Atorvastatin

Atorvastatin is a member of the medication class known as statins, which are used primarily as a lipid-lowering agent and for prevention of events associated with cardiovascular disease. Like all statins, atorvastatin works by inhibiting HMG-CoA reductase, an enzyme found in liver tissue that plays a key role in production of cholesterol in the body.

Antilipidemic agent.

Inhibits HMG-CoA reductase. Reduces total LDL, cholesterol, serum triglyceride levels. There is little if any effect on serum HDL levels

Routes of Administration: Oral only

Condition: Hyperlipidemia

Dose: Adults Initial: 10 mg/d. Maintenance: 10-80 mg/d.

Condition: Homozygous familial hypercholesterolemia

Dose: Adults 10-80 mg/d.

Kidney disease: None.

Liver disease: None.

Elderly: None

Pediatric: Limited data available.

Food: No restriction.

Pregnancy: Category X—contraindicated.

Lactation: Appears in breast milk. Contraindicated.

Contraindications: Hypersensitivity to statins, active liver disease or unexplained persistent elevations of serum transaminase, pregnancy, lactation.

> Use with caution in patients with the following conditions: renal insufficiency, history of liver disease, alcohol abusers.

> Discontinue if drug-induced myopathy develops. This is characterized by myalgia, creatinine kinase levels >10x normal. May cause acute renal failure from rhabdomyolysis. May occur more frequently when drug is combined with gemfibrozil or niacin.

> Discontinue drug if patient experiences severe trauma, surgery, or serious illness.

> Drugs that increase effects/toxicity of HMG-CoA reductase inhibitors: gemfibrozil, clofibrate, erythromycin, cyclosporin, niacin, clarithromycin, itraconazole, protease inhibitors.

> HMG-CoA reductase inhibitors increase effects/toxicity of oral anticoagulants.

> Common: None.

> Serious: myopathy, rhabdomyolysis, neuropathy, cranial nerve abnormalities, hypersensitivity reactions, pancreatitis, hepatic injury including hepatic necrosis and cirrhosis, lens opacities

> Total cholesterol, LDL and HDL cholesterol, triglycerides. Values should be obtained prior to and periodically after treatment begins to ascertain drug efficacy.

> Serum BUN and creatinine.

> Monitor liver enzymes before beginning therapy, at 3, 6, and 12 months thereafter, and semiannually afterward.

> Signs and symptoms of myopathy: unexplained skeletal muscle pain, muscle tenderness or weakness particularly when accompanied by fever or fatigue. Check creatinine kinase levels. If these are markedly elevated or patient is sympto-matic, discontinue drug.

> Discontinue drug if transaminase levels exceed three times normal values. It may be advisable to take a liver biopsy if transaminase elevation persists after drug is discontinued.

> Patient’s ophthalmic state should be evaluated once a year following treatment. If lens opacity occurs, consider discontinuing drug.

> Avoid alcohol.

> Use of OTC medications only with approval from treating physician.

> Exercise regularly, reduce fat and alcohol intake, and stop smoking.

> Current literature suggests that the most effective reduction of total and LDL cholesterol occurs with a combination of exercise, weight reduction, low-fat diet, and lipid-lowering agents.