Expiration date: 12/2026
The composition and form of issue:
Tablets, film-coated. 1 tablet contains:
atorvastatin (calcium salt) 10, 20 or 40 mg
auxiliary substances: magnesium oxide heavy microcrystalline lactose monohydrate croscarmellose sodium hydroxypropyl cellulose LH21 nizkosoleva silicon dioxide colloidal magnesium stearate
the composition of the shell:: hypromellose 2910/5 macrogol 6000 titanium dioxide talc
in a contour acheikova packing 10 PCs in a package of aluminum foil 1 package or bundle in a cardboard 3 or 9 packs or in dark glass bottles of 30 or 90 PCs. in cardboard pack 1 bottle.
Feature:
Selective competitive inhibitor of HMG-COA reductase is the primary enzyme, converting 3-hydroxy-3-methylglutaryl-coenzyme a in mevalonova acid — a precursor of steroids including cholesterol.
Pharmacokinetics:
Suction
After intake of atorvastatin is rapidly absorbed from the gastrointestinal tract. Cmax in plasma achieved through 1-2 h. absorption and concentration of atorvastatin in plasma increased in proportion to dose.
The bioavailability of tablets of atorvastatin compared to solution — 95 -99%.
The absolute bioavailability is about 14%, system bioavailability and inhibiting activity for HMG-COA reductase is about 30%.
Low systemic bioavailability explain to presystemic clearance in gastrointestinal mucosa and/or metabolism when "first pass" through the liver.
Although food decreases the rate and extent of absorption by approximately 25 and 9%, respectively (as evidenced by the results of determination of C Max and AUC values); however, cholesterol Cholesterol-LDL cholesterol while taking atorvastatin on an empty stomach and during the meal is reduced to the same extent. After administration of atorvastatin in the evening, the levels in plasma are lower (Cmax and AUC by about 30%) than after intake in the morning. However, the degree of reduction in Cholesterol-LDL is not dependent on time of drug intake during the day.
Distribution
The average volume of distribution is approximately 381 L. Linking blood plasma proteins — 98%. The ratio of the levels of atorvastatin in erythrocyte/plasma is about 0.25, which indicates slight penetration of atorvastatin in the erythrocytes.
Metabolism
Atorvastatin is extensively metabolized with the formation of ortho - and parahydroxylated derivatives and various products of beta-oxidation. In vitro inhibitory effect of ortho - and parahydroxylated metabolites for HMG-COA reductase comparable to that of atorvastatin. The inhibitory activity against HMG-COA reductase in plasma about 70% due to active metabolites. In vitro studies suggest the importance of atorvastatin metabolism by the action of CYP3A4 in the liver. This is confirmed by the increasing concentrations of atorvastatin in human plasma while taking erythromycin, which is an inhibitor of this isoenzyme. In vitro studies also showed that atorvastatin is a weak inhibitor of CYP3A4.
In animals, orthohydroxy-metabolite undergoes further glucuronidation.
Excretion
Atorvastatin and its metabolites are excreted primarily in bile following hepatic and/or extrahepatic metabolism of atorvastatin, however, not appear to undergo enterohepatic recirculation. T1/2 is about 14 h, however, T1/2 active metabolites determining inhibitory activity against HMG-COA reductase is 20 to 30 h After ingestion in the urine detected less than 2% of the dose.
Pharmacokinetics in special clinical cases
The concentration of atorvastatin in plasma in the elderly (over 65 years) is higher (Cmax approximately 40%, AUC by approximately 30%) than in adult patients younger. However, differences in safety, effectiveness, or achieving lipid-lowering therapy in elderly patients compared to the General population is not detected.
Studies of the pharmacokinetics of the drug in children have not been conducted.
The concentration of atorvastatin in plasma in women is different (Cmax about 20% higher, a AUC on 10% below) the concentration in men. However, clinically significant difference influence of the drug on lipid metabolism in men and women is not revealed.
