AtorvaSTATin (Lexi-Drugs)

Pronunciation

(a TORE va sta tin)

Brand Names: US

Lipitor

Brand Names: Canada

AG-Atorvastatin; APO-Atorvastatin; Atorvastatin-10; Atorvastatin-20; Atorvastatin-40; Atorvastatin-80; Auro-Atorvastatin; DOM-Atorvastatin; GD-Atorvastatin [DSC]; JAMP-Atorvastatin; Lipitor; M-Atorvastatin; Mar-Atorvastatin; MYLAN-Atorvastatin; NOVO-Atorvastatin [DSC]; PMS-Atorvastatin; RAN-Atorvastatin; RATIO-Atorvastatin [DSC]; REDDY-Atorvastatin; RIVA-Atorvastatin; SANDOZ Atorvastatin; TEVA-Atorvastatin

Dosing: Adult

Note: Doses should be individualized according to the baseline LDL-cholesterol concentrations and patient response; adjustments should be made at intervals of 2 to 4 weeks

Hypercholesterolemia (heterozygous familial and nonfamilial) and mixed hyperlipidemia (Fredrickson types IIa and IIb): Oral: Initial: 10 or 20 mg once daily; patients requiring >45% reduction in LDL-C may be started at 40 mg once daily; range: 10 to 80 mg once daily

Homozygous familial hypercholesterolemia: Oral: 10 to 80 mg once daily

Prevention of cardiovascular disease/reduce the risk of atherosclerotic cardiovascular disease: Oral:

ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Grundy 2018]; ACC/AHA [Stone 2013]):

Note: When choosing to initiate therapy and selecting dose intensity, consider atherosclerotic cardiovascular disease (ASCVD) risk, risk enhancing factors, possibility for side effects, and drug interactions.

Primary Prevention:

LDL-C ≥190 mg/dL and age 20 to 75 years: High-intensity therapy: 80 mg once daily; if unable to tolerate, may reduce dose to 40 mg once daily

Diabetes, age 40 to 75 years, and an estimated 10-year ASCVD risk <7.5%: Moderate-intensity therapy: 10 to 20 mg once daily

Diabetes, age 40 to 75 years, and an estimated 10-year ASCVD risk ≥7.5%: High-intensity therapy: 80 mg once daily; if unable to tolerate, may reduce dose to 40 mg once daily

LDL-C 70 to 189 mg/dL, age 40 to 75 years and an estimated 10-year ASCVD risk ≥7.5%: Moderate- to high-intensity therapy: 10 to 80 mg once daily

Secondary prevention:

Patient has clinical ASCVD (eg, coronary heart disease, stroke/TIA, or peripheral arterial disease presumed to be of atherosclerotic origin) or is post-CABG (AHA [Kulik 2015]) and:

Age ≤75 years: High-intensity therapy: 80 mg once daily; if unable to tolerate, may reduce dose to 40 mg once daily

Age >75 years: Moderate- to high-intensity therapy: 10 to 80 mg once daily (ACC/AHA [Grundy 2018]); if a moderate-intensity dose (10 to 20 mg once daily) is started and tolerated, increase to a high-intensity dose (40 to 80 mg once daily) within 3 months (Rosenson 2019).

Not a candidate for high-intensity therapy: Moderate-intensity therapy: 10 to 20 mg once daily

US Preventive Services Task Force Recommendations (USPSTF 2016): Age 40 to 75 years, no history of CVD, with ≥1 CVD risk factor (dyslipidemia, diabetes, hypertension, or smoking), and calculated 10-year CVD event risk of ≥10%:

Primary prevention:

Moderate-intensity therapy: 10 to 20 mg once daily

Note: These recommendations do not pertain to patients with very high CVD risk factors (eg, LDL >190 mg/dL, familial hypercholesterolemia; were excluded from primary prevention trials); use clinical judgment in the treatment of these patients. In patients with a calculated 10-year CVD event risk of 7.5% to 10%, may consider use of a statin based on patient characteristics.

Cardiac risk reduction for non-cardiac surgery (off-label use): Oral: 20 mg once daily for 45 days; surgical intervention (vascular surgery) was performed during this period but not earlier than 2 weeks after therapy initiation (Durazzo 2004)

Noncardioembolic stroke/TIA (off-label use): Oral: Initial: 80 mg once daily; adjust based on patient tolerability (Amarenco 2006). Also consider the ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Grundy 2018]; ACC/AHA [Stone 2013]).

Dosage adjustment for atorvastatin with concomitant medications:

Boceprevir, nelfinavir: Use lowest effective atorvastatin dose (not to exceed 40 mg daily)

Clarithromycin, itraconazole, fosamprenavir, ritonavir (plus darunavir, fosamprenavir, or saquinavir): Use lowest effective atorvastatin dose (not to exceed 20 mg daily)

Lomitapide: Consider atorvastatin dose reduction (per lomitapide manufacturer).

Dosing: Geriatric

Refer to adult dosing.

Dosing: Renal Impairment: Adult

No dosage adjustment necessary.

Dialysis: Due to the high protein binding, atorvastatin is not expected to be cleared by dialysis (not studied)

Dosing: Hepatic Impairment: Adult

Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.

Dosing: Adjustment for Toxicity: Adult

Severe muscle symptoms or fatigue: Promptly discontinue use; evaluate CPK, creatinine, and urinalysis for myoglobinuria (ACC/AHA [Stone 2013]).

Mild to moderate muscle symptoms: Discontinue use until symptoms can be evaluated; evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution, resume the original or lower dose of atorvastatin. If muscle symptoms recur, discontinue atorvastatin use. After muscle symptom resolution, may then use a low dose of a different statin; gradually increase if tolerated. In the absence of continued statin use, if muscle symptoms or elevated CPK continues after 2 months, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (ACC/AHA [Stone 2013]).

Dosing: Pediatric

Dosage should be individualized according to the baseline LDL-C level, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks.

Heterozygous familial and nonfamilial hypercholesterolemia:

Note: Begin treatment if after adequate trial (6 to 12 months) of intensive lifestyle modification emphasizing body weight normalization and diet, the following are present (AACE [Jellinger 2017]):

LDL-C ≥190 mg/dL or

LDL-C remains ≥160 mg/dL and 2 or more cardiovascular risk factors: family history of premature atherosclerotic cardiovascular disease (<55 years of age); overweight; obesity; or other elements of insulin resistance syndrome or

LDL-C ≥130 mg/dL and diabetes mellitus (Daniels 2008; NHLBI 2011)

Children 6 to 10 years of age (Tanner stage I): Limited data available: Oral: Initial: 5 mg once daily; if target LDL-C not achieved after 4 weeks, may increase incrementally by doubling dose (10 mg/day, 20 mg/day) at monthly intervals until target LDL-C; usual maximum daily dose: 40 mg/day; however, in some cases doses up to 80 mg/day have been used; dosing based on a long-term trial (3 years) of 272 patients (age range: 6 to 15 years); doses of 80 mg/day were used in 12 patients <10 years of age; over the 3 year study duration, similar efficacy was observed without growth or maturation impairment (Langslet 2016).

Children and Adolescents 10 to 17 years: Oral: Initial: 10 mg once daily; if target LDL-C not achieved after 4 weeks, may increase incrementally by doubling dose (20 mg/day, 40 mg/day) at monthly intervals until target LDL-C up to a maximum daily dose: 80 mg/day (Langslet 2016)

Hyperlipidemia: Limited data available: Children and Adolescents 10 to 17 years (males and postmenarchal females): Oral: Initial: 10 mg once daily; if LDL-C target not achieved after 1 to 3 months, may increase to meet target LDL-C; in pediatric patients with heterozygous familial hypercholesterolemia, a maximum titrated dose based upon LDL response: 80 mg/day was used (Langslet 2016; McCrindle 2007; NHLBI 2011)

Prevention of graft coronary artery disease: Limited data available: Children and Adolescents: Oral: 0.2 mg/kg/day rounded to nearest 2.5 mg increment; not to exceed age-appropriate doses (Chin 2002; Chin 2008)

Dosage adjustment for atorvastatin with concomitant medications: There are no recommendations in the manufacturer’s labeling for patients <18 years. In adolescents ≥18 years, the following have been suggested:

Boceprevir, nelfinavir: Use lowest effective atorvastatin dose; maximum daily dose: 40 mg/day

Clarithromycin, itraconazole, fosamprenavir, ritonavir (plus darunavir, fosamprenavir, or saquinavir): Use lowest effective atorvastatin dose; maximum daily dose: 20 mg/day

Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥10 years and Adolescents: Discontinue use until symptoms can be evaluated; check CPK level; based on experience in adult patients, also evaluate patient for conditions that may increase the risk for muscle symptoms (eg, hypothyroidism, reduced renal or hepatic function, rheumatologic disorders such as polymyalgia rheumatica, steroid myopathy, vitamin D deficiency, or primary muscle diseases). Upon resolution (symptoms and any associated CPK abnormalities), resume the original or consider a lower dose of atorvastatin and retitrate. If muscle symptoms recur, discontinue atorvastatin use. After muscle symptom resolution, may then reinitiate a different statin at an initial low dose; gradually increase if tolerated. Based on experience in adult patients, if muscle symptoms or elevated CPK persists for 2 months in the absence of continued statin use, consider other causes of muscle symptoms. If determined to be due to another condition aside from statin use, may resume statin therapy at the original dose (NHLBI 2011; Stone 2013)

Dosing: Renal Impairment: Pediatric

Children ≥10 years and Adolescents: Because atorvastatin does not undergo significant renal excretion, dose modification is not necessary.

