Medically reviewed on Nov 15, 2018
(pi TA va sta tin)
- Pitavastatin Calcium
- Pitavastatin Magnesium
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as calcium [strength expressed as base]:
Livalo: 1 mg, 2 mg, 4 mg
Tablet, Oral, as magnesium [strength expressed as base]:
Zypitamag: 1 mg, 2 mg, 4 mg
Brand Names: U.S.
- Antilipemic Agent, HMG-CoA Reductase Inhibitor
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).
Vd: ~148 L
Hepatic, via UGT1A3 and UGT2B7; minimal metabolism via CYP2C9 and CYP2C8
Feces (79%); urine (15%)
Time to Peak
>99%, primarily to albumin and alpha 1-acid glycoprotein
Special Populations: Renal Function Impairment
Cmax and AUC were 60% and 102% higher in patients with GFR 30 to 59 mL/minute/1.73 m2 and 40% and 86% higher in patients with ESRD on hemodialysis, respectively.
Special Populations: Hepatic Function Impairment
Half-life was 15 and 10 hours for patients with moderate and mild impairment, respectively.
Special Populations: Elderly
Cmax and AUC were 10% and 30% higher, respectively, in elderly patients compared with younger patients.
Special Populations: Gender
Cmax and AUC were 60% and 54% higher, respectively, in women compared with men.
Special Populations: Race
Cmax and AUC were 21% and 5% lower, respectively, in black patients compared with white patients.
Use: Labeled Indications
Primary hyperlipidemia and mixed dyslipidemia: As an adjunctive therapy to diet to reduce elevated total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (apo B), and triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C) in adults with primary hyperlipidemia or mixed dyslipidemia
Off Label Uses
Cardiac risk reduction for noncardiac surgery (perioperative therapy)
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/Transient ischemic attack (secondary prevention)
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).
Primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD)
Based on the American College of Cardiology/American Heart Association (ACC/AHA) Guideline on the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults and the National Lipid Association Recommendations for Patient-Centered Management of Dyslipidemia, pitavastatin given for primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD) is effective and recommended in the management of this condition. Based on the US Preventive Services Task Force (USPSTF) recommendation statement on Statin Use for the Primary Prevention of Cardiovascular Disease (CVD) in Adults, initiation of low to moderate dose statin therapy is recommended in adults 40 to 75 years without a history of CVD who have ≥1 CVD risk factors (dyslipidemia, diabetes, hypertension, or smoking) and a calculated 10-year CVD event risk of ≥10%. Based on the American Heart Association (AHA) scientific statement for the secondary prevention after coronary artery bypass graft surgery, statin therapy (unless contraindicated) is recommended for all coronary artery bypass graft (CABG) surgery patients to help maintain long-term graft patency and help obtain the highest level of physical health and quality of life.
Hypersensitivity to pitavastatin or any component of the formulation; active liver disease, including unexplained persistent elevations of hepatic transaminase levels; pregnancy; lactation; coadministration with cyclosporine
Primary hyperlipidemia and mixed dyslipidemia: Oral: Initial: 2 mg once daily; 4 weeks after initiation or upon titration, analyze lipid levels and adjust dose accordingly; Maintenance: 1 to 4 mg once daily; maximum: 4 mg/day.
Note: Individualize dose according to the baseline LDL-cholesterol levels, recommended goal of therapy, and patient response.
Prevention of cardiovascular disease/reduce the risk of ASCVD (off-label use): Oral:
ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Stone 2013]): Age ≥21 years of age:
LDL-C ≥190 mg/dL: High intensity therapy necessary; use alternate statin therapy (eg, atorvastatin or rosuvastatin)
Type 1 or 2 diabetes and age 40 to 75 years: Moderate intensity therapy: 2 to 4 mg once daily
Type 1 or 2 diabetes, age 40 to 75 years, and an estimated 10-year ASCVD risk ≥7.5%: High intensity therapy necessary; use alternate statin therapy (eg, atorvastatin or rosuvastatin)
Age 40 to 75 years and an estimated 10-year ASCVD risk ≥7.5%: Moderate to high intensity therapy: 2 to 4 mg once daily or consider using high intensity statin therapy (eg, atorvastatin or rosuvastatin)
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 necessary; use alternate statin therapy (eg, atorvastatin or rosuvastatin)
Age >75 years or not a candidate for high intensity therapy: Moderate intensity therapy: 2 to 4 mg once daily
NLA Dyslipidemia Guideline recommendations (NLA [Jacobson 2015]): Age ≥20 years of age:
Primary or secondary prevention: Note: Treatment initiation using either moderate- or high-intensity statin therapy is recommended in qualifying patients based on ASCVD risk assessment criteria and baseline non-HDL-C and LDL-C values. Dosage should be individualized based on patient characteristics, tolerance to therapy, and with consideration for non-HDL-C and LDL-C treatment goals.
Moderate-intensity therapy (30% to 50% reduction of LDL-C generally): 2 to 4 mg once daily
High-intensity therapy (≥50% reduction of LDL-C generally): Use alternate statin therapy (eg, atorvastatin, rosuvastatin)
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%:
Low intensity therapy: 1 mg once daily
Moderate intensity therapy: 2 to 4 mg once daily
Note: These recommendations do not pertain to patients with very high cholesterol levels (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%, statin use may be considered based on patient characteristics.
Dosage adjustment with concomitant medications:
Erythromycin: Maximum pitavastatin dose: 1 mg/day
Rifampin: Maximum pitavastatin dose: 2 mg/day
Refer to adult dosing.
Dosing: Renal Impairment
GFR ≥60 mL/minute/1.73 m2: There are no dosage adjustments provided in the manufacturer’s labeling.