Kidney disease do not influence the concentration of atorvastatin in plasma or lipid metabolism. In this regard, a dosage adjustment in patients with impaired renal function is not required.
Although research in patients with end-stage kidney disease have not been conducted, hemodialysis is unlikely to significantly enhance clearance of atorvastatin since it is actively bound to plasma proteins.
The concentration of atorvastatin significantly increased (Cmax and AUC approximately 16 and 11 times respectively) in patients with alcoholic cirrhosis of the liver (class B on a scale child-Pugh).
Description pharmacological action:
In the liver triglycerides and Cholesterol are incorporated into VLDL, come in blood plasma and transported in peripheral tissues. Formed from VLDL LDL, which metaboliziruetsa when interacting with high-affinity LDL receptors. Atorvastatin reduces levels of Cholesterol and lipoproteins in plasma blood by inhibiting HMG-COA reductase in the liver, increasing the number of LDL receptors in the liver on the surface of cells that leads to increased grip and catabolism of Cholesterol-LDL.
Atorvastatin reduces the formation of Cholesterol-LDL and the number of particles of LDL. The drug causes a marked and persistent increase in activity of LDL-receptors and also has a beneficial effect on the quality of circulating LDL. Atorvastatin effectively reduces the level of Cholesterol-LDL in patients with homozygous hypercholesterolemia, which is usually not amenable to therapy with other lipid means.
In the study-dependence was the effect of atorvastatin was discovered that the drug (at a dose of 10-80 mg) reduced total Cholesterol (on 30-46%), Cholesterol-LDL (on 41-61%), apolipoprotein b (by 34-50%) and triglycerides (by 14-33%). The results of treatment were similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia (including patients with insulin-independent diabetes mellitus). Atorvastatin reduces levels of total Cholesterol, Cholesterol-LDL, XC-VLDL, apolipoprotein b, TG and Cholesterol, which is not part of HDL, and increases the level of HDL-C in patients with isolated hypertriglyceridemia. Atorvastatin lowers the level of cholesterol of lipoproteins of intermediate density (XC-LPPP) in patients with dysbetalipoproteinemia. Like LDL, lipoproteins containing TG (including VLDL, and their remnants LPPP), also accelerate the development of atherosclerosis. Increase the level of triglycerides in blood plasma are often found in combination with a reduction in HDL-C and the presence of LDL particles of small size, as well as in combination with lipidnami metabolic risk factors for coronary artery disease. It is not proven that raising the General level of TG in plasma is an independent risk factor for CHD. Also not proven that the increase in the level of HDL-C or reduce TG by itself affects the risk of coronary and other cardiovascular complications and mortality of patients.
Atorvastatin and some of its metabolites are pharmacologically active. The primary target organ for the action of atorvastatin is the liver, where the cholesterol synthesis and clearance of LDL.
Dynamics of the level of CH-LDL is better correlated with the dose of atorvastatin than with its concentration in the blood plasma. The dose of the drug should be selected taking into account the therapeutic effect.
Dosage:
Release form, composition and packaging
Tablets, film-coated from white to almost white, oval, biconvex.
1 tablet contains:
atorvastatin (calcium salt) 10, 20 or 40 mg
Other ingredients: magnesium oxide heavy, cellulose microcrystalline, lactose monohydrate, croscarmellose sodium, hydroxypropyl cellulose LH21 nizkosoleva, silica colloidal anhydrous, magnesium stearate.
The composition of the shell: hypromellose 2910/5, macrogol 6000, titanium dioxide, talc.
