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Lipitor (Atorvastatin)
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Pharmacology
Atorvastatin is a synthetic lipid-lowering agent. It is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzymeA (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol.
Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic low density lipoprotein (LDL) receptors on the cell-surface for enhanced uptake and catabolism of low density lipoprotein (LDL).
Atorvastatin reduces LDL-cholesterol (LDL-C) and the number of LDL particles. Atorvastatin also reduces very low density lipoprotein-cholesterol (VLDL-C), serum triglycerides (TG) and intermediate density lipoproteins (IDL), as well as the number of apolipoproteinB (apo B)-containing particles, but increases high density lipoprotein-cholesterol (HDL-C). Elevated serum cholesterol due to elevated LDL-C is a major risk factor for the development of cardiovascular disease. Elevated plasma TG is also a risk factor for cardiovascular disease, particularly if due to increased IDL, or associated with decreased HDL-C or increased LDL-C.
Pharmacokinetics: Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations occur within 1to 2hours. Atorvastatin tablets are 95 to 99% bioavailable compared to solutions.
Mean distribution of atorvastatin is approximately 381L. Atorvastatin is ³98% bound to plasma proteins. Atorvastatin is extensively metabolized by cytochrome P450 3A4 to ortho- and para-hydroxylated derivatives and to various beta-oxidation products. Approximately 70% of circulating inhibitory activity for HMG Co-A reductase is attributed to active metabolites.
Atorvastatin and its metabolites are eliminated by biliary excretion. Less than 2% of a dose of atorvastatin is recovered in urine following oral administration. Mean plasma elimination half-life of atorvastatin in humans is approximately 14hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20to 30hours due to the contribution of longer-lived active metabolites.
Atorvastatin is a synthetic lipid-lowering agent. It is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzymeA (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol.
Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic low density lipoprotein (LDL) receptors on the cell-surface for enhanced uptake and catabolism of low density lipoprotein (LDL).
Atorvastatin reduces LDL-cholesterol (LDL-C) and the number of LDL particles. Atorvastatin also reduces very low density lipoprotein-cholesterol (VLDL-C), serum triglycerides (TG) and intermediate density lipoproteins (IDL), as well as the number of apolipoproteinB (apo B)-containing particles, but increases high density lipoprotein-cholesterol (HDL-C). Elevated serum cholesterol due to elevated LDL-C is a major risk factor for the development of cardiovascular disease. Elevated plasma TG is also a risk factor for cardiovascular disease, particularly if due to increased IDL, or associated with decreased HDL-C or increased LDL-C.
Pharmacokinetics: Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations occur within 1to 2hours. Atorvastatin tablets are 95 to 99% bioavailable compared to solutions.
Mean distribution of atorvastatin is approximately 381L. Atorvastatin is ³98% bound to plasma proteins. Atorvastatin is extensively metabolized by cytochrome P450 3A4 to ortho- and para-hydroxylated derivatives and to various beta-oxidation products. Approximately 70% of circulating inhibitory activity for HMG Co-A reductase is attributed to active metabolites.
Atorvastatin and its metabolites are eliminated by biliary excretion. Less than 2% of a dose of atorvastatin is recovered in urine following oral administration. Mean plasma elimination half-life of atorvastatin in humans is approximately 14hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20to 30hours due to the contribution of longer-lived active metabolites.
Indications
Atorvastatin Is A Synthetic Lipid-lowering Agent. It Is A Selective, Competitive Inhibitor Of 3-hydroxy-3-methylglutaryl-coenzymeA (HMG-CoA) Reductase. This Enzyme Catalyzes The Conversion Of HMG-CoA To Mevalonate, Which Is An Early And Rate-limiting Step In The Biosynthesis Of Cholesterol.
Atorvastatin Lowers Plasma Cholesterol And Lipoprotein Levels By Inhibiting HMG-CoA Reductase And Cholesterol Synthesis In The Liver And By Increasing The Number Of Hepatic Low Density Lipoprotein (LDL) Receptors On The Cell-surface For Enhanced Uptake And Catabolism Of Low Density Lipoprotein (LDL).
Atorvastatin Reduces LDL-cholesterol (LDL-C) And The Number Of LDL Particles. Atorvastatin Also Reduces Very Low Density Lipoprotein-cholesterol (VLDL-C), Serum Triglycerides (TG) And Intermediate Density Lipoproteins (IDL), As Well As The Number Of ApolipoproteinB (apo B)-containing Particles, But Increases High Density Lipoprotein-cholesterol (HDL-C). Elevated Serum Cholesterol Due To Elevated LDL-C Is A Major Risk Factor For The Development Of Cardiovascular Disease. Elevated Plasma TG Is Also A Risk Factor For Cardiovascular Disease, Particularly If Due To Increased IDL, Or Associated With Decreased HDL-C Or Increased LDL-C.
Pharmacokinetics: Atorvastatin Is Rapidly Absorbed After Oral Administration; Maximum Plasma Concentrations Occur Within 1to 2hours. Atorvastatin Tablets Are 95 To 99% Bioavailable Compared To Solutions.
Mean Distribution Of Atorvastatin Is Approximately 381L. Atorvastatin Is ³98% Bound To Plasma Proteins. Atorvastatin Is Extensively Metabolized By Cytochrome P450 3A4 To Ortho- And Para-hydroxylated Derivatives And To Various Beta-oxidation Products. Approximately 70% Of Circulating Inhibitory Activity For HMG Co-A Reductase Is Attributed To Active Metabolites.