Dialysis: Due to the high protein binding, atorvastatin is not expected to be cleared by dialysis (has not been studied).

Dosing: Hepatic Impairment: Pediatric

Children ≥10 years and Adolescents: Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.

Use: Labeled Indications

Dyslipidemias:

Dysbetalipoproteinemia: Treatment of primary dysbetalipoproteinemia (Fredrickson type III).

Heterozygous familial and nonfamilial hypercholesterolemia and mixed dyslipidemia: To reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), and triglyceride levels, and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson type IIa and IIb).

Heterozygous familial hypercholesterolemia: To reduce total-C, LDL-C, and apo B levels in pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia with LDL-C ≥190 mg/dL, LDL-C ≥160 mg/dL with positive family history of premature cardiovascular disease (CVD), or LDL-C ≥160 mg/dL with two or more other CVD risk factors.

Homozygous familial hypercholesterolemia: To reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (eg, LDL apheresis) or if such treatments are unavailable.

Hypertriglyceridemia: Treatment of elevated serum triglyceride levels (Fredrickson type IV).

Limitations of use: Has not been studied in conditions where the major lipid abnormality is elevation of chylomicrons (Fredrickson types I and V).

Prevention of cardiovascular disease (CVD):

Primary prevention of cardiovascular disease (high-risk for CVD): To reduce the risk of MI, stroke, and revascularization procedures and angina in adult patients without clinically evident coronary heart disease (CHD) who have multiple CHD risk factors (eg, age, smoking, hypertension, low high-density lipoprotein cholesterol [HDL-C], family history of early CHD); to reduce the risk of MI and stroke in patients with type 2 diabetes and without clinically evident CHD but with multiple risk factors for CHD (eg, retinopathy, albuminuria, smoking, hypertension).

Secondary prevention of cardiovascular disease: To reduce the risk of nonfatal MI, fatal and nonfatal stroke, revascularization procedures, hospitalization for decompensated heart failure, and angina in patients with clinically evident CHD.

Use: Off-Label: Adult

  Cardiac risk reduction for noncardiac surgery (perioperative therapy)Level of Evidence [B, G]

Data from a prospective, randomized, placebo-controlled, double-blind clinical trial supports the perioperative initiation of atorvastatin for reduction in cardiovascular events in patients who must undergo non-cardiac (vascular) surgery Ref. Additional trials may be necessary to further define the role of atorvastatin in this setting.

Based on the 2014 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery, perioperative initiation of statins is reasonable for patients undergoing vascular surgery and may be considered in patients with clinical indications according to guideline-directed medical therapy who are undergoing elevated risk procedures. In patients undergoing non-cardiac surgery who are currently receiving a statin, the statin should be continued.

  Noncardioembolic stroke/TIA (secondary prevention)Level of Evidence [A, G]

HMG-CoA reductase inhibitors have demonstrated reductions in the risk of stroke in patients with CAD and those considered to be high-risk of cardiovascular events. Data from a randomized, double-blind, placebo-controlled trial in patients with an LDL-C concentration between 100-190 mg/dL without known CAD who had suffered either a noncardioembolic stroke or TIA within the prior 6 months supports the use of atorvastatin in this setting. Patients randomized to atorvastatin experienced a lower incidence of stroke, the primary endpoint, and a 5-year absolute reduction in the incidence of cardiovascular events compared to those randomized to placebo Ref.

Based on the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the prevention of stroke in patients with stroke and transient ischemic attack, statin therapy with intensive lipid-lowering effects is recommended to reduce the risk of recurrent stroke and future cardiovascular events in patients with ischemic stroke or TIA presumed to be of atherosclerotic origin who have an LDL-C concentration ≥100 mg/dL (with or without evidence for other clinical atherosclerotic cardiovascular disease [ASCVD]) or who have an LDL-C concentration <100 mg/dL (without evidence for other clinical ASCVD).

Level of Evidence Definitions
  Level of Evidence Scale
Clinical Practice Guidelines

Coronary Artery Bypass Graft Surgery:

“AHA Scientific Statement, Secondary Prevention After Coronary Artery Bypass Graft Surgery,” February 2015

AHA/ACC/HRS, “2014 AHA/ACC/HRS Guideline for the Management of Patients with Atrial Fibrillation,” March 2014

Diabetes Mellitus:

AACE/ACE, “Consensus Statement on the Comprehensive Type 2 Diabetes Management Algorithm- 2019 Executive Summary,” January 2019

American Diabetes Association, “Standards of Medical Care in Diabetes – 2019,” January 2019

Diabetes Canada, “Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada,” 2018

Dyslipidemia:

AHA/ACC, “Guideline on the Management of Blood Cholesterol,” November 2018

AACE/ACE, “Guidelines for Management of Dyslipidemia and Prevention of Cardiovascular Disease,” April 2017

ACC/AHA, “2013 ACC/AHA Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults,” November 2013

Canadian Cardiovascular Society, “2012 Update of the Canadian Cardiovascular Society Guidelines for the Diagnosis and Treatment of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult,” 2012

NLA, “National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia” Part 1: April 2015; Part 2: December 2015

The Kidney Disease: Improving Global Outcomes (KDIGO), “Lipid Management in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2013 Clinical Practice Guideline,” December 2013

The Endocrine Society, “Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline,” September 2012

Ischemic Heart Disease:

ACC/AHA/AATS/PCNA/SCAI/STS, “2014 Focused Update of the Guideline for the Diagnosis and Management of Patients with Stable Ischemic Heart Disease,” July 2014

ACCF/AHA/ACP/AATS/PCNA/SCAI/STS, “2012 Guideline for the Diagnosis and Management of Patients with Stable Ischemic Heart Disease,” November 2012

Non-ST-Elevation Acute Coronary Syndromes:

AHA/ACC, “2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes,” September 2014.

Percutaneous Coronary Intervention:

“2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention,” November 2011

ST-Elevation Myocardial Infarction:

ACCF/AHA, “2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction,” December 2012.

Stroke:

AHA/ASA, “Guidelines for Prevention of Stroke in Patients with Stroke and Transient Ischemic Attack,” May 2014.

“Guidelines for the Primary Prevention of Stroke,” December 2010

Surgery:

ACC/AHA, “2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management of Patients Undergoing Noncardiac Surgery,” August 2014.

Administration: Oral

Administer with or without food; may take without regard to time of day. The manufacturer’s labeling states tablets should not be broken; however, available data do not indicate any safety or efficacy concerns with this practice.

Administration: Pediatric

Oral: May be taken without regard to meals or time of day. Swallow whole; do not break, crush, or chew.

Dietary Considerations

Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 3 to 6 months and the diet should be continued during drug therapy. Atorvastatin serum concentration may be increased when taken with grapefruit juice; avoid concurrent intake of large quantities (>1 quart/day).

Red yeast rice contains variable amounts of several compounds that are structurally similar to HMG-CoA reductase inhibitors, primarily monacolin K (or mevinolin) which is structurally identical to lovastatin; concurrent use of red yeast rice with HMG-CoA reductase inhibitors may increase the incidence of adverse and toxic effects (Lapi 2008; Smith 2003).

Storage/Stability

Store at 20°C to 25°C (68°F to 77°F).

Medication Patient Education with HCAHPS Considerations

• Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?)

• Patient may experience diarrhea, nausea, insomnia, rhinitis, or pharyngitis. Have patient report immediately to prescriber signs of a urinary tract infection (hematuria, burning or painful urination, polyuria, fever, lower abdominal pain, or pelvic pain), signs of severe cerebrovascular disease (change in strength on one side is greater than the other, difficulty speaking or thinking, change in balance, or vision changes), signs of liver problems (dark urine, fatigue, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or jaundice), urinary retention, change in amount of urine passed, difficulty swallowing, severe loss of strength and energy, confusion, memory impairment, severe joint pain, severe muscle pain, severe muscle tenderness, or severe muscle weakness (HCAHPS).

• Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions.

Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for healthcare professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience and judgment in diagnosing, treating and advising patients.

Medication Safety Issues
  Sound-alike/look-alike issues:
Contraindications

Hypersensitivity to atorvastatin or any component of the formulation; active liver disease; unexplained persistent elevations of serum transaminases; pregnancy; breastfeeding

Canadian labeling: Additional contraindications (not in US labeling): Concurrent therapy with glecaprevir/pibrentasvir

Warnings/Precautions

Concerns related to adverse effects:

• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported.

• Hepatotoxicity: Persistent elevations in serum transaminases have been reported; upon dose reduction, drug interruption, or discontinuation, transaminase levels returned to or near pretreatment levels. Postmarketing reports of fatal and nonfatal hepatic failure have been reported and are rare. If serious hepatotoxicity with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, interrupt therapy promptly. If an alternate etiology is not identified, do not restart atorvastatin. Liver enzyme tests should be obtained at baseline and as clinically indicated and if signs/symptoms of liver injury occur. Ethanol may enhance the potential of adverse hepatic effects; instruct patients to avoid excessive ethanol consumption.

• Myopathy/rhabdomyolysis: Rhabdomyolysis with acute renal failure secondary to myoglobinuria and/or myopathy has been reported; patients should be monitored closely. This risk is dose-related and is increased with concurrent use of strong CYP3A4 inhibitors (eg, clarithromycin, itraconazole, protease inhibitors), cyclosporine, fibric acid derivatives (eg, gemfibrozil), or niacin (doses ≥1 g/day); if concurrent use is warranted, consider lower starting and maintenance doses of atorvastatin. Use caution in patients with inadequately treated hypothyroidism, and those taking other drugs associated with myopathy (eg, colchicine); these patients are predisposed to myopathy. Immune-mediated necrotizing myopathy (IMNM) associated with HMG-CoA reductase inhibitors use has also been reported. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine, particularly if accompanied by malaise or fever. Discontinue therapy if markedly elevated CPK levels occur or myopathy is diagnosed/suspected.

Disease-related concerns:

• Hepatic impairment and/or ethanol use: Use with caution in patients who consume large amounts of ethanol or have a history of liver disease; use is contraindicated in patients with active liver disease or unexplained persistent elevations of serum transaminases.

• Renal impairment: Use with caution in patients with renal impairment; these patients are predisposed to myopathy.

• Stroke: Patients with recent stroke or TIA receiving long-term therapy with high-dose (ie, 80 mg/day) atorvastatin may be at increased risk for hemorrhagic stroke (SPARCL Investigators 2006). A subsequent post-hoc analysis demonstrated that patients with lacunar or hemorrhagic stroke may be at higher risk of hemorrhagic stroke; however, this finding was determined to be hypothesis generating. The overall benefit of treatment with atorvastatin (ie, reduced risk of stroke and cardiovascular events) in this population seems to outweigh the increased risk of hemorrhagic stroke if one truly exists (Goldstein 2008).

Concurrent drug therapy issues:

• Drug-drug interactions: Potentially significant interactions may exist, requiring dose or frequency adjustment, additional monitoring, and/or selection of alternative therapy. Consult drug interactions database for more detailed information.

Special populations:

• Elderly: Use with caution in patients with advanced age, these patients are predisposed to myopathy.

• Surgical patients: The manufacturer recommends temporary discontinuation for elective major surgery, acute medical or surgical conditions, or in any patient experiencing an acute, serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis, hypotension, trauma, uncontrolled seizures, severe metabolic, endocrine, or electrolyte disorders). Based on current research and clinical guidelines, HMG-CoA reductase inhibitors should be continued in the perioperative period for noncardiac and cardiac surgery (ACC/AHA [Fleisher 2014]; ACC/AHA [Hillis 2011]). Perioperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.

Dosage form specific issues:

• Polysorbate 80: Some dosage forms may contain polysorbate 80 (also known as Tweens). Hypersensitivity reactions, usually a delayed reaction, have been reported following exposure to pharmaceutical products containing polysorbate 80 in certain individuals (Isaksson 2002; Lucente 2000; Shelley 1995).

Other warnings/precautions:

• Appropriate use: Secondary causes of hyperlipidemia should be ruled out prior to therapy. Atorvastatin has not been studied when the primary lipid abnormality is chylomicron elevation (Fredrickson types I and V).

Geriatric Considerations

Effective and well tolerated in the elderly, although age ≥65 years is a risk factor for myopathy. The definition of and, therefore, when to treat hyperlipidemia in the elderly is a controversial issue. According to the ACC/AHA, high-intensity statin doses are indicated for patients <75 years of age with existing clinical atherosclerotic cardiovascular disease (ASCVD); patients without clinical ASCVD if LDL-C is >190 mg/dL; patients without clinical ASCVD who are 40-75 years with type 1 or type 2 diabetes and with an estimated 10-year ASCVD risk ≥7.5%. Patients 40-75 years with a 10-year ASCVD risk >7.5% are candidates for moderate- to high-intensity statin therapy. Patients >75 years with existing clinical ASCVD are candidates for moderate-intensity statin doses. There are no data or recommendations on managing patients >75 years without clinical ASCVD who have type 1 or 2 diabetes or with a 10-year risk of ASCVD >7.5% (with or without diabetes) (Stone 2013). It is the authors’ belief that pharmacologic treatment be reserved for those whom the benefits of treatment are believed to outweigh the potential adverse effects, drug interactions, and cost of treatment.

Pregnancy Considerations

Atorvastatin is contraindicated in pregnant females or those who may become pregnant.

There are reports of congenital anomalies following maternal use of HMG-CoA reductase inhibitors in pregnancy; however, maternal disease, differences in specific agents used, and the low rates of exposure limit the interpretation of the available data (Godfrey 2012; Lecarpentier 2012). Cholesterol biosynthesis may be important in fetal development; serum cholesterol and triglycerides increase normally during pregnancy. The discontinuation of lipid-lowering medications temporarily during pregnancy is not expected to have significant impact on the long-term outcomes of primary hypercholesterolemia treatment.

Atorvastatin should be discontinued immediately if an unplanned pregnancy occurs during treatment.

Adequate contraception is recommended if an HMG-CoA reductase inhibitor is required in females of reproductive potential. Females planning a pregnancy should discontinue the HMG-CoA reductase inhibitor 1 to 2 months prior to attempting to conceive (AHA/ACC [Grundy 2018]).

Breast-Feeding Considerations

Use is contraindicated in breastfeeding women.

It is not known if atorvastatin is present in breast milk.

Briggs’ Drugs in Pregnancy & Lactation
Adverse Reactions

>10%:

Gastrointestinal: Diarrhea (7% to 14%)

Neuromuscular & skeletal: Arthralgia (9% to 12%)

Respiratory: Nasopharyngitis (13%)

1% to 10%:

Cardiovascular: Hemorrhagic stroke (2%)

Central nervous system: Insomnia (5%), malaise (<2%), nightmares (<2%)

Dermatologic: Urticaria (<2%)

Endocrine & metabolic: Diabetes mellitus (6%), hyperglycemia (<2%)

Gastrointestinal: Nausea (7%), dyspepsia (6%), abdominal distress (<2%), cholestasis (<2%), eructation (<2%), flatulence (<2%)

Genitourinary: Urinary tract infection (7% to 8%), urine abnormality (white blood cells positive in urine: <2%)

Hepatic: Increased serum transaminases (≤2%), abnormal hepatic function tests (<2%), hepatitis (<2%), increased serum alkaline phosphatase (<2%)

Neuromuscular & skeletal: Limb pain (9%), myalgia (4% to 8%), musculoskeletal pain (5%), muscle spasm (4% to 5%), increased creatine phosphokinase (<2%), joint swelling (<2%), muscle fatigue (<2%), neck pain (<2%)

Ophthalmic: Blurred vision (<2%)

Otic: Tinnitus (<2%)

Respiratory: Pharyngolaryngeal pain (3% to 4%), epistaxis (<2%)

Miscellaneous: Fever (<2%)

Frequency not defined: Central nervous system: Myasthenia

<1%, postmarketing, and/or case reports: Abdominal pain, alopecia, amnesia (reversible), anaphylaxis, anemia, angioedema, anorexia, back pain, bullous rash, chest pain, cognitive dysfunction (reversible), confusion (reversible), cystitis (interstitial; Huang 2015), depression, dizziness, dysgeusia, elevated glycosylated hemoglobin (HbA1c), erythema multiforme, fatigue, gynecomastia, hepatic failure, hypoesthesia, increased serum glucose, interstitial pulmonary disease, jaundice, memory impairment (reversible), myopathy, myositis, pancreatitis, paresthesia, peripheral edema, peripheral neuropathy, pruritus, rhabdomyolysis, rupture of tendon, Stevens-Johnson syndrome, thrombocytopenia, toxic epidermal necrolysis, vomiting, weight gain

