Atorvastatin | Atorvastatin-SZ tablets are covered.pl.ob. 10 mg 60 pcs. pack

Special Price $18.62 Regular Price $26.00
In stock
SKU
BID515828
372.4 Reward Points will be used to purchase this product
Pharmacological action of

Pharmacotherapeutic group of the medicinal product:

Hypolipidemic agent - inhibitor of HMG-CoA reductase

ATX code: [C10AA05]

Pharmacological properties of the inhibitor 3-phase competitive antioxidant

-hydroxy-3-methylglutaryl-CoA in mevalonate is a precursor to steroids, including cholesterol, a synthetic lipid-lowering agent.

In patients with homozygous and heterozygous familial hypercholesterolemia, non-family forms of hypercholesterolemia and mixed dyslipidemia, atorvastatin reduces the plasma concentration of cholesterol (cholesterol), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo-B), as well as very low-density lipoprotein cholesterol (X-LDL and cholesterol) TG), causes an unstable increase in the concentration of high density lipoprotein cholesterol (HDL-C). Atorvastatin reduces the concentration of cholesterol and lipoproteins in blood plasma, inhibiting HMG-CoA reductase and 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-C.

Atorvastatin reduces the formation 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 cholesterol in patients with homozygous hereditary familial hypercholesterolemia, resistant to therapy with other hypolipidemic agents.

Atorvastatin in doses from 10 mg to 80 mg lowers cholesterol concentration by 30% - 46%, LDL-C - by 41% - 61%, apolipoprotein-on-B - by 34% - 50% and TG - by 14% - 33% The results of therapy are similar in patients with heterozygous familial hypercholesterolemia, non-family forms of hypercholesterolemia and mixed hyperlipidemia, including patients with type 2 diabetes mellitus. In patients with isolated hypertriglyceridemia, atorvastatin lowers cholesterol, cholesterol-LDL, cholesterol-VLDL, apo-B and TG and increases the concentration of HDL-cholesterol. In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate-density lipoprotein cholesterol.

In patients with type IIa and IIb hyperlipoproteinemia according to the Fredrickson classification, the average increase in the concentration of HDL-C during treatment with atorvastatin (10-80 mg) compared with the initial value is 5.1% - 8.7% and does not depend on the dose. There is a significant dose-dependent decrease in the ratios: total cholesterol / cholesterol-HDL and cholesterol-LDL / cholesterol-HDL by 29% - 44% and 37% - 55%, respectively. The antisclerotic 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 cells of the inner lining of blood vessels. Under the influence of atorvastatin, endothelium-dependent expansion of blood vessels improves the concentration of LDL cholesterol, apolipoprotein B, and TG decreases there is an increase in the concentration of HDL cholesterol and apolipoprotein A. Atorvastatin reduces blood plasma viscosity and the activity of certain platelet coagulation and aggregation factors. Due to this, it improves hemodynamics and normalizes the state of the coagulation system. HMG-CoA reductase inhibitors also affect the metabolism of macrophages, block their activation and prevent rupture of atherosclerotic plaques.

Atorvastatin-SZ at a dose of 80 mg significantly reduces the risk of developing ischemic complications and mortality by 16% after a 16-week course, and the risk of re-hospitalization for angina pectoris, accompanied by signs of myocardial ischemia, by 26%. In patients with different initial concentrations of LDL-C, Atorvastatin-SZ reduces 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 under the age of 65) . A decrease in plasma concentration of LDL-C correlates better with the dose of the drug than with its concentration in the blood plasma. The dose is selected taking into account the therapeutic effect (see section "Dosage and administration"). The therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum after 4 weeks and persists throughout the entire period of therapy.