Atorvastatin And Its Metabolites Are Eliminated By Biliary Excretion. Less Than 2% Of A Dose Of Atorvastatin Is Recovered In Urine Following Oral Administration. Mean Plasma Elimination Half-life Of Atorvastatin In Humans Is Approximately 14hours, But The Half-life Of Inhibitory Activity For HMG-CoA Reductase Is 20to 30hours Due To The Contribution Of Longer-lived Active Metabolites.
Atorvastatin Is A Synthetic Lipid-lowering Agent. It Is A Selective, Competitive Inhibitor Of 3-hydroxy-3-methylglutaryl-coenzymeA (HMG-CoA) Reductase. This Enzyme Catalyzes The Conversion Of HMG-CoA To Mevalonate, Which Is An Early And Rate-limiting Step In The Biosynthesis Of Cholesterol.
Atorvastatin Lowers Plasma Cholesterol And Lipoprotein Levels By Inhibiting HMG-CoA Reductase And Cholesterol Synthesis In The Liver And By Increasing The Number Of Hepatic Low Density Lipoprotein (LDL) Receptors On The Cell-surface For Enhanced Uptake And Catabolism Of Low Density Lipoprotein (LDL).
Atorvastatin Reduces LDL-cholesterol (LDL-C) And The Number Of LDL Particles. Atorvastatin Also Reduces Very Low Density Lipoprotein-cholesterol (VLDL-C), Serum Triglycerides (TG) And Intermediate Density Lipoproteins (IDL), As Well As The Number Of ApolipoproteinB (apo B)-containing Particles, But Increases High Density Lipoprotein-cholesterol (HDL-C). Elevated Serum Cholesterol Due To Elevated LDL-C Is A Major Risk Factor For The Development Of Cardiovascular Disease. Elevated Plasma TG Is Also A Risk Factor For Cardiovascular Disease, Particularly If Due To Increased IDL, Or Associated With Decreased HDL-C Or Increased LDL-C.
Pharmacokinetics: Atorvastatin Is Rapidly Absorbed After Oral Administration; Maximum Plasma Concentrations Occur Within 1to 2hours. Atorvastatin Tablets Are 95 To 99% Bioavailable Compared To Solutions.
Mean Distribution Of Atorvastatin Is Approximately 381L. Atorvastatin Is ³98% Bound To Plasma Proteins. Atorvastatin Is Extensively Metabolized By Cytochrome P450 3A4 To Ortho- And Para-hydroxylated Derivatives And To Various Beta-oxidation Products. Approximately 70% Of Circulating Inhibitory Activity For HMG Co-A Reductase Is Attributed To Active Metabolites.
Atorvastatin And Its Metabolites Are Eliminated By Biliary Excretion. Less Than 2% Of A Dose Of Atorvastatin Is Recovered In Urine Following Oral Administration. Mean Plasma Elimination Half-life Of Atorvastatin In Humans Is Approximately 14hours, But The Half-life Of Inhibitory Activity For HMG-CoA Reductase Is 20to 30hours Due To The Contribution Of Longer-lived Active Metabolites.
Contraindications
Hypersensitivity to any component of this medication. Active liver disease or unexplained persistent elevations of serum transaminases exceeding 3times the upper limit of normal.
Hypersensitivity to any component of this medication. Active liver disease or unexplained persistent elevations of serum transaminases exceeding 3times the upper limit of normal.
Safety Information / Warning
Pharmacokinetic Interactions : The use of HMG-CoA reductase inhibitors has been associated with severe myopathy, including rhabdomyolysis, which may be more frequent when they are coadministered with drugs that inhibit the cytochrome P450 enzyme system. Atorvastatin is metabolized by cytochrome P450 isoform 3A4 and as such may interact with agents that inhibit this enzyme (see Warnings, Muscle Effects and Precautions, Drug Interactions and Cytochrome P450-mediated Interactions).
Hepatic Effects: In clinical trials, persistent increases in serum transaminases greater than 3times the upper limit of normal occurred in <1% of patients who received atorvastatin. When the dosage of atorvastatin was reduced, or when drug treatment was interrupted or discontinued, serum transaminase levels returned to pretreatment levels. The increases were generally not associated with jaundice or other clinical signs or symptoms. Most patients continued treatment with a reduced dose of atorvastatin without clinical sequelae.
Liver function tests should be performed before the initiation of treatment, and periodically thereafter. Special attention should be paid to patients who develop elevated serum transaminase levels, and in these patients measurements should be repeated promptly and then performed more frequently.
If increases in ALT or AST show evidence of progression, particularly if they rise to greater than 3times the upper limit of normal and are persistent, the dosage should be reduced or the drug discontinued.
Atorvastatin should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease. Active liver disease or unexplained transaminase elevations are contraindications to the use of atorvastatin; if such a condition should develop during therapy, the drug should be discontinued.
Muscle Effects: Myopathy, defined as muscle aching or muscle weakness in conjunction with increases in creatinine phosphokinase (CPK) values to greater than 10times the upper limit of normal, should be considered in any patient with diffuse myalgia, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Atorvastatin therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected.
The risk of myopathy and rhabdomyolysis during treatment with HMG-CoA reductase inhibitors is increased with concurrent administration of cyclosporine, fibric acid derivatives, erythromycin, clarithromycin, niacin (nicotinic acid), azole antifungals or nefazodone. As there is no experience to date with the use of atorvastatin given concurrently with these drugs, with the exception of pharmacokinetic studies conducted in healthy subjects with erythromycin and clarithromycin, the benefits and risks of such combined therapy should be carefully considered (see Precautions, Pharmacokinetic Interaction Studies and Potential Drug Interactions).
Rhabdomyolysis has been reported in very rare cases with atorvastatin (see Precautions, Drug Interactions).
Rhabdomyolysis with renal dysfunction secondary to myoglobinuria has also been reported with HMG-CoA reductase inhibitors. Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (such as severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).
