ATORVAST 20 Atorvastatin 20mg Film-Coated Tablet 1's

An adjunct to lifestyle changes, including diet for the reduction of elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and apolipoprotein B (apo B), the total cholesterol: high-density lipoprotein cholesterol (TC:HDL-C) ratio and for increasing HDL-C; in hyperlipidemic and dyslipidemic conditions including: Primary hypercholesterolemia (type IIa); combined (mixed) hyperlipidemia (type IIb), including familial combined hyperlipidemia, regardless of whether cholesterol or TG are the lipid abnormality of concern; dysbetalipoproteinemia (type III); hypertriglyceridemia (type IV); familial hypercholesterolemia (homozygous and heterozygous).
For homozygous familial hypercholesterolemia, atorvastatin should be used as an adjunct to treatments eg, LDL apheresis or as monotherapy if such treatments are not available.
An adjunct to diet to reduce total-C, LDL-C and apo B levels in boys and postmenarchal girls 10-17 years with heterozygous familial hypercholesterolemia, if after an adequate trial of diet therapy the following findings are still present: LDL-C remains ≥4.9 mmol/L (190 mg/dL) or ≥4.1 mmol/L (160 mg/dL), and there is a positive family history of premature cardiovascular disease (CVD) or ≥2 other CVD risk factors are present in the pediatric patient.
Prior to initiating therapy with atorvastatin, secondary causes should be excluded for elevations in plasma lipid levels (eg, poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease and alcoholism) and a lipid profile performed to measure total-C, LDL-C, HDL-C and TG. For patients with TG <4.52 mmol/L (<400 mg/dL), LDL-C can be estimated using the following equation: (See equation.)

For patients with TG levels >4.52 mmol/L (>400 mg/dL), this equation is less accurate and LDL-C concentrations should be measured directly or by ultracentrifugation.
Patients with high or very high TG levels ie, >2.2 mmol/L (200 mg/dL) or >5.6 mmol/L (500 mg/dL), respectively, may require TG-lowering therapy (fenofibrate, bezafibrate or nicotinic acid) alone or in combination with atorvastatin.
In general, combination therapy with fibrates must be undertaken cautiously and only after risk-benefit analysis (see Precautions and Interactions).
Elevated serum TG are most often observed in patients with the metabolic syndrome [abdominal obesity, atherogenic dyslipidemia (elevated TG, small dense LDL particles and low HDL-C), insulin resistance with or without glucose intolerance, raised blood pressure and prothrombic and pro-inflammatory states].
When drugs are prescribed attention to therapeutic lifestyle changes (reduced intake of saturated fats and cholesterol, weight reduction, increased physical activity, ingestion of soluble fibers) should always be maintained and reinforced.
Prevention of Cardiovascular Disease: To reduce the risk of myocardial infarction in adult hypertensive patients without clinically evident coronary heart disease (CHD), but with at least 3 additional risk factors for CHD eg, age ≥55 years, male sex, smoking, type 2 diabetes, left ventricular hypertrophy, other specified abnormalities on electrocardiogram (ECG), microalbuminuria or proteinuria, ratio of plasma total-C to HDL-C ≥6 or premature family history of CHD.
To reduce the risk of myocardial infarction and stroke in adult patients with type 2 diabetes mellitus and hypertension without clinically evident CHD, but with other risk factors eg, age ≥55 years, retinopathy, albuminuria or smoking.
To reduce the risk of myocardial infarction in patients with clinically evident CHD.

 