Pharmacokinetics

Absorption

Atorvastatin is rapidly absorbed after oral administration: the time to reach its maximum concentration (TCmax) in blood plasma is 1-2 hours. In women, the maximum concentration (Cmax) of atorvastatin is 20% higher, and the area under the concentration-time curve (AUC) is 10% lower than in men. The degree of absorption and concentration in blood plasma increase in proportion to the dose. The absolute bioavailability is about 14%, and the systemic bioavailability of the inhibitory activity against HMG-CoA reductase is about 30%. Low systemic bioavailability is due to a presystemic metabolism in the mucous membrane of the gastrointestinal tract and / or during the “primary passage” through the liver. Eating reduces the speed and degree of absorption of the drug (by 25% and 9%, respectively), as evidenced by the results of the determination of Cmax and AUC, however, the decrease in LDL-C is similar to that of atorvastatin on an empty stomach. Despite, that after taking atorvastatin in the evening, its plasma concentration is lower (Cmax and AUC, about 30%) than after taking in the morning, the decrease in the concentration of LDL-C does not depend on the time of day at which the drug is taken.

Distribution

The average volume of distribution of atorvastatin is about 381 liters. Communication with blood plasma proteins is not less than 98%. The ratio of the content in red blood cells / blood plasma is about 0.25, i.e., atorvastatin does not penetrate well into red blood cells.

Metabolism

Atorvastatin is extensively metabolized to form ortho- and para-hydroxylated derivatives and various -oxidation products. In vitro ortho- and para-hydroxylated metabolites have an inhibitory effect on HMG-CoA reductase, comparable to that of atorvastatin. An approximately 70% decrease in the activity of HMG-CoA reductase occurs due to the action of active circulating metabolites. The results of the studies invitro suggest that the isoenzyme of liver CYPZA4 plays an important role in the metabolism of atorvastatin. This fact is supported by an increase in the concentration of the drug in blood plasma while taking erythromycin, which is an inhibitor of this isoenzyme. In vitro studies have also shown that atorvastatin is a weak inhibitor of the CYP3A4 isoenzyme. Atorvastatin does not have a clinically significant effect on the plasma concentration of terfenadine, which is metabolized mainly by the CYPZA4 isoenzyme, therefore, it is unlikely to significantly affect the pharmacokinetics of other substrates of the SYPZA4 isoenzyme (see the section “Interaction with other medicinal products”).

Excretion of

Atorvastatin and its metabolites are excreted mainly with bile after hepatic and / or extrahepatic metabolism (atorvastatin does not undergo severe enterohepatic recirculation). The half-life (T1 / 2) of atorvastatin is about 14 hours, while the inhibitory effect of the drug against HMG-CoA reductase is approximately 70% determined by the activity of circulating metabolites and lasts about 20-30 hours due to their presence. After oral administration, less than 2% of the accepted dose of the drug is found in the urine.

Special patient groups

Elderly patients

The plasma concentrations of atorvastatin are higher for patients over 65 years of age (Cmax

by about 40%, AUC by about 30%) than in adult patients. Differences in the effectiveness and safety of the drug, or achievement of the goals of lipid-lowering therapy in elderly patients compared with the general population was not detected.

Children

Studies of the pharmacokinetics of the drug in children have not been conducted.

Insufficiency of renal function

Impaired renal function does not affect the concentration of atorvastatin in the blood plasma or its effect on lipid metabolism therefore, a dose change in patients with impaired renal function is not required.

Atorvastatin is not excreted during hemodialysis due to intense binding to plasma proteins.

Atorvastatin has not been studied in patients with end-stage renal failure.

Lack of liver function

The concentration of the drug rises significantly (РЎmax approximately 16 times, AUC is approximately 11 times) in patients with alcoholic cirrhosis of the liver (stage B on the Child-Pugh scale) (see section "Contraindications").
Pharmacological action of

Pharmacotherapeutic group of the medicinal product:

Hypolipidemic agent - inhibitor of HMG-CoA reductase

ATX code: [C10AA05]

Pharmacological properties of the inhibitor 3-phase competitive antioxidant

-hydroxy-3-methylglutaryl-CoA in mevalonate is a precursor to steroids, including cholesterol, a synthetic lipid-lowering agent.