Pharmacokinetic Interactions : The use of HMG-CoA reductase inhibitors has been associated with severe myopathy, including rhabdomyolysis, which may be more frequent when they are coadministered with drugs that inhibit the cytochrome P450 enzyme system. Atorvastatin is metabolized by cytochrome P450 isoform 3A4 and as such may interact with agents that inhibit this enzyme (see Warnings, Muscle Effects and Precautions, Drug Interactions and Cytochrome P450-mediated Interactions).
Hepatic Effects: In clinical trials, persistent increases in serum transaminases greater than 3times the upper limit of normal occurred in <1% of patients who received atorvastatin. When the dosage of atorvastatin was reduced, or when drug treatment was interrupted or discontinued, serum transaminase levels returned to pretreatment levels. The increases were generally not associated with jaundice or other clinical signs or symptoms. Most patients continued treatment with a reduced dose of atorvastatin without clinical sequelae.
Liver function tests should be performed before the initiation of treatment, and periodically thereafter. Special attention should be paid to patients who develop elevated serum transaminase levels, and in these patients measurements should be repeated promptly and then performed more frequently.
If increases in ALT or AST show evidence of progression, particularly if they rise to greater than 3times the upper limit of normal and are persistent, the dosage should be reduced or the drug discontinued.
Atorvastatin should be used with caution in patients who consume substantial quantities of alcohol and/or have a past history of liver disease. Active liver disease or unexplained transaminase elevations are contraindications to the use of atorvastatin; if such a condition should develop during therapy, the drug should be discontinued.
Muscle Effects: Myopathy, defined as muscle aching or muscle weakness in conjunction with increases in creatinine phosphokinase (CPK) values to greater than 10times the upper limit of normal, should be considered in any patient with diffuse myalgia, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Atorvastatin therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected.
The risk of myopathy and rhabdomyolysis during treatment with HMG-CoA reductase inhibitors is increased with concurrent administration of cyclosporine, fibric acid derivatives, erythromycin, clarithromycin, niacin (nicotinic acid), azole antifungals or nefazodone. As there is no experience to date with the use of atorvastatin given concurrently with these drugs, with the exception of pharmacokinetic studies conducted in healthy subjects with erythromycin and clarithromycin, the benefits and risks of such combined therapy should be carefully considered (see Precautions, Pharmacokinetic Interaction Studies and Potential Drug Interactions).
Rhabdomyolysis has been reported in very rare cases with atorvastatin (see Precautions, Drug Interactions).
Rhabdomyolysis with renal dysfunction secondary to myoglobinuria has also been reported with HMG-CoA reductase inhibitors. Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (such as severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).
Precautions
General: The effects of atorvastatin-induced changes in lipoprotein levels, including reduction of serum cholesterol on cardiovascular morbidity or mortality or total mortality have not been established.
Before instituting therapy with atorvastatin, an attempt should be made to control elevated serum lipoprotein levels with appropriate diet, exercise, and weight reduction in overweight patients, and to treat other underlying medical problems (see Indications). Patients should be advised to inform subsequent physicians of the prior use of atorvastatin or any other lipid-lowering agents.
Effect on the Lens: Current long-term data from clinical trials do not indicate an adverse effect of atorvastatin on the human lens.
Effect on Ubiquinone (CoQ 10) Levels: Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure.
Effect on Lipoprotein (a): In some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by a concomitant increase in Lp(a) levels. Until further experience is obtained, it is suggested, where feasible, that measurements of serum Lp(a) be followed up in patients placed on atorvastatin therapy.
Hypersensitivity: An apparent hypersensitivity syndrome has been reported with other HMG-CoA reductase inhibitors which has included 1 or more of the following features: anaphylaxis, angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, vasculitis, purpura, thrombocytopenia, leukopenia, hemolytic anemia, positive ANA, ESR increase, eosinophilia, arthritis, arthralgia, urticaria, asthenia, photosensitivity, fever, chills, flushing, malaise, dyspnea, toxic epidermal necrolysis, erythema multiforme, including Stevens-Johnson syndrome. Although to date hypersensitivity syndrome has not been described as such, atorvastatin should be discontinued if hypersensitivity is suspected.
Pregnancy: Atorvastatin is contraindicated during pregnancy (see Contraindications).
Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause harm to the fetus when administered to pregnant women.
There are no data on the use of atorvastatin during pregnancy. Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued and the patient apprised of the potential risk to the fetus.
Lactation : In rats, milk concentrations of atorvastatin are similar to those in plasma. It is not known whether this drug is excreted in human milk. Because of the potential for adverse reactions in nursing infants, women taking atorvastatin should not breast-feed (see Contraindications).
Children: Treatment experience in a pediatric population is limited to doses of atorvastatin up to 80mg/day for 1year in 8patients with homozygous familial hypercholesterolemia. No clinical or biochemical abnormalities were reported in these patients.
Geriatrics: Treatment experience in adults 70years or older (N=221) with doses of atorvastatin up to 80mg/day has demonstrated that the safety and effectiveness of atorvastatin in this population was similar to that of patients <70years of age. Pharmacokinetic evaluation of atorvastatin in subjects over the age of 65years indicates an increased AUC. As a precautionary measure, the lowest dose should be administered initially.
Renal Insufficiency: Plasma concentrations and LDL-C lowering efficacy of atorvastatin was shown to be similar in patients with moderate renal insufficiency compared with patients with normal renal function. However, since several cases of rhabdomyolysis have been reported in patients with a history of renal insufficiency of unknown severity, as a precautionary measure and pending further experience in renal disease, the lowest dose (10mg/day) of atorvastatin should be used in these patients. Similar precautions apply in patients with severe renal insufficiency (creatinine clearance <30mL/min [<0.5 mL/s]); the lowest dosage should be used and implemented cautiously (see Warnings, Muscle Effects; Precautions, Drug Interactions).
