus, fatigue. The most frequently develop adverse effects on the gastrointestinal tract: constipation, flatulence, dyspepsia, abdominal pain; Usually, these phenomena diminish as treatment continues. During clinical studies, drug withdrawal due to side effects was required in less than 2% of patients.


There is no specific antidote. In case of overdose, the necessary symptomatic and supportive therapy should be carried out. Monitoring of liver function and serum CK level is necessary. Hemodialysis is ineffective.

Interaction with other drugs and other forms of interaction

The risk of myopathy in the treatment of HMG-CoA reductase inhibitors is increased when used in combination with cyclosporine, fibrates, macrolide antibiotics (including erythromycin), azole antifungal agents or nicotinic acid.

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In some rare cases, these combinations cause rhabdio myolysis, accompanied by renal failure due to myoglobinuria. In this regard, a thorough assessment of the balance of risks and benefits of the combined treatment is necessary.

Inhibitors of isoenzyme pitochrome P450 CYP ZA4

Atorvastatin is metabolized with the participation of the cytochrome P450 CYP 3A4 isoenzyme. When using atorvastatin in combination with cytochrome P450 CYP ZA4 isoenzyme inhibitors (for example, cyclosporine, macrolide antibiotics, for example, erythromycin and clarithromycin, nefazodone, azole antifungal drugs, for example, itraconazole, and HIV protease inhibitors), drugs may arise. With the combined use of drugs, elevated plasma concentrations of atorvastatin may be noted. In this regard, special care should be taken when using atorvastatin in combination with the above-mentioned drugs.

Simultaneous use with drugs that reduce the concentration of endogenous steroid hormones (including cimetidine, ketoconazole, spironolactone) increases the risk of reducing endogenous steroid horomones (caution should be exercised).

P-glycoprotein inhibitors

Atorvastatin and its metabolites are substrates for P-glycoprotein. P-glycoprotein inhibitors (for example, cyclosporin) may increase the bioavailability of atorvastatin.

Erythromycin, clarithromycin

With simultaneous use of atorvastatin and erythromycin (500 mg 4 times / day) or clarithromycin (500 mg 2 times / day), which inhibit cytochrome P450 ZA4, an increase in atorvastatin concentration in the blood plasma was observed.

With simultaneous use of atorvastatin / 10 mg times / day.) And azithromycin (500f 1 times / day.), The concentration of atorvastatin in the blood plasma did not change.


With the combined use of atorvastatin at a dose of 40 mg and itraconazole at a dose of 200 mg once a day, an increase in AUC was detected to a level that exceeded the norm three times.

Protease inhibitors

The simultaneous use of atorvastatin with protease inhibitors, known as inhibitors of cytochrome P450 ZA4, was accompanied by an increase in plasma atorvastatin concentration.

Grapefruit juice

Grapefruit juice contains at least one ingredient that is a CYP3A4 inhibitor, and may cause an increase in the plasma concentration of those drugs that are metabolized by CYP3A4. Daily consumption of 240 ml of grapefruit juice increased Atorvastatin AUC by 37% and reduced the active orthohydroxy metabolite AUC by 20.4%. Consumption of a large amount of grapefruit juice (more than 1.2 liters per day for 5 days) increased the AUC of atorvastatin 2.5 times, and the AUC of active inhibitors of HMG-CoA reductase (atorvastatin + its metabolites) - 1.3 times. In this regard, the consumption of large quantities of grapefruit juice during the period of treatment with atorvastatin is not recommended.

Inductors of cytochrome P450

The effects of drugs inducing cytochrome P450 CYP ZA4 isoenzyme. (for example, rifampicin and phenazone), on atorvastatin is unknown. Interactions with atorvastatin and other substrates of this isoenzyme are unknown; however, the possibility of these interactions should be considered when using drugs with a low therapeutic index - in particular, class III antiarrhythmic drugs, for example, amiodarone.

Gemfibrozil / Fibrates

The risk of atorvastatin myopathy may increase with concomitant use of fibrates. In vitro studies suggest that gemfibrozil may also interact with atorvastatin by inhibiting eiro glucuronidation, which may cause an increase in plasma atorvastatin concentrations.