In patients with homozygous and heterozygous familial hypercholesterolemia, non-family forms of hypercholesterolemia and mixed dyslipidemia, atorvastatin reduces the plasma concentration of cholesterol (cholesterol), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo-B), as well as very low-density lipoprotein cholesterol (X-LDL and cholesterol) TG), causes an unstable increase in the concentration of high density lipoprotein cholesterol (HDL-C). Atorvastatin reduces the concentration of cholesterol and lipoproteins in blood plasma, inhibiting HMG-CoA reductase and 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-C.

Atorvastatin reduces the formation 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 cholesterol in patients with homozygous hereditary familial hypercholesterolemia, resistant to therapy with other hypolipidemic agents.

Atorvastatin in doses from 10 mg to 80 mg lowers cholesterol concentration by 30% - 46%, LDL-C - by 41% - 61%, apolipoprotein-on-B - by 34% - 50% and TG - by 14% - 33% The results of therapy are similar in patients with heterozygous familial hypercholesterolemia, non-family forms of hypercholesterolemia and mixed hyperlipidemia, including patients with type 2 diabetes mellitus. In patients with isolated hypertriglyceridemia, atorvastatin lowers cholesterol, cholesterol-LDL, cholesterol-VLDL, apo-B and TG and increases the concentration of HDL-cholesterol. In patients with dysbetalipoproteinemia, atorvastatin reduces the concentration of intermediate-density lipoprotein cholesterol.

In patients with type IIa and IIb hyperlipoproteinemia according to the Fredrickson classification, the average increase in the concentration of HDL-C during treatment with atorvastatin (10-80 mg) compared with the initial value is 5.1% - 8.7% and does not depend on the dose. There is a significant dose-dependent decrease in the ratios: total cholesterol / cholesterol-HDL and cholesterol-LDL / cholesterol-HDL by 29% - 44% and 37% - 55%, respectively. The antisclerotic 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 cells of the inner lining of blood vessels. Under the influence of atorvastatin, endothelium-dependent expansion of blood vessels improves the concentration of LDL cholesterol, apolipoprotein B, and TG decreases there is an increase in the concentration of HDL cholesterol and apolipoprotein A. Atorvastatin reduces blood plasma viscosity and the activity of certain platelet coagulation and aggregation factors. Due to this, it improves hemodynamics and normalizes the state of the coagulation system. HMG-CoA reductase inhibitors also affect the metabolism of macrophages, block their activation and prevent rupture of atherosclerotic plaques.

Atorvastatin-SZ at a dose of 80 mg significantly reduces the risk of developing ischemic complications and mortality by 16% after a 16-week course, and the risk of re-hospitalization for angina pectoris, accompanied by signs of myocardial ischemia, by 26%. In patients with different initial concentrations of LDL-C, Atorvastatin-SZ reduces 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 under the age of 65) . A decrease in plasma concentration of LDL-C correlates better with the dose of the drug than with its concentration in the blood plasma. The dose is selected taking into account the therapeutic effect (see section "Dosage and administration"). The therapeutic effect is achieved 2 weeks after the start of therapy, reaches a maximum after 4 weeks and persists throughout the entire period of therapy.

Pharmacokinetics

Absorption

Atorvastatin is rapidly absorbed after oral administration: the time to reach its maximum concentration (TCmax) in blood plasma is 1-2 hours. In women, the maximum concentration (Cmax) of atorvastatin is 20% higher, and the area under the concentration-time curve (AUC) is 10% lower than in men. The degree of absorption and concentration in blood plasma increase in proportion to the dose. The absolute bioavailability is about 14%, and the systemic bioavailability of the inhibitory activity against HMG-CoA reductase is about 30%. Low systemic bioavailability is due to a presystemic metabolism in the mucous membrane of the gastrointestinal tract and / or during the “primary passage” through the liver. Eating reduces the speed and degree of absorption of the drug (by 25% and 9%, respectively), as evidenced by the results of the determination of Cmax and AUC, however, the decrease in LDL-C is similar to that of atorvastatin on an empty stomach. Despite, that after taking atorvastatin in the evening, its plasma concentration is lower (Cmax and AUC, about 30%) than after taking in the morning, the decrease in the concentration of LDL-C does not depend on the time of day at which the drug is taken.