Allergy and Idiosyncratic Reactions
Metabolism/Transport Effects

Substrate of CYP3A4 (major), OATP1B1/1B3 (SLCO1B1/1B3), P-glycoprotein/ABCB1; Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential

Drug Interactions 

Acipimox: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Aliskiren: AtorvaSTATin may increase the serum concentration of Aliskiren. Risk C: Monitor therapy

Amiodarone: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Antihepaciviral Combination Products: May increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

Aprepitant: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Asunaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Azithromycin (Systemic): May enhance the myopathic (rhabdomyolysis) effect of AtorvaSTATin. Risk C: Monitor therapy

Bexarotene (Systemic): May decrease the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Bezafibrate: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Bezafibrate may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). More specifically, bezafibrate may increase the serum concentration of fluvastatin Management: Monitor patients closely for myopathy with concomitant use of bezafibrate and HMG-CoA reductase inhibitors. Concomitant use is contraindicated in patients predisposed to myopathy and alternative therapy should be considered. Risk D: Consider therapy modification

Bosentan: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Cimetidine: AtorvaSTATin may enhance the adverse/toxic effect of Cimetidine. Specifically, there is a theoretical potential for enhanced effects on reducing endogenous steroid activity.Risk C: Monitor therapy

Ciprofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid the use of HMG-CoA reductase inhibitors and ciprofibrate if possible. If concomitant therapy is considered, benefits should be carefully weighed against the risks, and patients should be monitored closely for signs/symptoms of muscle toxicity. Risk D: Consider therapy modification

Clarithromycin: May increase the serum concentration of AtorvaSTATin. Management: Limit atorvastatin to a maximum dose of 20 mg/day (for adults) when used with clarithromycin. If this combination is used, monitor patients more closely for evidence of atorvastatin toxicity. Risk D: Consider therapy modification

Clofazimine: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Cobicistat: May increase the serum concentration of AtorvaSTATin. Management: Avoid the combined use of atorvastatin with atazanavir/cobicistat. Atorvastatin dose should not exceed 20 mg daily when combined with other cobicistat-containing regimens. Risk D: Consider therapy modification

Colchicine: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Colchicine may increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk D: Consider therapy modification

Conivaptan: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination

CycloSPORINE (Systemic): May increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

CYP3A4 Inducers (Moderate): May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

CYP3A4 Inducers (Strong): May increase the metabolism of CYP3A4 Substrates (High risk with Inducers). Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Risk D: Consider therapy modification

CYP3A4 Inhibitors (Moderate): May decrease the metabolism of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

CYP3A4 Inhibitors (Strong): May decrease the metabolism of CYP3A4 Substrates (High risk with Inhibitors). Risk D: Consider therapy modification

Cyproterone: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid use of statins metabolized by CYP3A4 (eg, simvastatin) and consider avoiding fluvastatin as well in patients receiving high dose cyproterone (300 mg/day). Consider use of pravastatin, rosuvastatin, or pitavastatin if statin therapy is needed.Risk D: Consider therapy modification

Dabigatran Etexilate: AtorvaSTATin may decrease the serum concentration of Dabigatran Etexilate. Risk C: Monitor therapy

Dabrafenib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Seek alternatives to the CYP3A4 substrate when possible. If concomitant therapy cannot be avoided, monitor clinical effects of the substrate closely (particularly therapeutic effects). Risk D: Consider therapy modification

Daclatasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Danazol: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Concurrent use of simvastatin with danazol is contraindicated. Do not exceed 20 mg per day of lovastatin if combined with danazol. Fluvastatin, pravastatin, and rosuvastatin may pose lower risk. Risk D: Consider therapy modification

DAPTOmycin: HMG-CoA Reductase Inhibitors (Statins) may enhance the adverse/toxic effect of DAPTOmycin. Specifically, the risk of skeletal muscle toxicity may be increased. Management: Consider temporarily stopping HMG-CoA reductase inhibitor therapy prior to daptomycin. If used together, regular (i.e., at least weekly) monitoring of CPK concentrations is recommended. Risk D: Consider therapy modification

Deferasirox: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Digoxin: AtorvaSTATin may increase the serum concentration of Digoxin. Risk C: Monitor therapy

DilTIAZem: AtorvaSTATin may increase the serum concentration of DilTIAZem. DilTIAZem may increase the serum concentration of AtorvaSTATin. Management: Consider using lower atorvastatin doses when used together with diltiazem. Risk D: Consider therapy modification

Dronedarone: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Duvelisib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Efavirenz: May decrease the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Elbasvir: May increase the serum concentration of AtorvaSTATin. Management: Limit the dose of atorvastatin to a maximum of 20 mg/day when used together with elbasvir and grazoprevir. Monitor closely for evidence of statin-related toxicities such as myalgia or myopathy. Risk D: Consider therapy modification

Eltrombopag: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates. Risk C: Monitor therapy

Enzalutamide: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Concurrent use of enzalutamide with CYP3A4 substrates that have a narrow therapeutic index should be avoided. Use of enzalutamide and any other CYP3A4 substrate should be performed with caution and close monitoring. Risk D: Consider therapy modification

Erythromycin (Systemic): May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Etravirine: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). This applies to atorvastatin, lovastatin and simvastatin. Conversely, levels of fluvastatin may be increased. Management: Dose adjustment of the HMG-CoA reductase inhibitor may be warranted. No interaction is expected with rosuvastatin, pravastatin, or pitavastatin.Risk C: Monitor therapy

Fenofibrate and Derivatives: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Fluconazole: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Fosaprepitant: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Fosnetupitant: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Fosphenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk D: Consider therapy modification

Fusidic Acid (Systemic): May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for muscle toxicities, including rhabdomyolysis may be significantly increased. Management: Avoid concurrent use whenever possible. Use is listed as contraindicated in product characteristic summaries in several countries, although UK labeling suggests that use could be considered under exceptional circumstances and with close supervision. Risk X: Avoid combination

Fusidic Acid (Systemic): May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination

Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of AtorvaSTATin. Gemfibrozil may increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

Glecaprevir and Pibrentasvir: May increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

Grapefruit Juice: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Avoid concurrent use of GFJ with lovastatin or simvastatin. Avoid high quantities of GFJ with atorvastatin. Consider using a lower statin dose or a statin that is less likely to interact when possible. Risk D: Consider therapy modification

Grazoprevir: May increase the serum concentration of AtorvaSTATin. Management: Limit the dose of atorvastatin to a maximum of 20 mg/day when used together with elbasvir and grazoprevir. Monitor closely for evidence of statin-related toxicities such as myalgia or myopathy. Risk D: Consider therapy modification

Idelalisib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk X: Avoid combination

Itraconazole: May increase the serum concentration of AtorvaSTATin. Management: Limit atorvastatin to a maximum adult dose of 20 mg/day in patients receiving itraconazole. Assess clinical response to ensure that the lowest necessary dose of atorvastatin is used. Consider use of fluva-, rosuva-, pitava-, or pravastatin when possible. Risk D: Consider therapy modification

Ivosidenib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Ketoconazole (Systemic): AtorvaSTATin may enhance the adverse/toxic effect of Ketoconazole (Systemic). Specifically, there is a theoretical potential for additive effects on reducing endogenous steroid concentrations. Ketoconazole (Systemic) may increase the serum concentration of AtorvaSTATin. Management: Administer ketoconazole with atorvastatin cautiously, and monitor for toxic effects of atorvastatin (e.g., myalgia, rhabdomyolysis, liver function test abnormalities). Consider use of fluva-, rosuva-, pitava-, or pravastatin when possible. Risk D: Consider therapy modification

Lanthanum: HMG-CoA Reductase Inhibitors (Statins) may decrease the serum concentration of Lanthanum. Management: Administer HMG-CoA reductase inhibitors at least two hours before or after lanthanum. Risk D: Consider therapy modification

Larotrectinib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Letermovir: May increase the serum concentration of AtorvaSTATin. Management: Limit the atorvastatin dose to 20 mg daily when combined with letermovir. When letermovir is coadministered with cyclosporine, the use of atorvastatin (at any dose) is not recommended. Risk D: Consider therapy modification

Lorlatinib: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Avoid concurrent use of lorlatinib with any CYP3A4 substrates for which a minimal decrease in serum concentrations of the CYP3A4 substrate could lead to therapeutic failure and serious clinical consequences. Risk D: Consider therapy modification

Midazolam: AtorvaSTATin may increase the serum concentration of Midazolam. Risk C: Monitor therapy