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. digoxin concentration increased by about 20%. Patients receiving digoxin in combination with atorvastatin should be monitored.

Oral contraceptives

Taking atorvastatin in combination with an oral contraceptive containing norethisterone and ethinyl estradiol caused an increase in plasma concentrations of norethisterone and ethinyl estradiol. These increases in concentration should be considered when choosing doses of oral contraceptives. With simultaneous use of atorvastatin and a oral contraceptive containing norethisterone and ethinyl estradiol, there was a significant increase in the AUC of norethisterone 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 colestipol was administered in combination with atorvastatin, plasma levels of atorvastatin decreased by approximately 25%. However, with the combined use of atorvastatin and colestipol, the effect on lipids was more pronounced than when using each of these drugs separately.


With simultaneous ingestion of atorvastatin and a suspension containing magnesium and aluminum hydroxide, the concentration of atorvastatin in plasma decreased by approximately 35%; however, the degree of reduction in LDL levels did not change.


When taking atorvastatin in combination with warfarin, a slight decrease in prothrombin time was noted in the first days of atorvastatin administration; however, the prothrombin time returned to normal in the next 15 days. However, in the case of co-administration of atorvastatin and warfarin, patients should be carefully monitored.


With simultaneous use of atorvastatin does not affect the pharmacokinetics of phenazone, therefore, interaction with other drugs metabolized by the same cytochrome isoenzymes is not expected.


A study of the combined administration of cimetidine and atorvastatin did not reveal a significant interaction between these drugs.


With the combined administration of 80 mg of atorvastatin and 10 mg of amlodipine, no changes in the pharmacokinetic parameters of atorvastatin in the equilibrium state were found.


No clinically significant undesirable interaction of atorvastatin and antihypertensive agents has been noted. Studies of the interaction with all specific drugs were not conducted.

Atorvastatin did not have a clinically significant effect on the concentration of terfenadine in plasma, which is metabolized mainly by cytochrome P450 ZA4; therefore, it seems unlikely that atorvastatin can significantly affect the pharmacokinetic parameters of other cytochrome P450 ZA4 substrates.

Special instructions

Before starting treatment with Atorvastatin, 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 the biochemical parameters that deactivate liver function. Liver function should be monitored before starting therapy, 6 weeks, 12 weeks after starting atorvastatin 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 atorvastatin. Patients who have increased levels of enzymes should be monitored until the level of enzymes returns to normal. In the case of a persistent increase in the values of alanine aminotransferase (ALT) or aspartate aminotransferase (ACT) to a level that exceeds the upper permissible limit by more than 3 times, it is recommended to reduce the dose of Atorvastatin or discontinue treatment.

Atorvastatin 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 atorvastatin.

Treatment with atorvastatin, like other HMG-CoA reductase inhibitors, can cause myopathy. The diagnosis of myopathy (pain and weakness in the muscles in combination with an increase in the activity of creatine phosphokinase (CPK) more than 10 times compared with the upper limit of the norm) should be discussed in patients with common myalgias or muscle weakness and / or a pronounced increase in the activity of CPK. 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. Atorvastatin therapy should be discontinued in case of a pronounced increase in CPK activity or in the presence of 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 cytochrome P450 ZA4, and / or the transport of drugs. Atorvastatin is biotransformed by CYP ZA4.

When prescribing atorvastatin in combination with fibrates, erythromycin, immunosuppressive agents, azole antifungals or nicotinic acid in lipid-lowering doses, the risk and the expected benefit of treatment should be carefully evaluated and patients should be regularly monitored to detect 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.

With the use of atorvastatin, as well as other means of this class, cases of rhabdomyolysis with acute renal failure caused by myoglobinuria are described.

Atorvastatin therapy should be temporarily discontinued or completely discontinued if there is evidence 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 convulsions).

Before starting treatment with atorvastatin, it is necessary to try to achieve control of hypercholesterolemia through adequate diet therapy, increased physical activity, weight loss in patients with obesity, and treatment of other conditions.

The impact on the ability to drive and work with mechanisms on the adverse effects of atorvastatin on the ability to drive and work with mechanisms was not reported.


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