Patients should be placed on a standard cholesterol-lowering 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.
Prior to initiating therapy with atorvastatin, secondary causes for elevations in plasma lipid levels should be excluded. A lipid profile should also be performed.
Primary Hypercholesterolemia and Combined (Mixed) Dyslipidemia, Including Familial Combined Hyperlipidemia: Recommended Starting Dose: 10 or 20 mg once daily, depending on patient's LDL-C reduction required. Patients who require a large reduction in LDL-C (>45%) may be started at 40 mg once daily. The dosage range of atorvastatin is 10-80 mg once daily. A significant therapeutic response is evident within 2 weeks and the maximum response is usually achieved within 2-4 weeks. The response is maintained during chronic therapy. Adjustments of dosage, if necessary, should be made at intervals of 2-4 weeks. The maximum dose is 80 mg/day.
The dosage of atorvastatin should be individualized according the baseline LDL-C, TC:HDL-C ratio and/or TG levels to achieve the recommended desired lipid values at the lowest dose needed to achieve LDL-C desired level. Lipid levels should be monitored periodically and if necessary, the dose of atorvastatin adjusted based on desired lipid levels recommended by guidelines.
Severe Dyslipidemias: In patients with severe dyslipidemias including homozygous and heterozygous familial hypercholesterolemia and dysbetalipoproteinemia (type III), higher dosages (up to 80 mg/day) may be required (see Precautions and Interactions).
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): Recommended Starting Dose: 10 mg/day. Maximum Recommended Dose: 20 mg/day (doses >20 mg/day have not been studied in this patient population). Doses should be individualized according to the recommended goal of therapy (see Pharmacology: Pharmacodynamics under Actions and Indications). Adjustments should be made at intervals of ≥4 weeks.
Prevention of Cardiovascular Disease: Clinical trials conducted that evaluated atorvastatin in the primary prevention of myocardial infarction used a dose of atorvastatin 10 mg once daily. For secondary prevention of myocardial infarction, optimal dosing may range from 10-80 mg atorvastatin once daily, to be given at the discretion of the prescriber, taking into account the expected benefit and safety considerations relevant to the patient to be treated.
Concomitant Therapy: See Interactions.
Renal Impairment: See Precautions.
Missed Dose: Take it as soon as possible. But if it is almost time for the next dose, skip the missed dose and just take the next dose. Don't take a double dose.
Administration: Doses can be given at any time of the day with or without food, and should preferably be given in the evening.

 

Overdosage

May be taken with or without food: Avoid excessive consumption (>1 L/day) of grapefruit juice.

Hypersensitivity to atorvastatin calcium or to any component of Atorvast-Natrapharm (see Description).
Active liver disease or unexplained persistent elevations of serum transaminases exceeding 3 times the upper limit of normal (ULN) (see Precautions).
Use in pregnancy: Atorvastatin is contraindicated during pregnancy. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Atorvastatin should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the possible harm. If the patient becomes pregnant while taking atorvastatin, the drug should be discontinued immediately and the patient apprised of the potential harm to the fetus. Atherosclerosis being a chronic process, discontinuation of lipid metabolism regulating drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia.