Refer also to Dosage.
Endocrine Function: HMG-CoA reductase inhibitors interfere with cholesterol synthesis and as such might theoretically blunt adrenal and/or gonadal steroid production. Clinical studies with atorvastatin and other HMG-CoA reductase inhibitors have suggested that these agents do not reduce plasma cortisol concentration or impair adrenal reserve and do not reduce basal plasma testosterone concentration. However, the effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown.
Patients treated with atorvastatin who develop clinical evidence of endocrine dysfunction should be evaluated appropriately. Caution should be exercised if an HMG-CoA reductase inhibitor or other agent used to lower cholesterol levels is administered to patients receiving other drugs (e.g., ketoconazole, spironolactone or cimetidine) that may decrease the levels of endogenous steroid hormones.
Pharmacokinetic Interaction Studies and Potential Drug Interactions : Pharmacokinetic interaction studies conducted with drugs in healthy subjects may not detect the possibility of a potential drug interaction in some patients due to differences in underlying diseases and use of concomitant medications (see also Geriatrics; Renal Insufficiency; Patients with Severe Hypercholesterolemia).
Concomitant Therapy with Other Lipid Metabolism Regulators: Combined drug therapy should be approached with caution as information from controlled studies is limited.
Bile Acid Sequestrants: Patients With Mild to Moderate Hypercholesterolemia: LDL-C reduction was greater when atorvastatin 10mg and colestipol 20g were coadministered (-45%) than when either drug was administered alone (-35% for atorvastatin and -22% for colestipol).
Patients With Severe Hypercholesterolemia: LDL-C reduction was similar (-53%) when atorvastatin 40mg and colestipol 20g were coadministered when compared with that of atorvastatin 80mg alone. Plasma concentration of atorvastatin was lower (approximately 26%) when atorvastatin 40mg plus colestipol 20g were coadministered compared with atorvastatin 40mg alone.
However, the combination drug therapy was less effective in lowering the triglycerides than atorvastatin monotherapy in both types of hypercholesterolemic patients.
When atorvastatin is used concurrently with colestipol or any other resin, an interval of at least 2hours should be maintained between the two drugs since the absorption of atorvastatin may be impaired by the resin.
Fibric Acid Derivatives (Gemfibrozil, Fenofibrate, Bezafibrate) and Niacin (Nicotinic Acid): Although there is no experience with the use of atorvastatin given concurrently with fibric acid derivatives and niacin, the benefits and risks of such combined therapy should be carefully considered. The risk of myopathy during treatment with other drugs in this class is increased with concurrent administration (see Warnings, Muscle Effects).
Coumarin Anticoagulants: Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin therapy.
Digoxin: In healthy subjects, digoxin pharmacokinetics at steady-state were not significantly altered by coadministration of digoxin 0.25 mg and atorvastatin 10 mg daily. However, digoxin steady-state concentrations increased approximately 20% following coadministration of digoxin 0.25 mg and atorvastatin 80 mg daily. Patients taking digoxin should be monitored appropriately.
Antihypertensive Agents (amlodipine): In clinical studies, atorvastatin was used concomitantly with antihypertensive agents without evidence to date of clinically significant adverse interactions. In healthy subjects, atorvastatin pharmacokinetics were not altered by the coadministration of atorvastatin 80 mg and amlodipine 10 mg at steady-state.
(quinapril): In a randomized, open-label study in healthy subjects, steady-state quinapril dosing (80mg once a day) did not significantly affect the pharmacokinetic profile of atorvastatin tablets (10mg once a day).
Oral Contraceptives and Hormone Replacement Therapy: Coadministration of atorvastatin with an oral contraceptive, containing 1mg norethindrone and 35µg ethinyl estradiol, increased plasma concentrations (AUC levels) of norethindrone and ethinyl estradiol by approximately 30%and 20%, respectively. These increases should be considered when selecting an oral contraceptive. In clinical studies, atorvastatin was used concomitantly with estrogen replacement therapy without evidence to date of clinically significant adverse interactions.
Antacids: Administration of aluminum- and magnesium-based antacids, such as MaaloxTC suspension, with atorvastatin decreased plasma concentrations of atorvastatin by approximately 35%. LDL-C reduction was not altered but the triglyceride-lowering effect of atorvastatin may be affected.
Cimetidine: Administration of cimetidine with atorvastatin did not alter plasma concentrations or LDL-C lowering efficacy of atorvastatin, however, the triglyceride-lowering effect of atorvastatin was reduced from 34 to 26%.
Cytochrome P450-mediated Interactions : Atorvastatin is metabolized by the cytochrome P450 isoenzyme, CYP3A4. Erythromycin, a CYP3A4 inhibitor, increased atorvastatin plasma levels by 40%. Coadministration of CYP3A4 inhibitors, such as grapefruit juice, some macrolide antibiotics (i.e., erythromycin, clarithromycin), immunosuppressants (cyclosporine), azole antifungal agents (i.e., itraconazole, ketoconazole), protease inhibitors or the antidepressant, nefazodone, may have the potential to increase plasma concentrations of HMG CoA reductase inhibitors, including atorvastatin. Caution should thus be exercised with concomitant use of these agents (see Warnings, Pharmacokinetic Interactions, Muscle Effects; Precautions, Renal Insufficiency, Endocrine Function; and Dosage).