Distribution

The average volume of distribution of atorvastatin is about 381 liters. Communication with blood plasma proteins is not less than 98%. The ratio of the content in red blood cells / blood plasma is about 0.25, i.e., atorvastatin does not penetrate well into red blood cells.

Metabolism

Atorvastatin is extensively metabolized to form ortho- and para-hydroxylated derivatives and various -oxidation products. In vitro ortho- and para-hydroxylated metabolites have an inhibitory effect on HMG-CoA reductase, comparable to that of atorvastatin. An approximately 70% decrease in the activity of HMG-CoA reductase occurs due to the action of active circulating metabolites. The results of the studies invitro suggest that the isoenzyme of liver CYPZA4 plays an important role in the metabolism of atorvastatin. This fact is supported by an increase in the concentration of the drug in blood plasma while taking erythromycin, which is an inhibitor of this isoenzyme. In vitro studies have also shown that atorvastatin is a weak inhibitor of the CYP3A4 isoenzyme. Atorvastatin does not have a clinically significant effect on the plasma concentration of terfenadine, which is metabolized mainly by the CYPZA4 isoenzyme, therefore, it is unlikely to significantly affect the pharmacokinetics of other substrates of the SYPZA4 isoenzyme (see the section “Interaction with other medicinal products”).

Excretion of

Atorvastatin and its metabolites are excreted mainly with bile after hepatic and / or extrahepatic metabolism (atorvastatin does not undergo severe enterohepatic recirculation). The half-life (T1 / 2) of atorvastatin is about 14 hours, while the inhibitory effect of the drug against HMG-CoA reductase is approximately 70% determined by the activity of circulating metabolites and lasts about 20-30 hours due to their presence. After oral administration, less than 2% of the accepted dose of the drug is found in the urine.

Special patient groups

Elderly patients

The plasma concentrations of atorvastatin are higher for patients over 65 years of age (Cmax

by about 40%, AUC by about 30%) than in adult patients. Differences in the effectiveness and safety of the drug, or achievement of the goals of lipid-lowering therapy in elderly patients compared with the general population was not detected.

Children

Studies of the pharmacokinetics of the drug in children have not been conducted.

Insufficiency of renal function

Impaired renal function does not affect the concentration of atorvastatin in the blood plasma or its effect on lipid metabolism therefore, a dose change in patients with impaired renal function is not required.

Atorvastatin is not excreted during hemodialysis due to intense binding to plasma proteins.

Atorvastatin has not been studied in patients with end-stage renal failure.

Lack of liver function

The concentration of the drug rises significantly (РЎmax approximately 16 times, AUC is approximately 11 times) in patients with alcoholic cirrhosis of the liver (stage B on the Child-Pugh scale) (see section "Contraindications").

Indications

• Primary hypercholesterolemia (heterozygous familial and non-familial hypercholesterolemia (IIa type according to the Fredrickson classification)

• Combined (mixed) hyperlipidemia (IIa and IIb types according to the Fredrickson classification) typederiponephenophenemia to diet)

• Familial endogenous hypertriglyceridemia (type IV according to the classification of Fredrickson), diet-resistant

• Homozygous familial hypercholesterolemia with insufficient efficacy of diet therapy and other non-pharmacological treatments for

• Prevention of cardiovascular disease:

- Primary prevention of cardiovascular complications in patients without clinical signs of coronary heart disease (CHD), but with several its development: age over 55 years, nicotine addiction, arterial hypertension, diabetes mellitus, genetic predisposition, including on the background

dyslipidemia - Secondary prophylaxis of cardiovascular complications in patients with coronary artery disease in order to reduce the total mortality rate, myocardial infarction, stroke, re-hospitalization for angina pectoris and the need for revascularization.