General: Before instituting therapy with atorvastatin calcium, 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.
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 co-administered with drugs that inhibit the cytochrome P-450 (CYP450) enzyme system. Atorvastatin is metabolized by CYP450 isoform 3A4 (CYP3A4) and as such may interact with agents that inhibit this enzyme (see Muscle effects as follows and Interactions).
Muscle Effects: Effects on skeletal muscle eg, myalgia, myopathy and rarely, rhabdomyolysis have been reported in patients treated with atorvastatin.
Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobulinuria have been reported with atorvastatin and with other HMG-CoA reductase inhibitors.
Myopathy, defined as muscle pain or muscle weakness in conjunction with increases in creatine kinase (CK) values to >10 x ULN, should be considered in any patient with diffuse myalgia, muscle tenderness or weakness, and/or marked elevation of CK. Patients should be advised to report promptly any unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Patients who develop any signs or symptoms suggestive of myopathy should have their CK levels measured. Atorvastatin therapy should be discontinued if markedly elevated CK levels are measured or myopathy is diagnosed or suspected.
Pre-Disposing Factors for Myopathy/Rhabdomyolysis: Atorvastatin, as with other HMG-CoA reductase inhibitors, should be prescribed with caution in patients with pre-disposing factors for myopathy/rhabdomyolysis. Such factors include: Personal or family history of hereditary muscular disorders, previous history of muscle toxicity with another HMG-CoA reductase inhibitor, concomitant use of a fibrate or niacin, hypothyroidism, alcohol abuse, excessive physical exercise, age >65 years, renal and hepatic impairment, diabetes with hepatic fatty change, surgery and trauma, frailty and situations where an increase in plasma levels of atorvastatin calcium may occur.
The risk of myopathy and rhabdomyolysis during treatment with HMG-CoA reductase inhibitors is increased with concurrent administration of drugs that interfere with metabolism of atorvastatin via CYP3A4 eg, cyclosporine, fibric acid derivatives, erythromycin, clarithromycin, niacin (nicotinic acid), azole antifungals or nefazodone. Concomitant use of strong inhibitors of CYP3A4 with atorvastatin should be used with caution. If such use must be instituted, lower starting and maintenance doses of atorvastatin should be considered and patients should be monitored closely for musculoskeletal effects (see Pharmacology: Pharmacokinetics under Actions, Pharmacokinetic Interactions as previously mentioned and Interactions).
In cases where co-administration of atorvastatin with cyclosporine is necessary, the dose of atorvastatin should not exceed 10 mg. Temporary suspension of atorvastatin during fusidic acid therapy is recommended (see Interactions).
Although patients with renal impairment are known to be predisposed to the development of rhabdomyolysis with administration of HMG-CoA reductase inhibitors (also known as statins), those with a history of renal impairment may also be predisposed to the development of rhabdomyolysis. Such patients merit close monitoring for skeletal muscle effects.
Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute serious condition suggestive of myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis, severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).
Atorvastatin therapy should be discontinued if markedly elevated creatine phosphokinase (CPK) levels occur or myopathy is diagnosed or suspected.
Cardiovascular: Hemorrhagic Stroke in Patients with Recent Stroke or Transient Ischemic Attack (TIA): A post hoc analysis of a clinical study in 4,731 patients without CHD who had a stroke or TIA with in the preceding 6 months revealed a higher incidence of hemorrhagic stroke in the atorvastatin 80 mg group compared to placebo. Patients with hemorrhagic stroke on entry appeared to be at increased risk for recurrent hemorrhagic stroke. The potential risk of hemorrhagic stroke should be carefully considered before initiating treatment with atorvastatin in patients with recent (1-6 months) stroke or TIA.
Effect on Ubiquinone (CoQ10) 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.
Endocrine and Metabolism: 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 (eg, ketoconazole, spironolactone or cimetidine) that may decrease the levels of endogenous steroid hormones.
Effect on Lipoprotein (a): In some patients, the beneficial effect of lowered total-C and LDL-C levels may be partly blunted by a concomitant increase in Lp(a) lipoprotein concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for CHD. It is thus desirable to maintain and reinforce lifestyle changes in high risk patients placed on atorvastatin therapy.
Patients with Severe Hypercholesterolemia: Higher drug dosages (80 mg/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 with digoxin or CYP3A4 inhibitors (see Dosage & Administration, Pharmacokinetic Interactions and Muscle Effects as previously mentioned and Interactions).
Hepatic/Biliary/Pancreatic: Hepatic Effects: In clinical trials, persistent increases in serum transaminases >3 x ULN 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 alanine aminotransferase (ALT) or aspartate aminotransferase (AST) show evidence of progression, particularly if they rise to >3 x ULN and are persistent, the dosage should be reduced or the drug should be discontinued.
Atorvastatin, as well as other HMG-CoA reductase inhibitors, 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.
Ophthalmologic: Effect on the Lens: Current long-term data from clinical trials do not indicate an adverse effect of atorvastatin on the human lens.
Renal: 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 (10 mg/day) of atorvastatin should be used in these patients. Similar precautions apply in patients with severe renal insufficiency [CrCl <30 mL/min (<0.5 mL/sec)]; the lowest dosage should be used and implemented cautiously (see Muscle Effects as previously mentioned and Interactions). Refer also to Dosage & Administration.
Sensitivity/Resistance: Hypersensitivity: An apparent hypersensitivity syndrome has been reported with other HMG-CoA reductase inhibitors which has included ≥1 of the following features: Anaphylaxis, angioedema, lupus erythematous-like syndrome, polymyalgia rheumatica, vasculitis, purpura, thrombocytopenia, leukopenia, hemolytic anemia, positive antinuclear antibodies (ANA), increase erythrocyte sedimentation rate (ESR), 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.
Use in 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 breastfeed.
Use in children: Safety and effectiveness of atorvastatin in patients 10-17 years (N=140) with heterozygous familial hypercholesterolemia have been evaluated in a controlled clinical trial of 6 months duration in adolescent boys and postmenarchal girls. Patients treated with atorvastatin had a safety and tolerability profile generally similar to that of placebo. Doses >20 mg have not been studied in this patient population.
Safety and effectiveness of atorvastatin in pediatric patients has not been determined in the prevention of myocardial infarction.
Atorvastatin had no effect on growth or sexual maturation in boys and in girls. The effects on menstrual cycle were not assessed (see Pharmacology: Pharmacodynamics under Actions, Dosage & Administration and Adverse Reactions).
Adolescent females should be counseled on appropriate contraceptive methods while on atorvastatin therapy (see Contraindications). Atorvastatin has not been studied in controlled clinical trials involving pre-pubertal patients or patients <10 years.
Doses of atorvastatin up to 80 mg/day for 1 year have been evaluated in 8 pediatric patients with homozygous familial hypercholesterolemia (see Pharmacology: Pharmacodynamics under Actions).
Use in the elderly: Treatment experience in adults ≥70 years (N=221) with doses of atorvastatin up to 80 mg/day has demonstrated that the safety and effectiveness of atorvastatin in this population was similar to that of patients <70 years. Pharmacokinetic evaluation of atorvastatin in subjects >65 years indicates an increased AUC. As a precautionary measure, the lowest dose should be administered initially (see Pharmacology: Pharmacokinetics under Actions).
Elderly patients may be more susceptible to myopathy (see Muscle Effects: Predisposing Factors for Myopathy/Rhabdomyolysis as previously mentioned).

