Atorvastatin Verte Tablets 40mg N30
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Active ingredients
Atorvastatin
Release form
Pills
Composition
Atorvastatin (in the form of atorvastatin calcium trihydrate) 40 mg adjuvants: microcrystalline cellulose - 103.72 mg, lactose monohydrate - 100 mg, calcium carbonate - 20 mg, crospovidone - 15 mg, sodium carboxymethyl starch - 9 mg, hyprolose - 6 mg, magnesium stearate - mg composition of the film membrane: hypromellose - 4.5 mg, talc - 1.764 mg, hyprolosis - 1.746 mg, titanium dioxide - 0.99 mg.
Pharmacological effect
Pharmacodynamics. Atorvasterol is a selective competitive inhibitor of HMG-CoA reductase, an enzyme that slows down and is responsible for the conversion of 3-hydroxy-3-methylglutarycoenzyme A to mevalonate (a precursor of sterols, including cholesterol). In the liver, TG and cholesterol are incorporated into the composition of VLDL and enter the blood plasma for transport to peripheral tissues. LDL derived from VLDL is catabolized mainly by interaction with high affinity LDL receptors. Atorvasterol reduces the level of cholesterol and lipoproteins in the blood plasma, inhibiting the activity of HMG-CoA reductase and the synthesis of cholesterol in the liver. Atorvasterol also increases the number of LDL liver receptors on the surface of the cell membrane of hepatocytes, which leads to increased uptake and catabolism of LDL. Atorvasterol reduces the formation of LDL and the number of LDL particles, causes a pronounced and prolonged increase in the activity of LDL receptors, which has a beneficial effect on the quality of LDL fractions . Atorvastatin significantly reduces the level of LDL cholesterol in patients with homozygous familial hypercholesterolemia, which usually cannot be treated with other lipid-lowering drugs. In studies of dose dependence, atorvastatin reduced the level of total cholesterol (by 30–46%), LDL cholesterol (41–61%), apolipoprotein B (by 34–50%) and TG (by 14–33%), but caused a non-constant increase in HDL cholesterol and apolipoprotein A1. These results were obtained in patients with heterozygous familial hypercholesterolemia, non-familial hypercholesterolemia and mixed hyperlipidemia, including patients with non-insulin-dependent diabetes mellitus. It was confirmed that a decrease in total cholesterol cholesterol, LDL cholesterol and lipoprotein B reduces the risk of developing heart failure, heart failure, heart failure, heart failure, heart failure, heart failure, heart rate, heart failure, heart failure, heart failure, heart failure, heart failure, heart failure, heart failure, non-insulin dependent diabetes mellitus and diabetes mellitus.Studies of the effects of atorvastatin on the course of diseases and mortality are currently underway. The MIRACL study on the prevention of early recurrence of ischemic conditions analyzed the use of atorvastatin at a dose of 80 mg in 3086 patients (atorvastatin n = 1538; placebo = 1548) with acute coronary vascular diseases, including angina pectoris . The treatment was started 24–96 hours after the patient was hospitalized. The risk of re-hospitalization due to angina with clear signs of coronary heart disease was reduced by 26% (p = 0.018). Pharmacokinetics Absorption. Atorvastatin is rapidly absorbed after oral administration and reaches Cmax in the blood plasma in 1–2 hours. The volume of absorption increases in proportion to the dose of atorvastatin. The bioavailability of atorvastatin after ingestion in the form of coated pills is 95–99% compared with the bioavailability of atorvastatin in the form of p-ra. Absolute bioavailability is about 12%, and systemic availability of the active HMG-CoA reductase inhibitor is about 30%. Low system availability is explained by presystemic clearance in the gastrointestinal mucosa and / or metabolism during the first passage through the liver. Despite the fact that the amount and degree of absorption of the drug decreases when taken simultaneously with food by approximately 25 and 9%, respectively, estimating by Cmax and AUC, a decrease in the level of LDL cholesterol did not depend on whether atorvastatin was taken at the same time as food or not. When taking atorvastatin in the evening, its plasma concentration was lower (about 30% for Cmax and AUC) than when taken in the morning. However, a decrease in the level of LDL cholesterol does not depend on the time of taking the drug. Distribution. The average distribution of atorvastatin is about 381 liters. Atorvastatin is> 98% bound to plasma proteins. Metabolism. Atorvastatin is metabolized with the participation of cytochrome P450 ZA4 to ortho- and para-hydroxylated derivatives and various beta-oxidation products. Such substances are further metabolized by glucuronization. In vitro inhibition of HMG-CoA reductase due to the action of