Contraindications

Hypersensitivity to any component of the drug. Active liver disease or an increase in the activity of “liver” transaminases in blood plasma of unclear origin more than 3 times in comparison with the upper limit of normal. Age up to 18 years (insufficient clinical data on the effectiveness and safety of the drug in this age group). Lactose intolerance, lactase deficiency, glucose-galactose malabsorption. Hypersensitivity to soy and peanuts. Pregnancy and the period of breastfeeding. Use in women planning a pregnancy and not using reliable methods of contraception.

With caution

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

Use during pregnancy and lactation

Atorvastatin-SZ is contraindicated in pregnancy. Women of reproductive age should use adequate methods of contraception during treatment. The drug Atorvastatin-SZ can be prescribed to women of reproductive age only if the probability of pregnancy is very low, and the patient is informed about the possible risk of treatment for the fetus. The drug Atorvastatin-SZ is contraindicated during lactation. It is not known whether atorvastatin is excreted in breast milk. If it is necessary to prescribe the drug during lactation, breastfeeding should be stopped to avoid the risk of adverse events in infants.

Special instructions

Before starting therapy with Atorvastatin, the patient must be prescribed a standard hypocholesterol diet, which he must follow during the entire period of treatment.

The use of HMG-CoA reductase inhibitors to lower blood lipids can lead to a change in biochemical parameters that reflect liver function. Liver function should be monitored before starting therapy, 6 weeks, 12 weeks after starting atorvastatin and after each dose increase, and periodically, for example, every 6 months. An increase in the activity of “liver” enzymes in the blood serum can be observed during therapy with Atorvastatin. Patients with an increase in enzyme levels should be monitored until the enzyme levels return to normal. In the event that the values ​​of alanine aminotransferase (ALT) or aspartic aminotransferase (AST) are more than 3 times the level of the upper acceptable limit, it is recommended to reduce the dose of Atorvastatin or stop 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 unknown origin serve as contraindications to the appointment of Atorvastatin.

Treatment with atorvastatin may cause myopathy. The diagnosis of myopathy (muscle pain and weakness in combination with an increase in the activity of creatine phosphokinase (CPK) by more than 10 times compared with the upper limit of the norm) should be discussed in patients with common myalgia, pain or muscle weakness and / or a marked increase in CPK activity. 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 malaise or fever. Atorvastatin therapy should be discontinued if there is a marked 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 3A4 and / or drug transport. Atorvastatin is biotransformed under the influence of CYP 3A4. When prescribing atorvastatin in combination with fibrates, erythromycin, immunosuppressive drugs, azole antifungal agents or nicotinic acid in hypolipidemic doses, the expected benefit and risk of treatment should be carefully weighed and patients should be regularly observed to detect muscle pain or weakness, 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 control does not prevent the development of severe myopathy.

When using Atorvastatin, as well as other drugs of this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria are described. Atorvastatin therapy should be temporarily discontinued or completely discontinued if there are signs of a possible myopathy or a risk factor for the development of renal failure due to rhabdomyolysis (for example, severe acute infection, arterial hypotension, serious surgery, trauma, severe metabolic, endocrine and electrolyte disturbances and uncontrolled seizures).

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

Patients should be warned that they should immediately consult a doctor if unexplained muscle pain or weakness occurs, especially if they are accompanied by malaise or fever.

Influence on ability to drive a car and work with mechanisms

No adverse effects of Atorvastatin on ability to drive a car and work with mechanisms were reported.