 

Use In Pregnancy & Lactation

Adverse reactions with atorvastatin have usually been mild and transient. In the atorvastatin placebo-controlled clinical trial database of 16,066 (8,755 atorvastatin vs 7,311 placebo) patients treated for a median period of 53 weeks, 5.2% of patients on atorvastatin discontinue due to adverse reactions compared to 4% of the patients on placebo.
Adverse experiences occurring at an incidence ≥1% in patients participating in placebo-controlled clinical studies of atorvastatin and reported to be possibly, probably or definitely drug related are shown in Table 1 as follows. (See Table 1.)

The following additional adverse events were reported in placebo-controlled clinical trials during atorvastatin therapy: Muscle cramps, myositis, muscle fatigue, myopathy, paresthesia, peripheral neuropathy, pancreatitis, hepatitis, cholestatic jaundice, cholestasis, anorexia, vomiting, abdominal discomfort, alopecia, pruritus, rash, urticaria, erectile dysfunction, nightmare, blurred vision, tinnitus, eructation, neck pain, malaise, pyrexia and white blood cells urine positive.
In summary, the adverse events occurring at a frequency <1% are listed as follows: General Disorders and Administration Site Conditions: Malaise, pyrexia.
Gastrointestinal Disorders: Abdominal discomfort, eructation.
Hepatobiliary Disorders: Hepatitis, cholestasis.
Musculoskeletal and Connective Tissue Disorders: Muscle fatigue, neck pain.
Psychiatric Disorders: Nightmare.
Skin and Subcutaneous Tissue Disorders: Urticaria.
Eye Disorders: Blurred vision.
Ear and Labyrinth Disorders: Tinnitus.
Investigations: White blood cells urine positive.
Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10-17 years): In a 26-week controlled study in boys and postmenarchal girls (n=187, where 140 patients received atorvastatin), the safety and tolerability profile of atorvastatin 10-20 mg daily was similar to that of placebo. The adverse events reported in ≥1% of patients were as follows: Abdominal pain, depression and headache (see Pharmacology: Pharmacodynamics under Actions and Use in children under Precautions).
Laboratory Changes and Adverse Events: The criteria for clinically significant laboratory changes were >3 x ULN for liver enzymes and >5 x ULN for CK. A total of 8 unique subjects met ≥1 of these criteria during the double-blind phase. Hence, the incidence of patients who experienced abnormally high enzymatic levels (AST/ALT and CK) was >4% (8/187).
Five (5) atorvastatin and 1 placebo subjects had increases in CK >5 x ULN during the double-blind phase; 2 of the 5 atorvastatin-treated subjects had increases in CK >10 x ULN.
There were 2 subjects who had clinically significant increases in ALT.
Abnormal Hematologic and Clinical Chemistry Findings: Laboratory Tests: Increases in serum transaminase levels and serum glucose have been noted in clinical trials (see Precautions).
Post-Market Adverse Drug Reactions: The following adverse events have also been reported during post-marketing experience with atorvastatin, regardless of causality assessment: Rare Reports: Severe myopathy with or without rhabdomyolysis (see Precautions and Interactions).
Isolated Reports: Gynecomastia, thrombocytopenia, arthralgia and allergic reactions including urticaria, angioneurotic edema, anaphylaxis and bullous rashes (including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis); fatigue, back pain, chest pain, malaise, dizziness, amnesia, peripheral edema, weight gain, abdominal pain, insomnia, hypoesthesia, tinnitus, tendon rupture and dysgeusia.
Ophthalmologic Observations: see Precautions.
Cases of erectile dysfunction have been reported in association with the use of statins.
The following adverse events have been reported with some statins: Sleep disturbances including insomnia and nightmares; mood related disorders including depression; very rare cases of interstitial lungs disease, especially with long-term therapy. If it is suspected a patient has developed interstitial lung disease, statin therapy should be discontinued.