ortho and para-hydroxylated metabolites is equivalent to inhibition by atorvastatin. About 70% of the inhibitory effect on HMG-CoA reductase is exerted by active metabolites. Excretion.Atorvastatin is excreted mainly with bile after hepatic and / or extrahepatic metabolism. However, the drug is not subject to severe extrahepatic recirculation. The average T1 / 2 of atorvastatin from human blood plasma is about 14 hours. Due to the active metabolites, the half-time inhibitory activity on HMG-CoA reductase is about 20–30 hours. Separate groups of patients Patients of old age. Plasma concentrations of atorvastatin and its active metabolites in healthy older volunteers are higher than in younger patients, but the effects on blood lipid levels are similar in both age groups. Children. There are no data regarding pharmacokinetics in children. Pol. The concentrations of atorvastatin and its active metabolites in women (Cmax in plasma are approximately 20% higher, and the AUC value is approximately 10% lower) differ from those in men. Such differences have no clinical significance, and the difference in the effect on the level of lipids in the blood in men and women is not significant. Impaired kidney function. In kidney diseases, no effect on the concentration of atorvastatin and its metabolites in the blood plasma, as well as on the effectiveness of their influence on the levels of lipids in the blood, was noted. Abnormal liver function. Plasma concentrations of atorvastatin and its metabolites are significantly increased (Cmax - approximately 16 times, AUC - 11 times) in patients with chronic alcoholic liver disease (Child-Pugh class B). Data from preclinical studies of atorvastatin non-carcinogenic in animals. The maximum doses that were applied were 63 times higher than the maximum dose for a person (80 mg / day) when converted to mg / kg body weight, and 8–16 times higher than the values of AUC0-24 determined by the total inhibitory activity. In a 2-year animal study, the incidence of hepatocellular adenoma in males and hepatocellular carcinoma in females was increased when the animals were administered maximum doses that were 250 times the maximum dose for humans, expressed in mg / kg body weight. In animals, the effect was 6–11 times higher, which was established in terms of AUC0-24. Atorvastatin did not have a mutagenic effect, did not lead to malformations of the reproductive organs in 4 in vitro studies and in one in vivo test.In animal studies, atorvastatin did not affect male fertility when administered in doses up to 175 mg / kg body weight per day and females when administered in doses up to 225 mg / kg / day, and did not lead to malformations.
Indications
as an addition to the diet for the treatment of patients with elevated levels of total cholesterol, LDL cholesterol, apolipoprotein B, and TG, in order to increase LDL cholesterol in patients with primary hypercholesterolemia (hereditary hereditary and non-hereditary hypercholesterolemia), combined (mixed) hyperlipidemia (type IIa and II Fredrickson), elevated serum TG (type IV according to Fredrikson) and in patients with dysbetalipoproteinemia (type III according to Fredrikson) in cases when the diet does not provide a proper effect. To reduce the level of total cholesterol and cholesterol P in patients with homozygous hereditary hypercholesterolemia, when diet and other non-pharmacological agents do not provide the proper effect. Patients without clinical manifestations of cardiovascular diseases, with or without dyslipidemia, who have several risk factors for developing cardiovascular diseases, such as smoking, hypertension , diabetes mellitus, low HDL cholesterol or a family history of cardiovascular diseases at a young age in order to: reduce the risk of fatal manifestations of coronary heart disease and efatal myocardial infarction; reducing the risk of stroke; reducing the risk of angina and the need for myocardial revascularization. In patients with clinical symptoms of coronary diseases, atorvastatin is shown to: reduce the risk of developing nonfatal myocardial infarction; reduce the risk of developing fatal and nonfatal stroke; procedures for revascularization; reducing the risk of hospitalization for congestive heart failure; reducing the risk of of angina pectoris. Children aged 10–17 years Atorvasterol is prescribed in addition to the diet to reduce total cholesterol, LDL cholesterol and apoliprotein B in boys and girls in the post-menarchial period, aged 10–17 years with heterozygous hereditary hypercholesterolemia, even if adequate diets if: a) LDL cholesterol level remains ≥190 mg / dL, b) LDL cholesterol level remains ≥160 mg / dL and: c) a family history of cardiovascular disease at a young age; d) in children who have children and more risk factors occur I have heart disease.