In healthy subjects, coadministration of maximum doses of both atorvastatin (80mg) and terfenadine (120mg), a CYP3A4 substrate, was shown to produce a modest increase in terfenadine AUC. The QTc interval remained unchanged. However, since an interaction between these two drugs cannot be excluded in patients with predisposing factors for arrhythmia, (e.g., pre-existing prolonged QT interval, severe coronary artery disease, hypokalemia), caution should be exercised when these agents are coadministered (see Warnings, Pharmacokinetic Interactions; and Dosage).
Antipyrine: Antipyrine was used as a nonspecific model for drugs metabolized by the microsomal hepatic enzyme system (cytochrome P450 system). Atorvastatin had no effect on the pharmacokinetics of antipyrine, thus interactions with other drugs metabolized via the same cytochrome isozymes are not expected.
Macrolide Antibiotics (azithromycin, clarithromycin, erythromycin): In healthy adults, coadministration of atorvastatin (10 mg once a day) and azithromycin (500 mg once a day) did not significantly alter the plasma concentrations of atorvastatin. However, coadministration of atorvastatin (10 mg once a day) with erythromycin (500 mg q.i.d.) or clarithromycin (500 mg b.i.d.), which are both CYP3A4 inhibitors, increased plasma concentrations of atorvastatin approximately 40% and 80%, respectively (see Warnings, Muscle Effects).
Protease Inhibitors (nelfinavir mesylate): In healthy adults, coadministration of nelfinavir mesylate (1250mg b.i.d.), a known CYP3A4 inhibitor, and atorvastatin (10mg once a day) resulted in increased plasma concentrations of atorvastatin. AUC and C max of atorvastatin were increased by 74% and 122% respectively.
Patients with Severe Hypercholesterolemia: Higher drug dosages (80mg/day) required for some patients with severe hypercholesterolemia (including familial hypercholesterolemia) are associated with increased plasma levels of atorvastatin. Caution should be exercised in such patients who are also severely renally impaired, elderly, or are concomitantly being administered digoxin or CYP3A4 inhibitors (see Warnings, Pharmacokinetic Interactions, Muscle Effects; Precautions, Drug Interactions; and Dosage).
Drug/Laboratory Test Interactions : Atorvastatin may elevate serum transaminase and creatinine phosphokinase levels (from skeletal muscle). In the differential diagnosis of chest pain in a patient on therapy with atorvastatin, cardiac and noncardiac fractions of these enzymes should be determined.
General: The effects of atorvastatin-induced changes in lipoprotein levels, including reduction of serum cholesterol on cardiovascular morbidity or mortality or total mortality have not been established.
Before instituting therapy with atorvastatin, an attempt should be made to control elevated serum lipoprotein levels with appropriate diet, exercise, and weight reduction in overweight patients, and to treat other underlying medical problems (see Indications). Patients should be advised to inform subsequent physicians of the prior use of atorvastatin or any other lipid-lowering agents.
Effect on the Lens: Current long-term data from clinical trials do not indicate an adverse effect of atorvastatin on the human lens.
Effect on Ubiquinone (CoQ 10) Levels: Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure.
Effect on Lipoprotein (a): In some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by a concomitant increase in Lp(a) levels. Until further experience is obtained, it is suggested, where feasible, that measurements of serum Lp(a) be followed up in patients placed on atorvastatin therapy.
Hypersensitivity: An apparent hypersensitivity syndrome has been reported with other HMG-CoA reductase inhibitors which has included 1 or more of the following features: anaphylaxis, angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, vasculitis, purpura, thrombocytopenia, leukopenia, hemolytic anemia, positive ANA, ESR increase, eosinophilia, arthritis, arthralgia, urticaria, asthenia, photosensitivity, fever, chills, flushing, malaise, dyspnea, toxic epidermal necrolysis, erythema multiforme, including Stevens-Johnson syndrome. Although to date hypersensitivity syndrome has not been described as such, atorvastatin should be discontinued if hypersensitivity is suspected.
Pregnancy: Atorvastatin is contraindicated during pregnancy (see Contraindications).
Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause harm to the fetus when administered to pregnant women.
There are no data on the use of atorvastatin during pregnancy. Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued and the patient apprised of the potential risk to the fetus.
Lactation : In rats, milk concentrations of atorvastatin are similar to those in plasma. It is not known whether this drug is excreted in human milk. Because of the potential for adverse reactions in nursing infants, women taking atorvastatin should not breast-feed (see Contraindications).
Children: Treatment experience in a pediatric population is limited to doses of atorvastatin up to 80mg/day for 1year in 8patients with homozygous familial hypercholesterolemia. No clinical or biochemical abnormalities were reported in these patients.
Geriatrics: Treatment experience in adults 70years or older (N=221) with doses of atorvastatin up to 80mg/day has demonstrated that the safety and effectiveness of atorvastatin in this population was similar to that of patients <70years of age. Pharmacokinetic evaluation of atorvastatin in subjects over the age of 65years indicates an increased AUC. As a precautionary measure, the lowest dose should be administered initially.
Renal Insufficiency: Plasma concentrations and LDL-C lowering efficacy of atorvastatin was shown to be similar in patients with moderate renal insufficiency compared with patients with normal renal function. However, since several cases of rhabdomyolysis have been reported in patients with a history of renal insufficiency of unknown severity, as a precautionary measure and pending further experience in renal disease, the lowest dose (10mg/day) of atorvastatin should be used in these patients. Similar precautions apply in patients with severe renal insufficiency (creatinine clearance <30mL/min [<0.5 mL/s]); the lowest dosage should be used and implemented cautiously (see Warnings, Muscle Effects; Precautions, Drug Interactions).
Refer also to Dosage.