MiFEPRIStone: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Minimize doses of CYP3A4 substrates, and monitor for increased concentrations/toxicity, during and 2 weeks following treatment with mifepristone. Avoid cyclosporine, dihydroergotamine, ergotamine, fentanyl, pimozide, quinidine, sirolimus, and tacrolimus. Risk D: Consider therapy modification

Mitotane: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Doses of CYP3A4 substrates may need to be adjusted substantially when used in patients being treated with mitotane. Risk D: Consider therapy modification

Netupitant: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Niacinamide: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Palbociclib: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Risk C: Monitor therapy

PAZOPanib: AtorvaSTATin may enhance the hepatotoxic effect of PAZOPanib. AtorvaSTATin may increase the serum concentration of PAZOPanib. Risk X: Avoid combination

P-glycoprotein/ABCB1 Inhibitors: May increase the serum concentration of P-glycoprotein/ABCB1 Substrates. P-glycoprotein inhibitors may also enhance the distribution of p-glycoprotein substrates to specific cells/tissues/organs where p-glycoprotein is present in large amounts (e.g., brain, T-lymphocytes, testes, etc.). Risk C: Monitor therapy

Phenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Risk D: Consider therapy modification

Pitolisant: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Combined use of pitolisant with a CYP3A4 substrate that has a narrow therapeutic index should be avoided. Other CYP3A4 substrates should be monitored more closely when used with pitolisant. Risk D: Consider therapy modification

Posaconazole: May increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

Protease Inhibitors: May increase the serum concentration of AtorvaSTATin. Management: See full monograph for recommended dose limits. Avoid atorvastatin with tipranavir/ritonavir.Risk D: Consider therapy modification

QuiNINE: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Consider using a lower starting dose and lower maintenance/maximum doses of atorvastatin, simvastatin, or lovastatin when used together with quinine. Risk D: Consider therapy modification

Raltegravir: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Risk C: Monitor therapy

Ranolazine: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Risk X: Avoid combination

Repaglinide: HMG-CoA Reductase Inhibitors (Statins) may increase the serum concentration of Repaglinide. Risk C: Monitor therapy

Rifamycin Derivatives: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Consider use of noninteracting antilipemic agents (note: pitavastatin concentrations may increase with rifamycin treatment). Monitor for altered HMG-CoA reductase inhibitor effects. Rifabutin and fluvastatin, or possibly pravastatin, may pose lower risk. Risk D: Consider therapy modification

Rupatadine: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Specifically, the risk for increased CPK and/or other muscle toxicities may be increased.Risk C: Monitor therapy

Sarilumab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Siltuximab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Simeprevir: May increase the serum concentration of AtorvaSTATin. Management: The maximum atorvastatin dose should not exceed 40 mg/day with concurrent use of simeprevir, and use of the lowest necessary atorvastatin dose is recommended. Risk D: Consider therapy modification

Spironolactone: AtorvaSTATin may enhance the adverse/toxic effect of Spironolactone. Specifically, there is a theoretical potential for enhanced effects on reducing endogenous steroid activity. Risk C: Monitor therapy

St John’s Wort: May increase the metabolism of HMG-CoA Reductase Inhibitors (Statins). Management: Consider avoiding the concomitant administration of St Johns Wort with interacting HMG-CoA reductase inhibitors in order to avoid the potential for decreased antilipemic effects. Monitor for decreased effects during concomitant therapy. Risk D: Consider therapy modification

St John’s Wort: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Management: Consider an alternative for one of the interacting drugs. Some combinations may be specifically contraindicated. Consult appropriate manufacturer labeling. Risk D: Consider therapy modification

Stiripentol: May increase the serum concentration of CYP3A4 Substrates (High risk with Inhibitors). Management: Use of stiripentol with CYP3A4 substrates that are considered to have a narrow therapeutic index should be avoided due to the increased risk for adverse effects and toxicity. Any CYP3A4 substrate used with stiripentol requires closer monitoring. Risk D: Consider therapy modification

Telithromycin: May increase the serum concentration of AtorvaSTATin. Management: Consider limiting atorvastatin to a max (adult) dose of 20 mg/day when used with telithromycin. Although not a specific recommendation in atorvastatin labeling, this is consistent with dosing for other strong CYP3A4 inhibitors, including clarithromycin. Risk D: Consider therapy modification

Teriflunomide: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates. Risk C: Monitor therapy

Ticagrelor: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Tipranavir: May increase the serum concentration of AtorvaSTATin. Risk X: Avoid combination

Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates (High risk with Inducers). Risk C: Monitor therapy

Tolvaptan: May increase the serum concentration of OATP1B1/1B3 (SLCO1B1/1B3) Substrates. Risk D: Consider therapy modification

Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Risk C: Monitor therapy

Velpatasvir: May increase the serum concentration of AtorvaSTATin. Risk C: Monitor therapy

Verapamil: AtorvaSTATin may increase the serum concentration of Verapamil. Verapamil may increase the serum concentration of AtorvaSTATin. Management: Consider using lower atorvastatin doses when used together with verapamil. Risk D: Consider therapy modification

Voriconazole: May increase the serum concentration of AtorvaSTATin. Management: Monitor for toxic effects of atorvastatin (e.g., myalgia, rhabdomyolysis, liver function test abnormalities) during concomitant treatment, and reduce atorvastatin dose when possible. Consider use of fluva-, rosuva-, pitava-, or pravastatin when possible. Risk D: Consider therapy modification

Voxilaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest statin dose possible if combined with voxilaprevir and monitor patients for increased statin effects/toxicities. Avoid concomitant use of voxilaprevir with rosuvastatin or pitavastatin, and limit pravastatin doses to 40 mg daily. Risk D: Consider therapy modification

Food Interactions

Atorvastatin serum concentrations may be increased by grapefruit juice. Management: Avoid concurrent intake of large quantities of grapefruit juice (>1 quart/day).

Monitoring Parameters

ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Grundy 2018]; ACC/AHA [Stone 2013]):

Lipid panel (total cholesterol, HDL, LDL, triglycerides): Lipid profile (fasting or nonfasting) before initiating treatment. Fasting lipid profile should be rechecked 4 to 12 weeks after starting therapy and every 3 to 12 months thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.

Hepatic transaminase levels: Baseline measurement of hepatic transaminase levels (AST and ALT); measure AST, ALT, total bilirubin, and alkaline phosphatase if symptoms suggest hepatotoxicity (eg, unusual fatigue or weakness, loss of appetite, abdominal pain, dark-colored urine or yellowing of skin or sclera) during therapy.

CPK: CPK should not be routinely measured. Baseline CPK measurement is reasonable for some individuals (eg, family history of statin intolerance or muscle disease, clinical presentation, concomitant drug therapy that may increase risk of myopathy). May measure CPK in any patient with symptoms suggestive of myopathy (pain, tenderness, stiffness, cramping, weakness, or generalized fatigue).

Evaluate for new-onset diabetes mellitus during therapy; if diabetes develops, continue statin therapy and encourage adherence to a heart-healthy diet, physical activity, a healthy body weight, and tobacco cessation.

If patient develops a confusional state or memory impairment, may evaluate patient for nonstatin causes (eg, exposure to other drugs), systemic and neuropsychiatric causes, and the possibility of adverse effects associated with statin therapy.

Reference Range

Treatment goals: May vary depending on clinical condition, different clinical practice guidelines and expert opinion. Refer to clinical practice guidelines for specific treatment goals.

Advanced Practitioners Physical Assessment/Monitoring

Rule out secondary causes of hyperlipidemia prior to initiation. Assess other medicines patient may be taking; alternate therapy or dosage adjustments may be needed. Obtain liver enzyme tests prior to therapy and as needed. Obtain CPK when myopathy is considered or in high-risk patients. Follow-up with lipid panel within 2 to 4 weeks of initiation or titration.

Nursing Physical Assessment/Monitoring

Check ordered labs and report and abnormalities. Monitor for and educate patient to report signs and symptoms of myopathy (muscle pain, weakness, fatigue). Consider dietary assessment and plan for teaching.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Lipitor: 10 mg, 20 mg, 40 mg, 80 mg

Generic: 10 mg, 20 mg, 40 mg, 80 mg

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral:

Lipitor: 10 mg, 20 mg, 40 mg, 80 mg [contains POLYSORBATE 80]

Generic: 10 mg, 20 mg, 40 mg, 80 mg

Anatomic Therapeutic Chemical (ATC) Classification
  • C10AA05
Generic Available (US)

Yes

Pricing: US

Tablets (Atorvastatin Calcium Oral)

10 mg (per each): $3.85 – $7.50

20 mg (per each): $5.43 – $10.70

40 mg (per each): $5.49 – $10.70

80 mg (per each): $5.49 – $10.70

Tablets (Lipitor Oral)

10 mg (per each): $12.58

20 mg (per each): $17.94

40 mg (per each): $18.84

80 mg (per each): $17.94

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer’s AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Mechanism of Action

Inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol synthesis (reduces the production of mevalonic acid from HMG-CoA); this then results in a compensatory increase in the expression of LDL receptors on hepatocyte membranes and a stimulation of LDL catabolism. In addition to the ability of HMG-CoA reductase inhibitors to decrease levels of high-sensitivity C-reactive protein (hsCRP), they also possess pleiotropic properties including improved endothelial function, reduced inflammation at the site of the coronary plaque, inhibition of platelet aggregation, and anticoagulant effects (de Denus 2002; Ray 2005).