Contraindications
hypersensitivity to the active substance or any other component of the drug in history, liver disease in the active phase or prolonged increase in transaminase levels (3 times higher than the average upper limit of normal) in blood plasma of unknown etiology, myopathy, pregnancy and lactation, women of reproductive age, who do not use effective methods of contraception; children under the age of 10 years.
Precautionary measures
Application for violations of liver functionWith caution, you should prescribe the drug for violations of the liver.It is not necessary to change the dose in case of renal dysfunction. The concentration of amplodipine in the blood plasma does not depend on the degree of reduction of renal function. Use in children It is contraindicated in children and adolescents under the age of 18. Application in elderly patients With caution in elderly patients.
Dosage and administration
Before starting therapy with Atorvasterol, it is necessary to try to control the level of hypercholesterolemia with the help of an appropriate diet, prescribe physical exercises and measures aimed at reducing body weight in patients with obesity, and treat other associated diseases. During treatment with Atorvasterol, patients should follow a standard cholesterol-lowering diet. The drug is prescribed in a dose of 10-80 mg once a day, every day, at any time of the day, regardless of the meal. The initial and maintenance doses should be selected individually, according to the initial value of the LDL cholesterol level, the goal of treatment and the patient's sensitivity to the drug. After 2–4 weeks after the start of treatment and / or after titration of the dose of Atorvasterol, it is necessary to monitor the level of lipoproteins, and depending on the results of the analysis, correct the dose of the preparation accordingly. For most patients, an effective dose of 10 mg / day. The therapeutic effect is achieved for 2 weeks, the maximum therapeutic effect - for 4 weeks. The effect is maintained for prolonged treatment. Homozygous familial hypercholesterolemia.For most patients with homozygous familial hypercholesterolemia, the result is achieved when using 80 mg of Atorvasterol 1 time per day, which reduces LDL cholesterol levels by more than 15% (18–45%). years old). It is recommended to prescribe Atorvasterol in the initial dose of 10 mg 1 time per day. The maximum recommended dose is 20 mg 1 time per day (doses exceeding 20 mg have not been studied in patients of this age group). The dose is determined individually, depending on the purpose of treatment. Every 4 weeks or more it is necessary to correct the dose of the drug. Use for the treatment of patients with liver failure. See CONTRAINDICATIONS and SPECIAL INSTRUCTIONS. Application for the treatment of patients with renal insufficiency. Kidney disease does not affect the concentration of atorvastatin or a decrease in the level of LDL cholesterol in the blood plasma. Therefore, there is no need for dose adjustment. Application for the treatment of elderly patients. Differences in safety, efficacy, or goal attainment in the treatment of hypercholesterolemia in elderly patients and patients of other age groups are not present. Use in combination with other drugs. If necessary, the simultaneous use of atorvastatin and cyclosporine atorvastatin dose should not exceed 10 mg (see SPECIAL INSTRUCTIONS and INTERACTIONS).
Side effects
Gastrointestinal symptoms, including constipation, flatulence, dyspepsia, and abdominal pain, are expected to be side effects that are noted most often. They tend to disappear with continued treatment. Due to atorvastatin side effects, less than 2% of patients discontinued their participation in clinical trials. The following list of adverse reactions is based on data obtained in clinical studies and during the post-marketing period. 100 <1/10); infrequently (≥1 / 1000, <1/100); rarely (≥1 / 10,000, <1/1000); very rarely (<1/10 000). From the digestive tract: often: constipation, flatulence, dyspepsia, nausea, diarrhea; infrequently: anorexia, vomiting. For the blood system and lymphatic system: infrequently: thrombocytopenia. For the immune system: often: hypersensitivity; very rarely: anaphylaxis. From the endocrine system: infrequently: alopecia, hyperglycemia or hypoglycemia, pancreatitis. From the psyche: often: insomnia; infrequently: amnesia. From the nervous system: often: headache,dizziness, paresthesia, hypesthesia; infrequently: peripheral neuropathy. From the hepatobiliary system: rarely: hepatitis, cholestatic jaundice. From the organ of hearing and balance: infrequently: tinnitus. From the skin and subcutaneous tissue: often: rash, itching; infrequently: urticaria; very rarely: angioedema, bullous eruptions (including erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis). On the part of the musculoskeletal system: often: myalgia, arthralgia; infrequently: myopathy; rarely: myositis, rhabdomyolysis, convulsions. On the part of the reproductive system: infrequently: impotence. General disorders: often: weakness, chest pain, back pain, peripheral edema; infrequently: malaise, impaired metabolism and