Composition

dosage of 10 mg of active substance: atorvastatin calcium in terms of atorvastatin - 10 mg

excipients (core): lactose monohydrate (milk sugar) - 62.0 mg calcium carbonate - 33.0 mg povidone K 30 (polyvinylpyrrolidone average ) - 6, 0 mg croscarmellose sodium (primellose) - 6.75 mg sodium stearyl fumarate - 1.5 mg silicon colloidal dioxide (aerosil) - 0.75 mg microcrystalline cellulose - 30.0 mg

excipients (coating):

Opadry II (polyvinyl alcohol partially hydrolyzed - 2.2 mg macrogol (polyethylene glycol) 3350 - 0.6175 mg talc - 1.0 mg titanium dioxide E 171 - 0.9585 mg soy lecithin E 322 - 0.175 mg aluminum varnish based on the dye indigo carmine - 0.003 mg aluminum dye-based varnish azorubin - 0.0255 mg dye-based aluminum varnish crimson [Ponceau 4R] - 0.0205 mg).

Tablets, film-coated, pink, round, biconvex. In a cross section, the tablet core is white or almost white.

Dosage and Administration

Inside.

Take at any time of the day, regardless of food intake. Before starting treatment with Atorvastatin-SZ, you should try to achieve control of hypercholesterolemia using diet, exercise and weight loss in patients with obesity, as well as therapy for the underlying disease.

When prescribing the drug, the patient should recommend a standard hypocholesterolemic diet, which he must adhere to during the entire period of therapy.

The dose of the drug varies from 10 mg to 80 mg once a day and is titrated taking into account the initial concentration of LDL-C, the purpose of the therapy and the individual effect on the therapy. The maximum daily dose for a single dose is 80 mg. At the beginning of treatment and / or during an increase in the dose of Atorvastatin-SZ, it is necessary to monitor the concentration of lipids in the blood plasma every 2 to 4 weeks and adjust the dose of the drug accordingly.

Primary hypercholesterolemia and combined (mixed) hyperlipidemia

For most patients - 10 mg once a day, the therapeutic effect is manifested for 2 weeks and usually reaches a maximum within 4 weeks. With prolonged treatment, the effect persists.

Homozygous familial hypercholesterolemia

The initial dose is selected individually depending on the severity of the disease. In most cases, the optimal effect is observed when using the drug in a dose of 80 mg once a day (a decrease in the concentration of LDL-C by 18 - 45%).

Insufficiency of liver function

Caution is necessary in case of insufficiency of liver function (due to the slowing down of elimination of the drug from the body). Clinical and laboratory parameters should be carefully monitored (regular monitoring of the activity of “liver” transaminases: aspartate aminotransferase (AST) and alanine aminotransferase (ALT)). With a significant increase in hepatic transaminases, the dose of Atorvastatin-SZ should be reduced or treatment should be discontinued.

Insufficiency of renal function

Impaired renal function does not affect the concentration of atorvastatin in the blood plasma or the degree of decrease in the concentration of LDL-C during treatment with Atorvastatin-SZ, therefore, dose adjustment is not required. Elderly patients There were no differences in the efficacy, safety, or therapeutic effect of Atorvastatin-SZ in elderly patients compared with the general population and dose adjustment is not required (see the Pharmacokinetics section).

Use in combination with other medicines

If necessary, simultaneous use with cyclosporine, telaprevir or a combination of tipranavir / ritonavir, the dose of the drug Atorvastatin-SZ should not exceed 10 mg / day. Caution should be exercised and the lowest effective dose of atorvastatin should be used while it is used with HIV protease inhibitors, hepatitis C inhibitors, clarithromycin and itraconazole. (see the section "Special Instructions").

Side effects of

From the nervous system - more often 2% - insomnia, dizziness less than 2% - headache, asthenia, malaise, drowsiness, nightmares, paresthesia, peripheral neuropathy, amnesia, emotional lability, ataxia, paralysis, paralysis , migraine, depression, hypesthesia, loss of consciousness.

On the part of the sensory organs: less than 2% - amblyopia, ringing in the ears, dryness of the conjunctiva, disturbed accommodation, hemorrhage in the retina, deafness, glaucoma, parosmia, loss of taste, perversion of taste.