Pharmacodynamics/Kinetics

Onset of action: Initial changes: 3 to 5 days; Maximal reduction in plasma cholesterol and triglycerides: 2 to 4 weeks; LDL reduction: 10 mg/day: 39% (for each doubling of this dose, LDL is lowered approximately 6%)

Absorption: Oral: Rapidly absorbed; extensive first-pass metabolism in GI mucosa and liver

Distribution: Vd: ~381 L

Protein binding: ≥98%

Metabolism: Hepatic via CYP3A4; forms active ortho- and parahydroxylated derivatives and an inactive beta-oxidation product; plasma concentrations are elevated in patients with chronic alcoholic liver disease and Childs-Pugh class A and B liver disease

Bioavailability: ~14% (parent drug); ~30% (parent drug and equipotent metabolites)

Half-life elimination: Parent drug: ~14 hours; Equipotent metabolites: 20 to 30 hours

Time to peak, serum: 1 to 2 hours

Excretion: Bile (following hepatic and/or extra-hepatic metabolism; does not appear to undergo enterohepatic recirculation); urine (<2% as unchanged drug)

Pharmacodynamics/Kinetics: Additional Considerations

Hepatic function impairment: Cmax and AUC are each 4-fold greater in patients with Child-Pugh class A disease; Cmax and AUC are ~16-fold and 11-fold increased, respectively, in patients with Child-Pugh class B disease.

Geriatric: Plasma concentrations are higher (~40% for Cmax and 30% for AUC).

Gender: Plasma concentrations in women differ from those in men (~ 20% higher for Cmax and 10% lower for AUC)

Local Anesthetic/Vasoconstrictor Precautions

No information available to require special precautions

Effects on Dental Treatment

Key adverse event(s) related to dental treatment: Assess unusual presentations of muscle weakness or myopathy resulting from lipid therapy such as patient having a difficult time brushing teeth or weakness with chewing. Refer patient back to their physician for evaluation and adjustment of lipid therapy.

Effects on Bleeding

No information available to require special precautions

Index Terms

Atorvastatin Calcium

FDA Approval Date
December 17, 1996
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January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society [published online March 28, 2014]. Circulation.[PubMed 24682347]

Jellinger PS, Handelsman Y, Rosenblit PD, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(suppl 2):1-87. doi: 10.4158/EP171764.APPGL.[PubMed 28437620]

Kernan WN, Ovbiagele B, Black HR, et al; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; Council on Peripheral Vascular Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association [published correction appears in Stroke. 2015;46(2):e54]. Stroke. 2014;45(7):2160-2236. doi: 10.1161/STR.0000000000000024.[PubMed 24788967]

Kulik A, Ruel M, Jneid H, et al. Secondary prevention after coronary artery bypass graft surgery: a scientific statement from the American Heart Association. Circulation. 2015;131(10):927-964. doi: 10.1161/CIR.0000000000000182.[PubMed 25679302]

Lapi F, Gallo E, Bernasconi S, et al. Myopathies associated with red yeast rice and liquorice: spontaneous reports from the Italian Surveillance System of Natural Health Products. Br J Clin Pharmacol. 2008;66(4):572-574.[PubMed 18637891]

LaRosa JC, Grundy SM, Waters DD, et al, “Intensive Lipid Lowering With Atorvastatin in Patients With Stable Coronary Disease,” N Engl J Med, 2005, 352(14):1425-35.[PubMed 15755765]

Lecarpentier E, Morel O, Fournier T, et al, “Statins and Pregnancy: Between Supposed Risks and Theoretical Benefits,” Drugs, 2012, 72(6):773-88.[PubMed 22480340]

LeManach Y, Godet G, Coriat P, et al, “The Impact of Postoperative Discontinuation or Continuation of Chronic Statin Therapy on Cardiac Outcome After Major Vascular Surgery,” Anesth Analg, 2007, 104(6):1326-33.[PubMed 17513620]

Levine GN, Bates ER, Blankenship JC, et al, “2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions,” Circulation, 2011, 124(23):e574-651.[PubMed 22064601]

Lipitor (atorvastatin) [prescribing information]. New York, NY: Parke-Davis; June 2017.

Lipitor (atorvastatin) [product monograph]. Kirkland, Quebec, Canada: Pfizer Canada ULC; January 2019.

Lucente P, Iorizzo M, Pazzaglia M. Contact sensitivity to Tween 80 in a child. Contact Dermatitis. 2000;43(3):172.[PubMed 10985636]

McPherson R, Frohlich J, Fodor G, et al, “Canadian Cardiovascular Society Position Statement–Recommendations for the Diagnosis and Treatment of Dyslipidemia and Prevention of Cardiovascular Disease,” [published correction appears in Can J Cardiol. 2006, 22(12):1077]. Can J Cardiol. 2006;22(11):913-927.[PubMed 16971976]

“MRC/BHF Heart Protection Study of Cholesterol Lowering With Simvastatin in 20,536 High-Risk Individuals: A Randomised Placebo-Controlled Trial. Heart Protection Study Collaborative Group,” Lancet, 2002, 360(9326):7-22.[PubMed 12114036]

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2013;128(25):e481.] Circulation. 2013;127(4):e362-425.[PubMed 23247304]

Pasceri V, Patti G, Nusca A, et al, “Randomized Trial of Atorvastatin for Reduction of Myocardial Damage During Coronary Intervention: Results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) Study,” Circulation, 2004, 110(6):674-8.[PubMed 15277322]

Pasternak RC, Smith SC Jr, Bairey-Merz CN, et al, “ACC/AHA/NHLBI Clinical Advisory on the Use and Safety of Statins,” Stroke, 2002, 33(9):2337-41. Available at http://stroke.ahajournals.org/cgi/content/short/33/9/2337[PubMed 12215610]

Patti G, Pasceri V, Colonna G, et al, “Atorvastatin Pretreatment Improves Outcomes in Patients With Acute Coronary Syndromes Undergoing Early Percutaneous Coronary Intervention: Results of the ARMYDA-ACS Randomized Trial,” J Am Coll Cardiol, 2007, 49(12):1272-8.[PubMed 17394957]

Pearson TA, Mensah GA, Alexander RW, et al, “Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association,” Circulation, 2003, 107(3):499-511.[PubMed 12551878]

Pederson TR, Faergerman O, Kastelein JJ, et al, “High-Dose Atorvastatin vs Usual-Dose Simvastatin for Secondary Prevention After Myocardial Infarction: The IDEAL Study: A Randomized Controlled Trial,” JAMA, 2005, 294(19):2437-45.[PubMed 16287954]

Pitt B, Waters D, Brown WV, et al, “Aggressive Lipid-Lowering Therapy Compared With Angioplasty in Stable Coronary Artery Disease. Atorvastatin Versus Revascularization Treatment Investigators,” N Engl J Med, 1999, 341(2):70-6.[PubMed 10395630]

Poldermans D, Bax JJ, Kertai MD, et al, “Statins Are Associated With a Reduced Incidence of Perioperative Mortality in Patients Undergoing Major Noncardiac Vascular Surgery,” Circulation, 2003, 107(14):1848-51.[PubMed 12695283]

Ray KK and Cannon CP. The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes. J Am Coll Cardiol. 2005;46(8):1425-1433.[PubMed 16226165]

Ridker PM, Danielson E, Fonseca FAH, et al, “Rosuvastatin to Prevent Vascular Events in Men and Women With Elevated C-Reactive Protein,” N Engl J Med, 2008, 359(21):2195-207.[PubMed 18997196]

Rosenson RS. Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. Accessed January 3, 2019.