nutrition, asthenia. Children aged 10-17 years The patients had adverse reactions similar to those in those who received a placebo. The most common side effects that were noted in both groups, without taking into account the causal relationship, were infections. In postmarketing studies, the following side effects were reported: from the blood system and lymphatic system: thrombocytopenia; on the part of the immune system: allergic reactions (including anaphylaxis); on the part of the metabolism: increase in body weight; on the part of the nervous system: hypesthesia, amnesia, dizziness; on the part of the organ of hearing: ringing in the ears; on the part of skin and subcutaneous tissue: Stephen-Johnson, toxic epidermal necrolysis, erythema multiforme, bullous eruption, urticaria, from the musculoskeletal system and connective tissue: rhabdomyolysis, arthralgia, back pain; general disorders: chest pain, peripheral edema, malaise, fatigue. Studies As with the use of other HMG-CoA reductase inhibitors, an increase in plasma transaminase levels was reported in patients using atorvastatin. Such changes were more often slight and temporary; there was no need to discontinue use of the drug. A clinically significant increase in serum transaminase levels (levels 3 times higher than the mean upper limit of normal) was noted in 0.8% of patients who received atorvastatin. Such increases were dose-dependent and reversible in all patients.In clinical studies, an increase in serum creatine phosphokinase levels (levels 3 times higher than the mean upper limit of normal) was observed in 2.5% of patients who used atorvastatin, which is typical of other HMG-CoA reductase inhibitors. Levels that were 10 times higher than the average upper limit of normal were detected in 0.4% of patients who used atorvastatin.
Overdose
There is no specific treatment for atorvastatin overdose. In cases of overdose, patient treatment should be symptomatic and supportive (if necessary). It is necessary to monitor indicators of liver function and the level of CPK. Since atorvastatin binds to plasma proteins, it is not expected that hemodialysis will significantly increase the clearance of atorvastatin.
Interaction with other drugs
the risk of myopathy during treatment with HMG-CoA reductase inhibitors increases with simultaneous use of cyclosporine, fibrates, macrolide antibiotics, including erythromycin, antifungal drugs of the azoles group, or niacin, and very rarely leads to the development of rhabdomyolysis and impaired kidney function due to myoglobinuria. Careful consideration should be given to the balance of possible benefits and risks, which are noted with concomitant treatment. Inhibitors of cytochrome P450 3A4. Atorvastatin is metabolized by cytochrome P450 3A4. Interactions can be detected with the simultaneous use of atorvastatin and cytochrome P450 ZA4 inhibitors (for example, cyclosporine, macrolide antibiotics, including erythromycin and clarithromycin, nefazodone, azole antifungal agents, including itraconazole, HIV protease inhibitors). Atorvastatin and these drugs are used at the same time with extreme caution, as this may lead to an increase in plasma plasma levels of atorvastatin. Erythromycin / clarithromycin. The simultaneous use of atorvastatin in a dose of 10 mg / day and such inhibitors of cytochrome P450 3A4, such as erythromycin (500 mg 4 times a day) or clarithromycin (500 mg 2 times a day) leads to an increase in plasma concentrations of atorvastatin. Clarithromycin increases Cmax of atorvastatin by 56% and AUC by 80%. P-glycoprotein inhibitors.Atorvastatin and its metabolites are substrates for P-glycoprotein. P-glycoprotein inhibitors (for example, cyclosporin) can increase the bioavailability of atorvastatin. Itraconazole. With simultaneous use of atorvastatin 40 mg and itraconazole 200 mg / day, the AUC value of atorvastatin increased 3 times. Protease inhibitors. The simultaneous use of atorvastatin with protease inhibitors, which inhibit the action of cytochrome P450 3A4, is accompanied by an increase in the concentration of atorvastatin in the blood plasma. Grapefruit juice. Contains one or more inhibitors of CYP 3A4 and may cause an increase in plasma concentrations of those drugs that are metabolized by CYP 3A4. The AUC value of atorvastatin is increased by 37%, and the AUC of active orthohydroxymetabolite is reduced by 20.4% after taking 240 ml of grapefruit juice. The use of grapefruit juice in large volumes (more than 1.2 liters per day for 5 days) leads to an increase in the AUC of atorvastatin 2.5 times and an increase of 1.3 times the AUC of the active inhibitors of HMG-CoA reductase (atorvastatin and active metabolites). Therefore, it is not recommended to use a large amount of grapefruit juice during treatment with atorvastatin. The cytochrome P450 3A4 inducers. The effect of cytochrome P450 ZA4 inducers (for example, rifampicin or phenytoin) on atorvastatin is unknown. Possible interactions with other substrates of this isoenzyme are unknown, but they should be considered in the case of the use of drugs with a narrow therapeutic window, for example, class III antiarrhythmic drugs, including amiodarone. Antipyrin. Since