Endocrine Function: HMG-CoA reductase inhibitors interfere with cholesterol synthesis and as such might theoretically blunt adrenal and/or gonadal steroid production. Clinical studies with atorvastatin and other HMG-CoA reductase inhibitors have suggested that these agents do not reduce plasma cortisol concentration or impair adrenal reserve and do not reduce basal plasma testosterone concentration. However, the effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown.
Patients treated with atorvastatin who develop clinical evidence of endocrine dysfunction should be evaluated appropriately. Caution should be exercised if an HMG-CoA reductase inhibitor or other agent used to lower cholesterol levels is administered to patients receiving other drugs (e.g., ketoconazole, spironolactone or cimetidine) that may decrease the levels of endogenous steroid hormones.
Pharmacokinetic Interaction Studies and Potential Drug Interactions : Pharmacokinetic interaction studies conducted with drugs in healthy subjects may not detect the possibility of a potential drug interaction in some patients due to differences in underlying diseases and use of concomitant medications (see also Geriatrics; Renal Insufficiency; Patients with Severe Hypercholesterolemia).
Concomitant Therapy with Other Lipid Metabolism Regulators: Combined drug therapy should be approached with caution as information from controlled studies is limited.
Bile Acid Sequestrants: Patients With Mild to Moderate Hypercholesterolemia: LDL-C reduction was greater when atorvastatin 10mg and colestipol 20g were coadministered (-45%) than when either drug was administered alone (-35% for atorvastatin and -22% for colestipol).
Patients With Severe Hypercholesterolemia: LDL-C reduction was similar (-53%) when atorvastatin 40mg and colestipol 20g were coadministered when compared with that of atorvastatin 80mg alone. Plasma concentration of atorvastatin was lower (approximately 26%) when atorvastatin 40mg plus colestipol 20g were coadministered compared with atorvastatin 40mg alone.
However, the combination drug therapy was less effective in lowering the triglycerides than atorvastatin monotherapy in both types of hypercholesterolemic patients.
When atorvastatin is used concurrently with colestipol or any other resin, an interval of at least 2hours should be maintained between the two drugs since the absorption of atorvastatin may be impaired by the resin.
Fibric Acid Derivatives (Gemfibrozil, Fenofibrate, Bezafibrate) and Niacin (Nicotinic Acid): Although there is no experience with the use of atorvastatin given concurrently with fibric acid derivatives and niacin, the benefits and risks of such combined therapy should be carefully considered. The risk of myopathy during treatment with other drugs in this class is increased with concurrent administration (see Warnings, Muscle Effects).
Coumarin Anticoagulants: Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin therapy.
Digoxin: In healthy subjects, digoxin pharmacokinetics at steady-state were not significantly altered by coadministration of digoxin 0.25 mg and atorvastatin 10 mg daily. However, digoxin steady-state concentrations increased approximately 20% following coadministration of digoxin 0.25 mg and atorvastatin 80 mg daily. Patients taking digoxin should be monitored appropriately.
Antihypertensive Agents (amlodipine): In clinical studies, atorvastatin was used concomitantly with antihypertensive agents without evidence to date of clinically significant adverse interactions. In healthy subjects, atorvastatin pharmacokinetics were not altered by the coadministration of atorvastatin 80 mg and amlodipine 10 mg at steady-state.
(quinapril): In a randomized, open-label study in healthy subjects, steady-state quinapril dosing (80mg once a day) did not significantly affect the pharmacokinetic profile of atorvastatin tablets (10mg once a day).
Oral Contraceptives and Hormone Replacement Therapy: Coadministration of atorvastatin with an oral contraceptive, containing 1mg norethindrone and 35µg ethinyl estradiol, increased plasma concentrations (AUC levels) of norethindrone and ethinyl estradiol by approximately 30%and 20%, respectively. These increases should be considered when selecting an oral contraceptive. In clinical studies, atorvastatin was used concomitantly with estrogen replacement therapy without evidence to date of clinically significant adverse interactions.
Antacids: Administration of aluminum- and magnesium-based antacids, such as MaaloxTC suspension, with atorvastatin decreased plasma concentrations of atorvastatin by approximately 35%. LDL-C reduction was not altered but the triglyceride-lowering effect of atorvastatin may be affected.
Cimetidine: Administration of cimetidine with atorvastatin did not alter plasma concentrations or LDL-C lowering efficacy of atorvastatin, however, the triglyceride-lowering effect of atorvastatin was reduced from 34 to 26%.
Cytochrome P450-mediated Interactions : Atorvastatin is metabolized by the cytochrome P450 isoenzyme, CYP3A4. Erythromycin, a CYP3A4 inhibitor, increased atorvastatin plasma levels by 40%. Coadministration of CYP3A4 inhibitors, such as grapefruit juice, some macrolide antibiotics (i.e., erythromycin, clarithromycin), immunosuppressants (cyclosporine), azole antifungal agents (i.e., itraconazole, ketoconazole), protease inhibitors or the antidepressant, nefazodone, may have the potential to increase plasma concentrations of HMG CoA reductase inhibitors, including atorvastatin. Caution should thus be exercised with concomitant use of these agents (see Warnings, Pharmacokinetic Interactions, Muscle Effects; Precautions, Renal Insufficiency, Endocrine Function; and Dosage).
In healthy subjects, coadministration of maximum doses of both atorvastatin (80mg) and terfenadine (120mg), a CYP3A4 substrate, was shown to produce a modest increase in terfenadine AUC. The QTc interval remained unchanged. However, since an interaction between these two drugs cannot be excluded in patients with predisposing factors for arrhythmia, (e.g., pre-existing prolonged QT interval, severe coronary artery disease, hypokalemia), caution should be exercised when these agents are coadministered (see Warnings, Pharmacokinetic Interactions; and Dosage).