Schwartz GG, Olsson AG, Ezekowitz MD, et al, “Effects of Atorvastatin on Early Recurrent Ischemic Events in Acute Coronary Syndromes: The MIRACL Study: A Randomized Controlled Trial,” JAMA, 2001, 285(13):1711-8.[PubMed 11277825]

Sever PS, Dahlof B, Poulter NR, et al, “Prevention of Coronary and Stroke Events With Atorvastatin in Hypertensive Patients Who Have Average or Lower-Than-Average Cholesterol Concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial – Lipid-Lowering Arm (ASCOT-LLA): A Multicentre Randomised Controlled Trial,” Lancet, 2003, 361(9364):1149-58.[PubMed 12686036]

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Shepherd J, Cobbe SM, Ford I, et al, “Prevention of Coronary Heart Disease With Pravastatin in Men With Hypercholesterolemia. West of Scotland Coronary Prevention Study Group,” N Engl J Med, 1995, 333(20):1301-7.[PubMed 7566020]

Siedlik PH, Olson, SC, Yang BB, et al, “Erythromycin Coadministration Increases Plasma Atorvastatin Concentrations,” J Clin Pharmacol, 1999, 39(5):501-4.[PubMed 10234598 ]

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Tonelli M, Wanner C; for the Kidney Disease: Improving Global Outcomes Lipid Guideline Development Work Group Members. Lipid Management in Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2013 Clinical Practice Guideline [published online ahead of print]. Ann Intern Med. 2013.[PubMed 24323134]

Waters DD, LaRosa JC, Barter P, et al, “Effects Of High-Dose Atorvastatin On Cerebrovascular Events In Patients With Stable Coronary Disease In The TNT (Treating To New Targets) Study,” J Am Coll Cardiol, 2006, 48(9):1793-9.[PubMed 17084252]

Brand Names: International

Acrovastin (EC); Actalipid (ID); Aditor (JO, LB); Aforsatin (VN); Ale (CN); Alipid (VN); Amicor (RO); Analip (CR, DO, GT, HN, NI, PA, SV); Anxolipo (TW); Aspavor (ZW); Astatin (QA); Astator (SI); Atacor (HK, MT); Atarva (AR); Atasin (BD); Ateroz (ET); Atocor (UA); Atofar (ID); Atolow (KR); Atopitar (PH); Ator (AE, BH, CY, IQ, IR, JO, KW, LB, LY, OM, PH, SA, SY, YE); Atorasat (BE); Atorcad (PH); Atorcal (TW); Atorin (TW); Atoris (BE, ES, HU, LT, LV, RU, SG); Atorlip (CO, HK, LB, PE, VN); Atorphil (PH); Atorsan (ID); Atorva (KR, LK, SA); Atorvaright (HK); Atorvas (IE, MY); Atorvast (EG); Atorwin (ID, PH); Atoty (TW); Atroact-10 (PH); Atrofit (TZ); Atstat (LK); Atswift (SG); Atvas (LK); Avamax (PH); Axo (DO, GT, HN, NI, PA, SV); Bestatin (PH); Carditor (TZ); Cardyl (ES); Carvastin (PH); Cheklip (VN); Chlovas (TH); Citalor (BR); Colestop (ET); Covetor (ID); Debostin (ID); Divator (HK); Enturion (SG); Fastor (ID); Hipolixan (CL); Leztrol (PH); Lipicon (LK); Lipiduce (HK, MY); Lipigo (PH); Lipikhan (HK, PH); Lipilou (KR); Lipinon (KR); Lipistad (HK, MY); Lipitas (ET, ZW); Lipiterol (KR); Lipitin (HR); Lipitor (AE, AR, AU, BB, BD, BE, BF, BH, BJ, BO, BR, CI, CL, CN, CO, CR, CY, DO, EC, EE, EG, ET, FI, GB, GH, GM, GN, GR, GT, HK, HN, ID, IE, IL, IQ, IR, JO, JP, KE, KR, KW, LB, LR, LU, LY, MA, ML, MR, MT, MU, MW, MX, MY, NE, NG, NI, NL, NO, OM, PA, PE, PH, PK, PR, PY, QA, SA, SC, SD, SE, SG, SL, SN, SV, SY, TH, TN, TR, TW, TZ, UG, UY, VE, YE, ZA, ZM, ZW); Lipivent (PH); Lipiwon (KR); Lipoactin (KR); Lipodar (AE, BH, CY, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE); Lipofix (ZW); Lipomax (EG, PY, QA, SA); Lipomet (KR); Liponorm (EC); Lipox (CL); Litorva (IL); Livostor (UA); Lopamol (LT); Lorstat (AU); Lowlipen (CO); Neustatin-A (KR); Newvast (KR); Olpit (KR); Orvakline (MY); Orvast (ID); Pelearto (VN); Plan (AR); Rotaqor (MY); Saatin (PH); Safena (VN); Shanleting (CN); Simtor (ID); Sortis (AT, BG, CH, CZ, DE, HR, LV, PL, SE, SI, SK); Statol (TR); Stator (ID); Stavinor (ID); Storvas (IN, MY, ZW); Tahor (FR, MU); TG-Tor (ZW); Tolevas (UA); Torid (IL); Torolac (JO); Torvacol (IE, QA); Torvalipin (SG); Torvast (IT); Torvatec (SG); Torvazin (VN); Tovast (KR); Trovas (AU); Truvast (PH); Truvaz (ID); Tulip (SG, SK, TW, UA); Vastor (JO); Vaztor (PH); X-Tor (LK); Xantor (PH); Xarator (TH); Xelpid (LK); Xentor (PH); Xerova (BD); You Jia (CN); Zapitor (BD); Zarator (AR, CL, DK, ES, NZ, PT)

Atorvastatin (Patient Education – Adult Medication)
You must carefully read the “Consumer Information Use and Disclaimer” below in order to understand and correctly use this information
Pronunciation

(a TORE va sta tin)

Brand Names: US

Lipitor

Brand Names: Canada

Lipitor

What is this drug used for?
  • It is used to prevent heart attacks.
  • It is used to prevent strokes.
  • It is used to prevent chest pain.
  • It is used to lower bad cholesterol and raise good cholesterol (HDL).
  • It is used to lower triglycerides.
  • It is used to slow the progress of heart disease.
  • It may be given to you for other reasons. Talk with the doctor.
What do I need to tell my doctor BEFORE I take this drug?
  • If you have an allergy to atorvastatin or any other part of this drug.
  • If you are allergic to any drugs like this one, any other drugs, foods, or other substances. Tell your doctor about the allergy and what signs you had, like rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other signs.
  • If you are pregnant or may be pregnant. Do not take this drug if you are pregnant.
  • If you are breast-feeding. Do not breast-feed while you take this drug.
  • If you have any of these health problems: Active liver disease or a rise in liver enzymes.
  • If you are taking any of these drugs: Cyclosporine, gemfibrozil, telaprevir, or tipranavir plus ritonavir.
  • This is not a list of all drugs or health problems that interact with this drug.
  • Tell your doctor and pharmacist about all of your drugs (prescription or OTC, natural products, vitamins) and health problems. You must check to make sure that it is safe for you to take this drug with all of your drugs and health problems. Do not start, stop, or change the dose of any drug without checking with your doctor.
What are some things I need to know or do while I take this drug?
  • Tell all of your health care providers that you take this drug. This includes your doctors, nurses, pharmacists, and dentists.
  • If you have high blood sugar (diabetes), you will need to watch your blood sugar closely.
  • Have blood work checked as you have been told by the doctor. Talk with the doctor.
  • Do not take more than what your doctor told you to take. Taking more than you are told may raise your chance of very bad side effects.
  • Follow the diet and workout plan that your doctor told you about.
  • If you drink grapefruit juice or eat grapefruit often, talk with your doctor.
  • Avoid or limit drinking alcohol to less than 3 drinks a day. Drinking too much alcohol may raise your chance of liver disease.
  • This drug may affect how much of some other drugs are in your body. If you are taking other drugs, talk with your doctor. You may need to have your blood work checked more closely while taking this drug with your other drugs.
  • If you are 65 or older, use this drug with care. You could have more side effects.
  • This drug may cause harm to the unborn baby if you take it while you are pregnant. If you are pregnant or you get pregnant while taking this drug, call your doctor right away.
  • Use birth control that you can trust to prevent pregnancy while taking this drug.
What are some side effects that I need to call my doctor about right away?
  • WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your doctor or get medical help right away if you have any of the following signs or symptoms that may be related to a very bad side effect:
  • Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing, swallowing, or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat.
  • Signs of a urinary tract infection (UTI) like blood in the urine, burning or pain when passing urine, feeling the need to pass urine often or right away, fever, lower stomach pain, or pelvic pain.
  • Weakness on 1 side of the body, trouble speaking or thinking, change in balance, drooping on one side of the face, or blurred eyesight.
  • Not able to pass urine or change in how much urine is passed.
  • Feeling very tired or weak.
  • Feeling confused.
  • Memory problems or loss.
  • Very bad joint pain.
  • This drug may cause muscle pain, tenderness, or weakness. Sometimes, a very bad muscle problem may happen that may lead to kidney problems. Rarely, deaths have happened in people who get these problems when taking drugs like this one. Call your doctor right away if you have muscle pain, tenderness, or weakness that is not normal (with or without fever or feeling out of sorts). Call your doctor right away if you have muscle signs that last after your doctor has told you to stop taking this drug.
  • Very bad and sometimes deadly liver problems have happened with this drug. Call your doctor right away if you have signs of liver problems like dark urine, feeling tired, not hungry, upset stomach or stomach pain, light-colored stools, throwing up, or yellow skin or eyes.
What are some other side effects of this drug?
  • All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away:
  • Diarrhea.
  • Joint pain.
  • Upset stomach.
  • Nose and throat irritation.
  • Not able to sleep.
  • These are not all of the side effects that may occur. If you have questions about side effects, call your doctor. Call your doctor for medical advice about side effects.
  • You may report side effects to your national health agency.
How is this drug best taken?
  • Use this drug as ordered by your doctor. Read all information given to you. Follow all instructions closely.
  • Take this drug at the same time of day.
  • Take with or without food.
  • Do not split or break tablet.
  • To gain the most benefit, do not miss doses.
  • Keep taking this drug as you have been told by your doctor or other health care provider, even if you feel well.
What do I do if I miss a dose?
  • Take a missed dose as soon as you think about it and go back to your normal time.
  • If it has been 12 hours or more since the missed dose, skip the missed dose and go back to your normal time.
  • Do not take 2 doses at the same time or extra doses.
How do I store and/or throw out this drug?
  • Store at room temperature.
  • Store in a dry place. Do not store in a bathroom.
  • Keep all drugs in a safe place. Keep all drugs out of the reach of children and pets.
  • Throw away unused or expired drugs. Do not flush down a toilet or pour down a drain unless you are told to do so. Check with your pharmacist if you have questions about the best way to throw out drugs. There may be drug take-back programs in your area.
General drug facts
  • If your symptoms or health problems do not get better or if they become worse, call your doctor.
  • Do not share your drugs with others and do not take anyone else’s drugs.
  • Keep a list of all your drugs (prescription, natural products, vitamins, OTC) with you. Give this list to your doctor.
  • Talk with the doctor before starting any new drug, including prescription or OTC, natural products, or vitamins.
  • Some drugs may have another patient information leaflet. If you have any questions about this drug, please talk with your doctor, nurse, pharmacist, or other health care provider.
  • If you think there has been an overdose, call your poison control center or get medical care right away. Be ready to tell or show what was taken, how much, and when it happened.
Atorvastatin (Patient Education – Pediatric Medication)
You must carefully read the “Consumer Information Use and Disclaimer” below in order to understand and correctly use this information
Pronunciation