From the side of the cardiovascular system: more often 2% - chest pain less than 2% - palpitations, vasodilation symptoms, orthostatic hypotension, increased blood pressure, phlebitis, arrhythmia, angina pectoris.

From the hemopoietic system: less than 2% - anemia, lymphadenopathy, thrombocytopenia.

From the respiratory system: more than 2% - bronchitis, rhinitis less often 2% - pneumonia, dyspnea, exacerbation of bronchial asthma, nosebleeds.

From the digestive system: more often 2% - nausea less than 2% - heartburn, constipation or diarrhea, flatulence, gastralgia, abdominal pain, decreased or increased appetite, dry mouth, belching, dysphagia, vomiting, stomatitis, esophagitis, glossitis, erosive and ulcerative lesions of the oral mucosa, gastroenteritis, hepatitis, biliary colic, cheilitis, duodenal ulcer, pancreatitis, cholestatic jaundice, impaired liver function, rectal bleeding, melena, bleeding gums, tenesmus.

From the side of the musculoskeletal system: more often 2% - arthritis less often 2% - leg muscle cramps, bursitis, tendosynovitis, myositis, myopathy, arthralgia, myalgia, rhabdomyolysis, torticollis, muscle hypertonicity, joint contractures.

From the genitourinary system: more than 2% - urogenital infections, peripheral edema, less than 2% - dysuria (including pollakiuria, nocturia, urinary incontinence or urinary retention, imperative urination), nephritis, hematuria, vaginal bleeding, nephrosis , metrorrhagia, epididymitis, decreased libido, impotence, impaired ejaculation.

From the skin: more than 2% - alopecia, xeroderma, increased sweating, eczema, seborrhea, ecchymosis, petechiae.

Allergic reactions: less than 2% - itchy skin, rash, contact dermatitis, rarely - urticaria, angioedema, facial edema, photosensitivity, anaphylaxis, erythema multiforme exudative (including Stevens-Johnson syndrome), toxic epidermal necrolysis (Lyell's syndrome).

Laboratory indicators: less than 2% - hyperglycemia, hypoglycemia, increased serum CPK, albuminuria.

Other: less than 2% - weight gain, gynecomastia, mastodynia, exacerbation of gout.

Overdose

In case of an overdose, the following general measures are necessary: ​​monitoring and maintaining the vital functions of the body, as well as preventing further absorption of the drug (gastric lavage, intake of activated charcoal or laxatives). With the development of myopathy, followed by rhabdomyolysis and acute renal failure (a rare but severe side effect), the drug must be immediately canceled and the infusion of diuretic and sodium bicarbonate started. If necessary, hemodialysis should be performed. Rhabdomyolysis can lead to hyperkalemia, which requires intravenous administration of a solution of calcium chloride or a solution of calcium gluconate, infusion of a 5% solution of dextrose (glucose) with insulin, and the use of potassium-exchange resins. Since the drug actively binds to plasma proteins, hemodialysis is ineffective.

Storage conditions

In a dry, dark place at a temperature of no higher than 25 РC. Keep out of the reach of children.

The Expiration of

is 3 years. Do not use after the expiry date stated on the packaging.

Deystvuyuschee substances

Atorvastatin

Form of Treatment

tablets

Appointment

for Adults on purpose doctor

Indications

prevention of heart attacks and strokes, atherosclerosis

Possible product names

Atorvastatin-SZ tablets coated. 10 mg 60 pcs.

Northern Star, Russia

Submit your review to Earn 10 Reward Points click here to login

Write Your Own Review
You're reviewing:Atorvastatin | Atorvastatin-SZ tablets are covered.pl.ob. 10 mg 60 pcs. pack

 Job in company (10-20 minutes a day | 400 - 1200 USD)! 

We are looking for partners!

 If you have PayPal and you are ready to earn in our team - contact us: [email protected] 

Copyright © 2011-2024 Buy-Pharm, Inc. All rights reserved.