10 PCs. - blisters (3) - packs cardboard.
10 PCs. - blisters (3) - foil sachets (1) - packs of cardboard.
10 PCs. - blisters (9) - packs of cardboard.
10 PCs. - blisters (9) - foil sachets (1) - packs of cardboard.
30 PCs. - vials dark glass (1) - packs of cardboard.
90 PCs. - vials dark glass (1) - packs of cardboard.
Pharmacological action
Hypolipidemic drug. Selective competitive inhibitor of HMG-COA reductase is the primary enzyme, converting 3-hydroxy-3-methylglutaryl-coenzyme a in mevalonova acid — a precursor of steroids including cholesterol. In the liver triglycerides and cholesterol are incorporated into VLDL, come in blood plasma and transported in peripheral tissues. Formed from VLDL LDL, which metaboliziruetsa when interacting with high-affinity LDL receptors. Atorvastatin reduces levels of cholesterol (TC) and lipoprotein in plasma, ingibiruya g-Koa-reductase in the liver and by increasing the number of LDL receptors in the liver on the surface of cells that leads to increased grip and catabolism of Cholesterol-LDL.
Atorvastatin reduces the formation of Cholesterol-LDL and the number of particles of LDL. The drug causes a marked and persistent increase in activity of LDL receptors, and also has a beneficial effect on the quality of circulating LDL. Atorvastatin effectively reduces the level of Cholesterol-LDL in patients with homozygous hypercholesterolemia, which is usually not amenable to therapy with other lipid means.
In the study-dependence was the effect of atorvastatin has been shown that the drug (at a dose of 10-80 mg) reduced total Cholesterol (on 30-46%), Cholesterol-LDL (41 - 61%), apolipoprotein b (by 34-50%) and triglycerides (by 14-33%). The results of treatment were similar in patients with heterozygous familial hypercholesterolemia, non-familial forms of hypercholesterolemia and mixed hyperlipidemia (including patients with insulin-dependent diabetes mellitus). Atorvastatin reduces levels of total Cholesterol, Cholesterol-LDL, XC-VLDL, apolipoprotein b, triglycerides, and Cholesterol, which is not part of HDL, and increases the level of HDL-C in patients with isolated hypertriglyceridemia. Atorvastatin lowers the level of cholesterol of lipoproteins of intermediate density (XC-LPPP) in patients with dysbetalipoproteinemia. Like LDL, lipoproteins, containing triglycerides (i.e. VLDL, and their remnants LPPP) also accelerate the development of atherosclerosis. The elevation of triglycerides in blood plasma are often found in combination with a reduction in HDL-C and the presence of LDL particles of small size, as well as in combination with lipidnami metabolic risk factors for coronary artery disease. It is not proven that raising the General level of triglycerides in plasma is an independent risk factor for CHD. Also not proven that the increase in the level of HDL-C or reducing triglycerides, in itself, affects the risk of coronary and other cardiovascular complications and mortality of patients.
Atorvastatin and some of its metabolites are pharmacologically active. The primary target organ for the action of atorvastatin is the liver, where the cholesterol synthesis and clearance of LDL.
Dynamics of the level of CH-LDL is better correlated with the dose of atorvastatin than with its concentration in the blood plasma. The dose of the drug should be selected taking into account the therapeutic effect.
Pharmacokinetics
Suction
After intake of atorvastatin is rapidly absorbed from the gastrointestinal tract. Cmax in plasma achieved through 1-2 h. absorption and concentration of atorvastatin in plasma increased in proportion to dose.
The bioavailability of tablets of atorvastatin compared to the solution is 95-99%.
The absolute bioavailability is approximately 14%, system bioavailability and inhibiting activity for HMG-COA reductase is about 30%.
Low systemic bioavailability explain to presystemic clearance in gastrointestinal mucosa and/or metabolism at the first passage through the liver.
Although food decreases the rate and extent of absorption by approximately 25% and 9% respectively (as evidenced by the results of determination of Cmax and AUC values), but the level of Cholesterol-LDL cholesterol while taking atorvastatin on an empty stomach and during the meal is reduced to the same extent. After administration of atorvastatin in the evening, the levels in plasma are lower (Cmax and AUC by about 30%) than after intake in the morning. However, the degree of reduction in Cholesterol-LDL is not dependent on time of drug intake during the day.