(a TORE va sta tin)

Brand Names: US

Lipitor

Brand Names: Canada

Lipitor

What is this drug used for?
  • It is used to prevent heart attacks.
  • It is used to prevent strokes.
  • It is used to prevent chest pain.
  • It is used to lower bad cholesterol and raise good cholesterol (HDL).
  • It is used to lower triglycerides.
  • It is used to slow the progress of heart disease.
  • It may be given to your child for other reasons. Talk with the doctor.
What do I need to tell the doctor BEFORE my child takes this drug?
  • If your child has an allergy to this drug or any part of this drug.
  • If your child is allergic to any drugs like this one or any other drugs, foods, or other substances. Tell the doctor about the allergy and what signs your child had, like rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other signs.
  • If your child has any of these health problems: Active liver disease or a rise in liver enzymes.
  • If your child is taking any of these drugs: Cyclosporine, gemfibrozil, telaprevir, or tipranavir plus ritonavir.
  • If your child is pregnant or breast-feeding a baby:
  • Do not give this drug to your child if she is pregnant.
  • Be sure your child does not breast-feed a baby while taking this drug.
  • This is not a list of all drugs or health problems that interact with this drug.
  • Tell the doctor and pharmacist about all of your child’s drugs (prescription or OTC, natural products, vitamins) and health problems. You must check to make sure that it is safe for your child to take this drug with all of his/her drugs and health problems. Do not start, stop, or change the dose of any drug your child takes without checking with the doctor.
What are some things I need to know or do while my child takes this drug?
  • Tell all of your child’s health care providers that your child is taking this drug. This includes your child’s doctors, nurses, pharmacists, and dentists.
  • If your child has high blood sugar (diabetes), you will need to watch his/her blood sugar closely.
  • Have your child’s blood work checked often. Talk with your child’s doctor.
  • Do not give your child more of this drug than what the doctor told you to give. Giving more of this drug than you are told may raise the chance of very bad side effects.
  • Have your child follow the diet and workout plan your child’s doctor told you about.
  • If your child drinks grapefruit juice or eats grapefruit often, talk with your child’s doctor.
  • Alcohol may interact with this drug. Be sure your child does not drink alcohol.
  • This drug may affect how much of some other drugs are in the body. If your child is taking other drugs, talk with the doctor. Your child may need to have blood work checked more closely while taking this drug with other drugs.
  • If your child is or may be sexually active:
  • Have your child use birth control to prevent pregnancy while taking this drug.
  • This drug may cause harm to the unborn baby if your child takes it during pregnancy. If your child is pregnant or gets pregnant while taking this drug, call the doctor right away.
What are some side effects that I need to call my child’s doctor about right away?
  • WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your child’s doctor or get medical help right away if your child has any of the following signs or symptoms that may be related to a very bad side effect:
  • Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing, swallowing, or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat.
  • Signs of a urinary tract infection (UTI) like blood in the urine, burning or pain when passing urine, feeling the need to pass urine often or right away, fever, lower stomach pain, or pelvic pain.
  • Weakness on 1 side of the body, trouble speaking or thinking, change in balance, drooping on one side of the face, or blurred eyesight.
  • Not able to pass urine or change in how much urine is passed.
  • Feeling very tired or weak.
  • Feeling confused.
  • Memory problems or loss.
  • Very bad joint pain.
  • This drug may cause muscle pain, tenderness, or weakness. Sometimes, a very bad muscle problem may happen that may lead to kidney problems. Rarely, deaths have happened in people who get these problems when taking drugs like this one. Call the doctor right away if your child has muscle pain, tenderness, or weakness that is not normal (with or without fever or feeling out of sorts). Call the doctor right away if your child has muscle signs that last after the doctor has told you to stop giving this drug.
  • Very bad and sometimes deadly liver problems have happened with this drug. Call your child’s doctor right away if your child has signs of liver problems like dark urine, feeling tired, not hungry, upset stomach or stomach pain, light-colored stools, throwing up, or yellow skin or eyes.
What are some other side effects of this drug?
  • All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your child’s doctor or get medical help if any of these side effects or any other side effects bother your child or do not go away:
  • Diarrhea.
  • Joint pain.
  • Upset stomach.
  • Nose and throat irritation.
  • Not able to sleep.
  • These are not all of the side effects that may occur. If you have questions about side effects, call your child’s doctor. Call your child’s doctor for medical advice about side effects.
  • You may report side effects to your national health agency.
How is this drug best given?
  • Give this drug as ordered by your child’s doctor. Read all information given to you. Follow all instructions closely.
  • Give this drug at the same time of day.
  • Give this drug with or without food.
  • Do not split or break tablet.
  • To gain the most benefit, do not miss giving your child doses.
  • Keep giving this drug to your child as you have been told by your child’s doctor or other health care provider, even if your child feels well.
What do I do if my child misses a dose?
  • Give a missed dose as soon as you think about it.
  • If it has been 12 hours or more since the missed dose, skip the missed dose and go back to your child’s normal time.
  • Do not put on 2 doses at the same time or extra doses.
How do I store and/or throw out this drug?
  • Store at room temperature.
  • Store in a dry place. Do not store in a bathroom.
  • Keep all drugs in a safe place. Keep all drugs out of the reach of children and pets.
  • Throw away unused or expired drugs. Do not flush down a toilet or pour down a drain unless you are told to do so. Check with your pharmacist if you have questions about the best way to throw out drugs. There may be drug take-back programs in your area.
General drug facts
  • If your child’s symptoms or health problems do not get better or if they become worse, call your child’s doctor.
  • Do not share your child’s drug with others and do not give anyone else’s drug to your child.
  • Keep a list of all your child’s drugs (prescription, natural products, vitamins, OTC) with you. Give this list to your child’s doctor.
  • Talk with your child’s doctor before giving your child any new drug, including prescription or OTC, natural products, or vitamins.
  • Some drugs may have another patient information leaflet. If you have any questions about this drug, please talk with your child’s doctor, nurse, pharmacist, or other health care provider.
  • If you think there has been an overdose, call your poison control center or get medical care right away. Be ready to tell or show what was taken, how much, and when it happened.