Trade Names:Lipitor- Tablets 10 mg- Tablets 20 mg- Tablets 40 mg- Tablets 80 mg
Increases rate at which body removes cholesterol from blood and reduces production of cholesterol by inhibiting enzyme that catalyzes early rate-limiting step in cholesterol synthesis; increases HDL; reduces LDL, VLDL, and triglycerides (TGs).
Rapidly absorbed; T max is 1 to 2 h. Bioavailability is approximately 14%; low bioavailability is because of presystemic Cl in GI mucosa and/or hepatic first-pass metabolism. Food decreases rate and extent of absorption approximately 25% and 9%, respectively, but does not alter efficacy.
Vd is approximately 381 L. At least 98% is protein bound.
Undergoes hepatic and extrahepatic metabolism, including first-pass metabolism and CYP3A4. Extensively metabolized to active metabolites, which produce approximately 70% of circulating inhibitory activity of HMG-CoA reductase.
Atorvastatin and metabolites eliminated primarily in bile. Less than 2% of dose is recovered in the urine. Plasma t ½ is approximately 14 h.
The t ½ of HMG-CoA reductase inhibition is 20 to 30 h.
Plasma levels are markedly increased in patients with chronic alcoholic liver disease.
Reduce risk of MI or stroke and reduce risk for revascularization procedures and angina in patients with multiple risk factors for coronary heart disease (CHD), such as age, smoking, hypertension, low HDL cholesterol (C), or family history of early CHD. Reduce risk of non-fatal MI and fatal and non-fatal stroke in patients with type 2 diabetes, and without clinically evident CHD, but with multiple risk factors for CHD, such as albuminuria, hypertension, retinopathy, or smoking. Reduce risk of angina, non-fatal MI, and fatal and non-fatal stroke, or hospitalization for CHD, and reduce risk for revascularization procedures in patients with clinically evident CHD.
HypercholesterolemiaAdjunct to diet to reduce elevated total-C, LDL-C, apolipoprotein B (apo B), and TG levels, and increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson types IIa and IIb). Adjunct to diet for treatment of patients with elevated serum TG levels (Fredrickson type IV). Treatment of primary dysbetalipoprotein (Fredrickson type III) in patients who do not respond adequately to diet. Reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatment (LDL aphaeresis), or if such treatments are unavailable. Adjunct to diet to reduce total-C, LDL-C, and apo B levels in boys and postmenarchal girls 10 to 17 yr of age with heterozygous familial hypercholesterolemia if, after an adequate trial of diet therapy, the following are present: LDL-C remains at a level of at least 190 mg/dL; LDC-C remains at a level of least 160 mg/dL and there is a positive family history of premature CV disease; 2 or more other CV disease risk factors are present in children.
Active liver disease or unexplained persistent elevation of serum transaminases; pregnancy; lactation; hypersensitivity to any component of the product.
PO 10 to 80 mg/day.
Heterozygous Familial HypercholesterolemiaChildren 10 to 17 yr of agePO Start with 10 mg/day (max, 20 mg/day).
Store tablets at controlled room temperature (68° to 77°F).
Coadministration may decrease atorvastatin levels.
Azole antifungal agents (eg, itraconazole), cyclosporine, diltiazem, gemfibrozil, grapefruit juice, macrolide antibiotics (eg, erythromycin), niacin, NNRTIs, protease inhibitors (eg, ritonavir), verapamilSevere myopathy or rhabdomyolysis may occur.
Contraceptives, oralMay increase AUC for norethindrone and ethinyl estradiol.
DigoxinElevated digoxin levels may occur.
None well documented.
Headache (17%); asthenia (4%); dizziness, insomnia (at least 2%).
Rash (4%); bullous rashes including erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (postmarketing).
Sinusitis (6%); pharyngitis (3%); rhinitis (at least 2%).
Diarrhea (5%); abdominal pain (4%); constipation, dyspepsia, flatulence (3%); nausea (at least 2%).
Albuminuria, hematuria, UTI (at least 2%).
Peripheral edema (at least 2%).
Myalgia (6%); arthralgia (5%); back pain (4%); arthritis (at least 2%); rhabdomyolysis (postmarketing).
Bronchitis (at least 2%).
Accidental injury (4%); flu-like symptoms (3%); chest pain (at least 2%); anaphylaxis, angioneurotic edema (postmarketing).
Category X .
Contraindicated in breast-feeding women.
Safety and efficacy not established, except in children 10 to 17 yr of age with heterozygous familial hypercholesterolemia.
Ensure secondary causes of hypercholesterolemia (eg, poorly controlled diabetes, hypothyroidism, drugs that increase LDL-C and decrease HDL-C) are excluded, or, if appropriate, treated, before starting therapy.
Ensure that LFTs (transaminases) are determined before and 12 wk following initiation of therapy, after increase in dose, and periodically thereafter (eg, every 6 mo).
Use with caution in patients who consume substantial quantities of alcohol or have a history of liver disease.
Ensure therapy is temporarily withheld in patient with an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (eg, hypotension, major surgery, sepsis, trauma).
Rhabdomyolysis with renal function impairment secondary to myoglobinuria has occurred in this class of drugs. Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, or marked elevation of CPK.
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