Antipyrine: Antipyrine was used as a nonspecific model for drugs metabolized by the microsomal hepatic enzyme system (cytochrome P450 system). Atorvastatin had no effect on the pharmacokinetics of antipyrine, thus interactions with other drugs metabolized via the same cytochrome isozymes are not expected.
Macrolide Antibiotics (azithromycin, clarithromycin, erythromycin): In healthy adults, coadministration of atorvastatin (10 mg once a day) and azithromycin (500 mg once a day) did not significantly alter the plasma concentrations of atorvastatin. However, coadministration of atorvastatin (10 mg once a day) with erythromycin (500 mg q.i.d.) or clarithromycin (500 mg b.i.d.), which are both CYP3A4 inhibitors, increased plasma concentrations of atorvastatin approximately 40% and 80%, respectively (see Warnings, Muscle Effects).
Protease Inhibitors (nelfinavir mesylate): In healthy adults, coadministration of nelfinavir mesylate (1250mg b.i.d.), a known CYP3A4 inhibitor, and atorvastatin (10mg once a day) resulted in increased plasma concentrations of atorvastatin. AUC and C max of atorvastatin were increased by 74% and 122% respectively.
Patients with Severe Hypercholesterolemia: Higher drug dosages (80mg/day) required for some patients with severe hypercholesterolemia (including familial hypercholesterolemia) are associated with increased plasma levels of atorvastatin. Caution should be exercised in such patients who are also severely renally impaired, elderly, or are concomitantly being administered digoxin or CYP3A4 inhibitors (see Warnings, Pharmacokinetic Interactions, Muscle Effects; Precautions, Drug Interactions; and Dosage).
Drug/Laboratory Test Interactions : Atorvastatin may elevate serum transaminase and creatinine phosphokinase levels (from skeletal muscle). In the differential diagnosis of chest pain in a patient on therapy with atorvastatin, cardiac and noncardiac fractions of these enzymes should be determined.
Side Effects / Adverse Effects
Atorvastatin is generally well-tolerated. Adverse reactions have usually been mild and transient. In controlled clinical studies (placebo-controlled and active-controlled comparative studies with other lipid lowering agents) involving 2502patients, <2% of patients were discontinued due to adverse experiences attributable to atorvastatin. Of these 2502patients, 1721 were treated for at least 6months and 1253 for 1year or more.
The following additional adverse events were reported in clinical trials; not all events listed below have been associated with a causal relationship to atorvastatin therapy: muscle cramps, myositis, myopathy, paresthesia, peripheral neuropathy, pancreatitis, hepatitis, cholestatic jaundice, anorexia, vomiting, alopecia, pruritus, rash, impotence, hyperglycemia and hypoglycemia.
Postmarketing Experience: Very rare reports: severe myopathy with or without rhabdomyolysis have been reported (see Warnings, Muscle Effects; Precautions, Renal Insufficiency and Drug Interactions). Isolated reports: thrombocytopenia, arthralgia and allergic reactions (including urticaria, angioneurotic edema, anaphylaxis and bullous rashes [including erytheme multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis]). These may have no causal relationship to atorvastatin.
Ophthalmologic Observations: see Precautions.
Laboratory Tests: Increases in serum transaminase levels have been noted in clinical trials (see Warnings).
Overdose: Symptoms and Treatment: There is no specific treatment for atorvastatin overdosage. Should an overdose occur, the patient should be treated symptomatically and supportive measures instituted as required. Due to extensive drug binding to plasma proteins, hemodialysis is not expected to significantly enhance atorvastatin clearance.
Atorvastatin is generally well-tolerated. Adverse reactions have usually been mild and transient. In controlled clinical studies (placebo-controlled and active-controlled comparative studies with other lipid lowering agents) involving 2502patients, <2% of patients were discontinued due to adverse experiences attributable to atorvastatin. Of these 2502patients, 1721 were treated for at least 6months and 1253 for 1year or more.
The following additional adverse events were reported in clinical trials; not all events listed below have been associated with a causal relationship to atorvastatin therapy: muscle cramps, myositis, myopathy, paresthesia, peripheral neuropathy, pancreatitis, hepatitis, cholestatic jaundice, anorexia, vomiting, alopecia, pruritus, rash, impotence, hyperglycemia and hypoglycemia.
Postmarketing Experience: Very rare reports: severe myopathy with or without rhabdomyolysis have been reported (see Warnings, Muscle Effects; Precautions, Renal Insufficiency and Drug Interactions). Isolated reports: thrombocytopenia, arthralgia and allergic reactions (including urticaria, angioneurotic edema, anaphylaxis and bullous rashes [including erytheme multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis]). These may have no causal relationship to atorvastatin.
Ophthalmologic Observations: see Precautions.
Laboratory Tests: Increases in serum transaminase levels have been noted in clinical trials (see Warnings).
Overdose: Symptoms and Treatment: There is no specific treatment for atorvastatin overdosage. Should an overdose occur, the patient should be treated symptomatically and supportive measures instituted as required. Due to extensive drug binding to plasma proteins, hemodialysis is not expected to significantly enhance atorvastatin clearance.
Overdose
Information not available
Information not available
Recommended Dosage
Dosage: Patients should be placed on a standard cholesterol-lowering diet (at least equivalent to the American Heart Association [AHA] Step 1 diet) before receiving atorvastatin, and should continue on this diet during treatment with atorvastatin. If appropriate, a program of weight control and physical exercise should be implemented.
Primary Hypercholesterolemia and Combined (Mixed) Hyperlipidemia, Including Familial Combined Hyperlipidemia: The recommended dose of atorvastatin is 10mg once aday. The majority of patients achieve and maintain target cholesterol levels with atorvastatin 10mg/day. A significant therapeutic response is evident within 2weeks, and the maximum response is usually achieved within 2to 4weeks. The response is maintained during chronic therapy.