atorvasterol does not alter the pharmacokinetics of antipyrine, the interaction between other drugs metabolized by the same cytochrome (such as terfenadine, tolbutamide, triazolam, oral contraceptives) is unlikely. Simultaneous use of other drugs Azithromycin. The simultaneous use of atorvastatin (10 mg per day) and azithromycin (500 mg per day) did not change the concentration of atorvastatin in the blood plasma. Gemibibrozil / fibrates. The risk of myopathy caused by the use of atorvastatin may increase with simultaneous use of fibrates. According to the results of in vitro studies, gemfibrozil suppresses atorvastatin glucuronization.This may cause an increase in plasma concentrations of atorvastatin. Digoxin. With long-term use of digoxin and the simultaneous use of 10 mg of atorvastatin, the level of digoxin in the blood plasma did not change. Nevertheless, the concentration of digoxin increased by approximately 20% with simultaneous use of 80 mg of atorvastatin per day. This interaction occurs due to inhibition of the membrane protein that transports the P-glycoprotein. The condition of patients who use digoxin should be carefully monitored. Oral contraceptives. When used simultaneously with oral contraceptives, concentrations of norethisterone and ethinyl estradiol increase. This effect should be considered when selecting doses of oral contraceptives. Colestipol. The concentration of atorvastatin and its active metabolites in the blood plasma is reduced (by about 25%) with the simultaneous use of atorvastatin and colestipol. At the same time, the hypolipidemic effect of the combination of atorvastatin and colestipol exceeded the effectiveness noted when using each of these drugs separately. Antacids. With simultaneous use of atorvastatin and antacids in the form of liquid forms for oral administration, which contain sodium hydroxide and aluminum hydroxide, plasma concentrations of atorvastatin are reduced by approximately 35%, however, there is no effect on reducing LDL cholesterol. Warfarin. The simultaneous use of atorvastatin and warfarin leads to a slight decrease in prothrombin time in the first days of such treatment, but after 15 days of atorvastatin use, this figure returns to normal. However, constant monitoring of the condition of patients taking warfarin is necessary if atorvastatin is added to the treatment regimen. Phenazone. The simultaneous use of atorvastatin and phenazone for a certain time leads to a slight effect on the clearance of phenazone, or does not reveal such an effect. Amlodipine. With simultaneous use of 80 mg of atorvastatin and 10 mg of amlodipine, the pharmacokinetic parameters of atorvastatin did not change in equilibrium. Terfenadine. The simultaneous use of atorvastatin and terfenadine did not cause significant changes in the pharmacokinetics of terfenadine. Other drugs.In clinical studies, no clinically significant interactions were noted with simultaneous administration of atorvastatin and antihypertensive or estrogen-substituting agents.
special instructions
Effect on the liver As with other hypolipoproteinemic drugs of this group, the treatment of transaminases of the blood plasma can be moderately increased during treatment with Atorvasterol (3 times higher than the upper normal level). Before starting treatment and periodically during treatment, liver function indicators should be determined. Monitoring of liver function should be carried out with the appearance of signs or symptoms of its possible defeat. Atorvasterol can cause an increase in transaminase activity. The condition of patients in whom the level of transaminases has increased should be monitored until the disappearance of pathological changes. In the case when the level of transaminases increases by 3 times compared with the average value of the upper limit of normal, it is recommended to reduce the dose of Atorvasterol or to cancel the drug. Increased transaminase activity was not accompanied by jaundice or other clinical manifestations. If the dose of the drug was reduced, a break was taken or treatment was stopped, the transaminase level returned to normal. Most patients continued treatment with low doses of atorvasterol without adverse effects. Atorvasterol should be used with caution in patients who abuse alcohol and / or have a history of liver disease. Liver diseases in the active phase or increased transaminase activity for some unknown reason are contraindicated for the use of the drug. Effect on skeletal muscles Like other HMG-CoA reductase inhibitors, atorvastatin is very rarely able to affect skeletal muscles and cause myalgia, myositis and myopathy, which can progress to the onset of rhabdomyolysis, a condition that potentially endangers the patient’s life and is characterized by a significant increase in CPK levels (more than 10 times higher than the upper limit of norm), myoglobinemia and myoglobinuria, which lead to impaired kidney function. The probability of occurrence of this condition should be considered in patients with diffuse myalgia, muscle soreness or weakness and / or a significant increase in the level of CPK. Patients should be warned about possible muscle pain and weakness