Distribution
Average Vd is approximately 381 L. Linking blood plasma proteins - 98%. The ratio of the levels of atorvastatin in erythrocyte/plasma is about 0.25, which indicates low permeability of atorvastatin in the erythrocytes.
Metabolism
Atorvastatin is extensively metabolized with the formation of ortho - and parahydroxylated derivatives and various products of beta-oxidation. In vitro inhibitory effect of ortho - and parahydroxylated metabolites for HMG-COA reductase comparable to that of atorvastatin. The inhibitory activity against HMG-COA reductase in plasma about 70% due to active metabolites. In vitro studies suggest the importance of atorvastatin metabolism by the action of CYP3A4 in the liver is evidenced by the increase in concentrations of atorvastatin in human plasma while taking erythromycin, which is an inhibitor of this isoenzyme. In vitro studies also showed that atorvastatin is a weak inhibitor of CYP3A4.
In animals, orthohydroxy - metabolite undergoes further glucuronidation.
Excretion
Atorvastatin and its metabolites are excreted primarily in bile following hepatic and/or extrahepatic metabolism of atorvastatin, however, not appear to undergo enterohepatic recirculation. T1/2 is about 14 h, however, the T 1/2 of active metabolites determining inhibitory activity against HMG-COA reductase is 20 to 30 h After ingestion in the urine less than 2% of the dose.
Pharmacokinetics in special clinical cases
The concentration of atorvastatin in plasma in the elderly (over 65 years) is higher (Cmax approximately 40%, AUC by approximately 30%) than in adult patients younger. However, differences in safety, effectiveness, or achieving lipid-lowering therapy in elderly patients compared to the General population is not detected.
Studies of the pharmacokinetics of the drug in children have not been conducted.
The concentration of atorvastatin in plasma in women is different (Cmax about 20% higher, a AUC on 10% below) the concentration in men. However, clinically significant difference influence of the drug on lipid metabolism in men and women is not revealed.
Kidney disease do not influence the concentration of atorvastatin in plasma or its effect on lipid metabolism. In this regard, a dosage adjustment in patients with impaired renal function is not required.
Although research in patients with end-stage kidney disease have not been conducted, however, hemodialysis is unlikely to significantly enhance clearance of atorvastatin since it is actively bound to plasma proteins.
The concentration of atorvastatin significantly increased (Cmax and AUC approximately 16 and 11 times respectively) in patients with alcoholic cirrhosis of the liver (class B on a scale child-Pugh).
Testimony
- in combination with diet to reduce elevated levels of total Cholesterol, Cholesterol-LDL, apolipoprotein b and triglycerides and increase the level of HDL - C in patients with primary hypercholesterolemia, heterozygous familial and non-family hypercholesterolemia and combined (mixed) hyperlipidemia (types IIa and IIb according to Frederickson)
- in combination with diet for the treatment of patients with elevated serum triglyceride levels (type IV according to Fredrickson) and patients with dysbetalipoproteinemia (type III Fredrickson), whose diet does not give adequate effect
- to reduce the levels of total Cholesterol and Cholesterol-LDL in patients with homozygous familial hypercholesterolemia, when diet and other nonpharmacologic therapies are not effective enough.
The dosage regimen
Before the appointment Torvacard patient must recommend a standard hypolipidemic diet, he must continue to observe during the whole period of therapy.
The initial dose is an average of 10 mg 1 times/day. Dose ranges from 10 to 80 mg 1 times/day. The drug can be taken anytime of day with food or regardless of mealtime. The dose is selected taking into account the initial levels of Cholesterol-LDL, the goal of therapy and individual effect. At the beginning of treatment and/or during increasing doses Torvacard necessary every 2-4 weeks to monitor the levels of lipids in plasma and accordingly to correct the dose.
When primary hypercholesterolemia and mixed hyperlipidemia in most cases it is enough to assign a dose of 10 mg Torvacard 1 times/day. Significant therapeutic effect is observed after 2 weeks, as a rule, the maximum therapeutic effect is usually observed after 4 weeks. With prolonged treatment, this effect persists.