 

Overview: 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 Precautions).
Concomitant Therapy with Other Lipid Metabolism Regulators: Based on post-marketing surveillance, gemfibrozil, fenofibrate, other fibrates and lipid-modifying doses of niacin (nicotinic acid) may increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone (see Precautions). Therefore, combined drug therapy should be approached with caution; lower starting and maintenance doses of atorvastatin should be considered.
Cytochrome P-450-Mediated Interactions: Atorvastatin is metabolized by the CYP450 isoenzyme, CYP3A4. Erythromycin, a CYP3A4 inhibitor, increased atorvastatin plasma levels by 40%. Co-administration of CYP3A4 inhibitors eg, grapefruit juice, some macrolide antibiotics (ie, erythromycin, clarithromycin), immunosuppressants (cyclosporine), azote antifungal agents (ie, itraconazole, ketoconazole), protease inhibitors or the antidepressant, nefazodone, have the potential to increase plasma concentrations of HMG-CoA reductase inhibitors, including atorvastatin (see Interactions). Concomitant use of strong inhibitors of CYP3A4 with atorvastatin should be used with caution. If such use must be instituted, lower starting and maintenance doses of atorvastatin should be considered and patients should be monitored closely for musculoskeletal effects (see Dosage & Administration and Precautions).
Transporter Inhibitors: Atorvastatin and atorvastatin-metabolites are substrates of the organic anion-transporting polypeptide (OATP1B1) transporter. Inhibitors of the OATP1B1 (eg, cyclosporine) can increase the bioavailability of atorvastatin (see Pharmacology: Pharmacokinetics under Actions).
Inducers of Cytochrome P-450 3A: Concomitant administration of atorvastatin with inducers of CYP3A4 (eg, efavirenz, rifampin) can lead to variable reductions in plasma concentrations of atorvastatin. Due to the dual interaction mechanism of rifampin, (CYP3A4 induction and inhibition of hepatocyte uptake transporter OATP1B1), simultaneous co-administration of atorvastatin with rifampin resulted in a mean increase in C_max and AUC of atorvastatin of 12% and 190%, respectively. In contrast, a delayed administration of atorvastatin after administration of rifampin has been associated with a significant reduction (approximately 80%) in atorvastatin plasma concentrations.
Drug-Drug Interactions: The drugs listed in Table 2a an 2b are based on either drug interactions studies, case reports or potential interactions due to the expected magnitude and seriousness of the interaction (ie, those identified as contraindicated). Interactions with other drugs have not been established. (See Table 2a and 2b.)

Drug-Food Interactions: Co-administration of grapefruit juice has the potential to increase plasma concentrations of HMG-CoA reductase inhibitors, including atorvastatin. The equivalent of 1.2 L/day resulted in a 2.5-fold increase in AUC of atorvastatin. Consumption of excessive grapefruit juice with atorvastatin is not recommended.
Drug-Herb Interactions: Interactions with herbal products have not been established.
Drug/Laboratory Test Interactions: Atorvastatin may elevate serum transaminase and CK 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.

Storage

Action

Dyslipidaemic Agents