Doses can be given at any time of the day, with or without food, and should preferably be given in the evening. Doses should be individualized according to baseline LDL-C and/or TG levels, the desired LDL-C and/or TG target (see the Detection and Management of Hypercholesterolemia, Working Group on Hypercholesterolemia and other Dyslipidemias [Canada] and/or the U.S. National Cholesterol Education Program [NCEP]), the goal of therapy and the patient's response. Adjustments of dosage, if necessary, should be made at intervals of 4weeks or more. The recommended dose range for most patients is 10to 40mg/day. The maximum dose is 80mg/day, which may be required in a minority of patients (see section below).
Lipid levels should be monitored periodically and, if necessary, the dose of atorvastatin adjusted based on target lipid levels recommended by guidelines.
The following reductions in total cholesterol and LDL-C levels have been observed in 2dose-response studies and may serve as a guide to treatment of patients with mild to moderate hypercholesterolemia.
Dose-response in Patients with Mild to Moderate Hypercholesterolemia (Mean % Change from Baseline)a
Severe Dyslipidemias: In patients with severe dyslipidemias, including homozygous and heterozygous familial hypercholesterolemia and dysbetalipoproteinemia (Type lll), higher dosages (up to 80mg/day) may be required (see Warnings, Pharmacokinetic Interactions, Muscle Effects and Precautions, Drug Interactions).
Concomitant Therapy: See Precautions, Drug Interactions.
Renal Insufficiency: See Precautions.
Information for the Patient: See Blue Section--Information for the Patient “Lipitor”.
Dosage: Patients should be placed on a standard cholesterol-lowering diet (at least equivalent to the American Heart Association [AHA] Step 1 diet) before receiving atorvastatin, and should continue on this diet during treatment with atorvastatin. If appropriate, a program of weight control and physical exercise should be implemented.
Primary Hypercholesterolemia and Combined (Mixed) Hyperlipidemia, Including Familial Combined Hyperlipidemia: The recommended dose of atorvastatin is 10mg once aday. The majority of patients achieve and maintain target cholesterol levels with atorvastatin 10mg/day. A significant therapeutic response is evident within 2weeks, and the maximum response is usually achieved within 2to 4weeks. The response is maintained during chronic therapy.
Doses can be given at any time of the day, with or without food, and should preferably be given in the evening. Doses should be individualized according to baseline LDL-C and/or TG levels, the desired LDL-C and/or TG target (see the Detection and Management of Hypercholesterolemia, Working Group on Hypercholesterolemia and other Dyslipidemias [Canada] and/or the U.S. National Cholesterol Education Program [NCEP]), the goal of therapy and the patient's response. Adjustments of dosage, if necessary, should be made at intervals of 4weeks or more. The recommended dose range for most patients is 10to 40mg/day. The maximum dose is 80mg/day, which may be required in a minority of patients (see section below).
Lipid levels should be monitored periodically and, if necessary, the dose of atorvastatin adjusted based on target lipid levels recommended by guidelines.
The following reductions in total cholesterol and LDL-C levels have been observed in 2dose-response studies and may serve as a guide to treatment of patients with mild to moderate hypercholesterolemia.
Dose-response in Patients with Mild to Moderate Hypercholesterolemia (Mean % Change from Baseline)a
Severe Dyslipidemias: In patients with severe dyslipidemias, including homozygous and heterozygous familial hypercholesterolemia and dysbetalipoproteinemia (Type lll), higher dosages (up to 80mg/day) may be required (see Warnings, Pharmacokinetic Interactions, Muscle Effects and Precautions, Drug Interactions).
Concomitant Therapy: See Precautions, Drug Interactions.
Renal Insufficiency: See Precautions.
Information for the Patient: See Blue Section--Information for the Patient “Lipitor”.
Supplied / Packaging
10mg: Each white, elliptical, film-coated tablet, coded “10” on one side and “PD155” on the other, contains: atorvastatin 10mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
20 mg: Each white, elliptical, film-coated tablet, coded “20” on one side and “PD156” on the other, contains: atorvastatin 20mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
40 mg: Each white, elliptical, film-coated tablet, coded “40” on one side and “PD157” on the other, contains: atorvastatin 40mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
80 mg: Each white, elliptical, film-coated tablet, coded “80” on one side and “PD158” on the other, contains: atorvastatin 80mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Blisters of 30 (3strips´10).
Store at controlled room temperature 15 to 30°C.
10mg: Each white, elliptical, film-coated tablet, coded “10” on one side and “PD155” on the other, contains: atorvastatin 10mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
20 mg: Each white, elliptical, film-coated tablet, coded “20” on one side and “PD156” on the other, contains: atorvastatin 20mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
40 mg: Each white, elliptical, film-coated tablet, coded “40” on one side and “PD157” on the other, contains: atorvastatin 40mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Bottles of90.
80 mg: Each white, elliptical, film-coated tablet, coded “80” on one side and “PD158” on the other, contains: atorvastatin 80mg. Nonmedicinal ingredients: calcium carbonate, candelilla wax, croscarmellose sodium, hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose monohydrate, magnesium stearate, microcrystalline cellulose, polyethylene glycol, polysorbate 80, simethicone emulsion, talc and titanium dioxide. Blisters of 30 (3strips´10).
Store at controlled room temperature 15 to 30°C.
Search for a drug
Brand Name
Lipitor
Lipitor
Generic Name
Atorvastatin
Atorvastatin
General Indications
Lipid Metabolism Regulator
Lipid Metabolism Regulator