When determining treatment goals you can use the following recommendations.
A. the recommendations of the National educational program on cholesterol (USA)
| Diagnosed atherosclerosis* | The presence of 2 or more risk factors** | Cholesterol-LDL, mg/DL (mmol/l) | ||
|---|---|---|---|---|
| The initial level | The minimum target level | |||
| no | no | >=190 (>=4.9) | <160 (<4.1) | |
| no | yes | >=160 (>=4.1) | <130 (<3.4) | |
| yes | yes or no | >=130*** (>=3.4) | <=100 (<=2.6) | |
*Coronary artery disease or peripheral atherosclerosis (including carotid arteries, accompanied by clinical symptoms).
**include: age (men >=45 years, women >=55 years or early menopause, which is not estrogen replacement therapy), early development of CHD in relatives, Smoking, hypertension, confirmed the level of HDL-C<35 mg/DL (<0.91 mmol/l) and diabetes. Subtract one risk factor if the level of HDL - C is >=60 mg/DL (>=1.6 mmol/l).
***in patients with CHD with the level of CH-LDL of 100 to 129 mg/DL, the issue of the appointment of drug therapy is decided by the doctor based on clinical experience.
B. Goals of lipid-lowering therapy of the European society of atherosclerosis
Patients with confirmed diagnosis of IHD and other patients with high risk of ischemic complications the goal of treatment is to reduce the level of Cholesterol-LDL<115 mg/DL (<3 mmol/l) and total Cholesterol<190 mg/DL (<5 mmol/l).
National recommendations for treatment
Homozygous familial hypercholesterolemia
In a study in adult patients with homozygous familial hypercholesterolemia therapy with atorvastatin 80 mg in most cases, led to lower Cholesterol levels-LDL by more than 15% (18-45%).
The use of the drug in patients with renal failure and renal disease has no influence on the level of atorvastatin in the blood plasma or the degree of reduce the content of Cholesterol-LDL in its application, so changing the dose is not required.
In applying the drug in elderly patients differences in security, efficiency, or achieving lipid-lowering therapy compared to the General population were noted.
Side effects
CNS and peripheral nervous system: headache, dizziness, asthenic syndrome, insomnia or drowsiness, nightmares, amnesia, paresthesia, peripheral neuropathy, emotional lability, ataxia, hyperkinesis, depression, hypersensitivity.
From the sensory organs: amblyopia, ringing in the ears, dryness of the conjunctiva, violation ccomodation, bleeding in the eye, deafness, increased intraocular pressure, parosmia, taste perversion, loss of taste sensations.
From the side of cardiovascular system: chest pain, palpitations, vasodilation, orthostatic hypotension, phlebitis, arrhythmia.
With the hematopoietic system: anemia, lymphadenopathy, thrombocytopenia.
The respiratory system: bronchitis, rhinitis, dyspnea, asthma, epistaxis.
From the digestive system: nausea, heartburn, constipation or diarrhea, flatulence, gastralgia, abdominal pain, anorexia or increased appetite, dry mouth, burp, dysphagia, vomiting, stomatitis, esophagitis, glossitis, gastroenteritis, hepatitis, hepatic colic, cheilitis, duodenal ulcer, pancreatitis, cholestatic jaundice, increased liver enzymes, rectal bleeding, melena, bleeding gums, tenesmus.
From the musculoskeletal: arthritis, muscle cramps feet, bursitis, myositis, myopathy, arthralgia, myalgia, rhabdomyolysis, joint contractures, pain in the back.
From the urogenital system: urogenital infections, peripheral edema, dysuria (W. pollakiuria, nocturia, incontinence or urinary retention, urgent need to urinate), nephritis, cystitis, hematuria, vaginal bleeding, uterine bleeding, urolithiasis, metrorrhagia, epididymitis, decreased libido, impotence, violation of ejaculation.