muscles, sometimes with indisposition or fever.In cases of elevated levels of CPK or an updated or probable diagnosis of myopathy, treatment with Atorvasterol should be discontinued. The risk of myopathy during treatment with drugs of this group increases with the simultaneous use of cyclosporine, fibrin acid derivatives, erythromycin, niacin or azole antifungal agents. Most of these agents inhibit the metabolism of cytochrome P450 ZA4 and / or the distribution of the drug in the body. Atorvasterol is biotransformed, first of all, with the help of the liver enzyme SUR ZA4. When administering atorvasterol in combination with fibrin acid derivatives, erythromycin, immunosuppressants or azole antifungals, or hypolipoproteinemic doses of niacin, positive results and negative effects should be weighed and patients should be monitored to determine manifestations such as muscle pain and muscle weakness, especially first months of treatment and after increasing the dose of one of these drugs. Periodic determination of CPK is recommended for this, but it should be remembered that this test is not sufficient for the timely diagnosis of severe myopathy. Atorvasterol can cause an increase in the level of CPK. When treating with Atorvasterol, as with the use of similar drugs in this group, cases of rhabdomyolysis in combination with secondary renal failure, which is manifested by myoglobinuria, are sometimes noted. Drug therapy should be discontinued or discontinued in the event of a patient’s serious condition if they are suspected that these changes are caused by myopathy, or if there are risk factors for the development of secondary renal failure in rhabdomyolysis (for example, severe acute infection, hypotension, serious surgical interventions, trauma, severe endocrine, metabolic or electrolyte disturbances and uncontrolled seizures). Before starting treatment, atorvastatin should be used with caution in patients prone to developed Iu rhabdomyolysis. Determining the level of CPK before starting treatment with statins is necessary in such cases: impaired renal function, hypothyroidism, a genetic myopathy in history, myopathy (in history) associated with previous use of statins or fibrates, abnormal liver function and / or alcohol abuse, in patientsold age (70 years and older). The need to define indicators should be assessed taking into account the above. In such cases, the risk associated with treatment and the possible benefits must be carefully considered. It is recommended to conduct a full clinical monitoring. If the CPK level is very high (5 times higher than the upper limit of the norm), treatment should not be started. Determining the CPK level You should not determine CPK levels after exercise or if there are any obvious reasons for increasing CPK, as this affects the interpretation of test results. If the level of CPK is significantly higher (5 times higher than the upper limit of normal), the analysis should be repeated after 5–7 days to confirm the result. During treatment: it is necessary to explain to patients the importance of immediately reporting to the doctor about the occurrence of myalgia, cramps or weakness, especially after indisposition and fever, if symptoms occur during the treatment with atorvastatin, you should determine the level of CPK, and in case of a marked increase in level (5 times higher than the upper limit of the norm), stop treatment; if the symptoms of the muscular system Common or daily discomfort should be considered, the drug should be discontinued, even if CPK levels do not exceed 5 times the upper limit of the norm, if the symptoms disappear and the CPK levels return to normal, treatment with atorvastatin or other statins can be considered in the minimum dose and under close monitoring; if there is a marked increase in CPK levels (10 times higher than the upper limit of normal) or if rhabdomyolysis is manifested or if such a condition is suspected, treatment with atorvastatin should be stopped. Menen during pregnancy and lactation. Atorvasterol is contraindicated during pregnancy and lactation. Women of reproductive age should use effective contraception during treatment. The safety of atorvastatin use during pregnancy and lactation has not been established. In animal studies, it has been established that HMG-CoA reductase inhibitors can influence the development of the embryo and fetus. After administration of atorvastatin to female animals at doses higher than 20 mg / kg / day, the development of the offspring was slowed down, and the rate of postnatal survival was reduced.In animals, the concentration of atorvastatin and its metabolites in plasma and milk is similar. It is not known whether atorvastatin is excreted in human breast milk. Children. In children, the drug should be used under the supervision of a specialist. Controlled clinical studies of the use of atorvastatin in patients with heterozygous familial hypercholesterolemia under the age of 10 years have not been conducted. The ability to influence the reaction rate in driving and working with other mechanisms. There is no evidence of any effect of atorvastatin on the ability to drive vehicles and work with mechanisms.