Dermatological reactions: alopecia, sweating, eczema, seborrhea, ekhimozy, photosensitivity.
Allergic reactions: skin itching, skin rash, contact dermatitis rarely urticaria, angioedema, face oedema, anaphylaxis, multiform exudative erythema, Stevens-Johnson syndrome, toxic epidermal necrolysis (Lyell's syndrome).
From the laboratory parameters: hyperglycemia, hypoglycemia, increased serum CPK, albuminuria, increased activity ACT, ALT.
Other: increased body weight, gynecomastia, aggravation of gout, fever.
Contraindications
- active liver disease or increased serum transaminases (more than 3 times compared with the upper limit of normal) of unknown origin
- pregnancy
- lactation
- child and adolescence to 18 years (efficacy and safety not established)
- hypersensitivity to the drug.
Caution should be used in chronic alcoholism, liver diseases in history, heavy violations elektrolitnogo balance, endocrine and metabolic disorders, arterial hypotension, severe acute infections (sepsis), uncontrolled epilepsy, extensive surgical interventions, injuries, diseases of skeletal muscles.
Pregnancy and lactation
Atorvastatin is contraindicated during pregnancy and lactation (breastfeeding).
Unknown, whether atorvastatin is allocated in breast milk. Given the possibility of adverse events in infants, if necessary, the use of the drug during lactation should decide the issue of termination of breastfeeding. Women of reproductive age during treatment should use adequate methods of contraception. Atorvastatin can be prescribed to women of reproductive age only if the probability of pregnancy they have very low, and the patient informed about the possible risk of treatment for the fetus.
Special instructions
Before starting therapy with Tarmacadam patient must assign default gipoholesterinovu diet which it should observe during the entire treatment period.
Inhibitors of HMG-COA reductase to reduce the level of lipids in blood may lead to changes in biochemical parameters reflecting liver function. Liver function should be monitored before therapy, after 6 weeks, 12 weeks after the start of Torvacard and after each dosage increase, and periodically (e.g. every 6 months). Increased activity of liver enzymes in the serum may occur during therapy with Torvacard. Patients who show increased levels of transaminases should be monitored prior to returning the enzyme levels to normal. In that case, if the values of ALT or AST more than 3 times the upper limit of normal (ULN), it is recommended to reduce the dose Torvacard or to stop treatment.
Torvacard should be used with caution in patients who abuse alcohol or have liver disease. Active liver disease or persistent increase in the aminotransferaz ambiguous Genesis are contraindications to the appointment Torvacard.
Treatment Torvacard can cause myopathy. In patients with widespread myalgia, tenderness or weakness of muscles and/or expressed by increased activity of KFK, keep in mind the possibility of myopathy (pain and weakness in the muscles in conjunction with increased activity of CPK more than 10 times compared with CAH). Patients should be warned that they should immediately inform the doctor about the appearance of unexplained pain or weakness in muscles, if they are accompanied by malaise or fever. Therapy Torvacard should be stopped in case of marked increase in the activity of CPK or the presence of confirmed or suspected myopathy. The risk of myopathy during treatment with other drugs in this class is increased with simultaneous use of cyclosporine, fibrates, erythromycin, nicotinic acid or azole antifungals. Many of these drugs inhibit the metabolism mediated by CYP3A4 and/or transport of drugs. Atorvastatin biotransformiroetsa under the action of CYP3A4. Assigning atorvastatin in combination with fibrates, erythromycin, immunosuppressive means, azole antifungal drugs or nicotinic acid in lipid lowering doses should carefully weigh the potential benefits and risks of treatment and regularly monitor patients to detect pain or weakness in muscles, especially during the first months of treatment and during periods of increasing doses of any drug. In such situations, it is possible to recommend periodic determination of activity of KFK, although such control cannot prevent the development of severe myopathy.
In the application of atorvastatin, like other drugs in this class, cases of rhabdomyolysis with acute renal failure due to myoglobinuria. Therapy Torvacard should temporarily stop or terminate at the appearance of signs of possible myopathy or having a risk factor for development of renal insufficiency on the background of rhabdomyolysis (e.g. severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures). Before starting therapy with Tarmacadam you should try to gain control of hypercholesterolemia through adequate diet, increasing physical activity, reducing body weight in patients with obesity and treat other conditions. Patients should be warned that they should immediately address to the doctor at occurrence of unexplained pain or weakness in muscles, particularly if accompanied by malaise or fever.
Effects on ability to drive and operate machinery
Regarding the adverse impact Torvacard on the ability to drive and work with mechanisms not reported.
Overdose
Symptoms: possible hypotension.
Treatment: symptomatic therapy. There is no specific antidote. Hemodialysis is ineffective.
Drug interactions
The risk of myopathy during treatment with other drugs in this class is increased with simultaneous use of cyclosporine, fibrates, erythromycin, antifungal agents belonging to azoles, and Niacin.
Simultaneous ingestion of atorvastatin and suspensions containing magnesium and aluminium hydroxide, decreased the concentration of plasma atorvastatin approximately 35%; however, the degree of reduction of level of Cholesterol-LDL is not changed.
With simultaneous use of atorvastatin does not affect the farmakokinetiku phenazone, therefore, interactions with other drugs metabolized by the same cytochrome isozymes are not expected.
While the application of colestipol atorvastatin concentration in plasma decreased by about 25%. However, the hypolipidemic effect of combination of atorvastatin and colestipol excelled itself each drug separately.
When re-administration of digoxin and atorvastatin dose 10 mg equilibrium concentration of digoxin in plasma were not changed. However, the application of digoxin in combination with atorvastatin 80 mg/day concentration of digoxin increased by approximately 20%. Patients, receiving digoxin combined with atorvastatin requires monitoring.
With simultaneous use of atorvastatin and erythromycin (500 mg 4 times/day) or clarithromycin (500 mg 2 times/day), which inhibit CYP3A4, there was an increase in concentrations of atorvastatin in plasma.
With simultaneous use of atorvastatin (10 mg 1 times/day) and azithromycin (500 mg 1 time/day) atorvastatin concentration in plasma did not change.
Atorvastatin had no clinically significant effect on the concentration of terfenadine in plasma, which is metabolized primarily by the CYP3A4 in this regard, it seems unlikely that atorvastatin can significantly affect the pharmacokinetic parameters of other CYP3A4 substrates.
With simultaneous use of atorvastatin and an oral contraceptive containing ethinyl estradiol and norethindrone, there was a significant increase in AUC norethindrone and ethinyl estradiol approximately 30% and 20% respectively. This effect should be considered when selecting oral contraceptive for women, receiving atorvastatin.
In the study of the interaction between atorvastatin with warfarin and cimetidine signs of clinically meaningful interaction is not detected.
With simultaneous use of atorvastatin 80 mg and amlodipine 10 mg pharmacokinetics of atorvastatin in equilibrium has not changed.
Simultaneous application of atorvastatin with protease inhibitors, known as CYP3A4 inhibitors, was accompanied by an increase in the concentration of atorvastatin in plasma.
Not clinically significant undesirable interactions atorvastatin and antigipertenziveh funds, as well as estrogens. Studies of the interaction with all the specific drugs have not been conducted.
Pharmaceutical incompatibility is unknown.
Terms and conditions storage
The drug should be stored out of reach of children at temperature of 10° to 30&°C. shelf Life - 2 years.
Conditions of supply of pharmacies
A drug dispensed by prescription.
Indications:
in combination with diet to reduce elevated levels of total Cholesterol, Cholesterol-LDL, apolipoprotein b and triglycerides and increase the level of HDL-C in patients with primary hypercholesterolemia, heterozygous familial and non-family hypercholesterolemia and combined (mixed) hyperlipidemia (types IIa and IIb according to Frederickson)