GFR 15 to 59 mL/minute/1.73 m2 (not receiving hemodialysis): Initial: 1 mg once daily; maximum: 2 mg/day
ESRD receiving hemodialysis: Initial: 1 mg once daily; maximum: 2 mg/day
Dosing: Hepatic Impairment
Contraindicated in active liver disease or in patients with unexplained persistent elevations of serum transaminases.
Dosing: Adjustment for Toxicity
Severe muscle symptoms or fatigue: Promptly discontinue use; evaluate CPK, creatinine, and urinalysis for myoglobinuria (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 pitavastatin. If muscle symptoms recur, discontinue pitavastatin 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 (Stone 2013).
Administer with or without food; may take without regard to time of 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).
Store at 15°C to 30°C (59°F to 86°F). Protect from light.
Acipimox: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
Asunaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
Atazanavir: May increase the serum concentration of Pitavastatin. 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. Consider therapy modification
Boceprevir: May increase the serum concentration of Pitavastatin. 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. Consider therapy modification
Clarithromycin: May increase the serum concentration of Pitavastatin. Monitor therapy
Cobicistat: May increase the serum concentration of Pitavastatin. Monitor therapy
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). Consider therapy modification
CycloSPORINE (Systemic): May increase the serum concentration of Pitavastatin. Avoid combination
Daclatasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
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. Consider therapy modification
Eltrombopag: May increase the serum concentration of OATP1B1/SLCO1B1 Substrates. Monitor therapy
Erythromycin (Systemic): May increase the serum concentration of Pitavastatin. Management: Limit pitavastatin to a maximum of 1 mg/day (adult dose) when used in combination with erythromycin. If this combination is used, monitor patients more closely for evidence of pitavastatin toxicity. Consider therapy modification
Fenofibrate and Derivatives: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
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. Avoid combination
Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of Pitavastatin. Gemfibrozil may increase the serum concentration of Pitavastatin. Avoid combination
Glecaprevir and Pibrentasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest statin dose possible if combined with glecaprevir/pibrentasvir and monitor for increased statin effects/toxicities. Avoid concomitant use with atorva-, simva-, or lovastatin. Limit rosuvastatin to 10 mg daily and reduce pravastatin dose 50% 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. Consider therapy modification
Letermovir: May increase the serum concentration of Pitavastatin. Avoid combination
Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
Niacinamide: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
Ombitasvir, Paritaprevir, Ritonavir, and Dasabuvir: May increase the serum concentration of Pitavastatin. Management: Canadian product labeling recommends use of the lowest pitavastatin dose with this combination. Monitor therapy
PAZOPanib: HMG-CoA Reductase Inhibitors (Statins) may enhance the hepatotoxic effect of PAZOPanib. Specifically, the risk for increased serum transaminase concentrations may be increased. Management: Simvastatin is specifically implicated in the interaction. There is a lack of data regarding risk with other statins, but caution appears warranted with any statins. Atorvastatin should be avoided due to P-gp inhibition. Monitor therapy
Raltegravir: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors (Statins). Monitor therapy
Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors (Statins). Avoid combination
Repaglinide: HMG-CoA Reductase Inhibitors (Statins) may increase the serum concentration of Repaglinide. Monitor therapy
Rifamycin Derivatives: May increase the serum concentration of Pitavastatin. Management: Limit pitavastatin dose to a maximum of 2 mg/day with concurrent rifampin. 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. Monitor therapy
Simeprevir: May increase the serum concentration of Pitavastatin. Monitor therapy
Telaprevir: May increase the serum concentration of Pitavastatin. Monitor therapy
Telithromycin: May increase the serum concentration of Pitavastatin. Monitor therapy
Teriflunomide: May increase the serum concentration of OATP1B1/SLCO1B1 Substrates. Monitor therapy
Tolvaptan: May increase the serum concentration of OATP1B1/SLCO1B1 Substrates. Consider therapy modification
Trabectedin: HMG-CoA Reductase Inhibitors (Statins) may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Monitor therapy
Vitamin K Antagonists (eg, warfarin): HMG-CoA Reductase Inhibitors (Statins) may enhance the anticoagulant effect of Vitamin K Antagonists. Monitor therapy
Voxilaprevir: May increase the serum concentration of Pitavastatin. Avoid combination
1% to 10%:
Central nervous system: Headache (<2%)
Endocrine & metabolic: Increased serum glucose (<2%)
Gastrointestinal: Constipation (4%), diarrhea (3%)
Hepatic: Increased serum alkaline phosphatase (<2%), increased serum bilirubin (<2%), increased serum transaminases (<2%; usually transient)
Infection: Influenza (<2%)
Neuromuscular & skeletal: Back pain (4%), myalgia (2% to 3%), arthralgia (<2%), increased creatine phosphokinase (<2%)
Respiratory: Nasopharyngitis (<2%)
<1%, postmarketing, and/or case reports: Abdominal distress, abdominal pain, cognitive dysfunction (reversible; including amnesia, confusion, forgetfulness, memory impairment), depression, dizziness, elevated glycosylated hemoglobin (Hb A1c), erectile dysfunction, fatigue, hepatic failure, hepatitis, hypoesthesia, immune-mediated necrotizing myopathy, insomnia, interstitial pulmonary disease, jaundice, malaise, muscle spasm, nausea, peripheral neuropathy, pruritus, myopathy, rhabdomyolysis (with acute renal failure), skin rash, urticaria, weakness
Concerns related to adverse effects:
• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported; however, the benefits of statin therapy far outweigh the risk of dysglycemia.
• Hepatotoxicity: Elevations in serum transaminases have been reported; elevations were transient and resolved or improved on continued therapy or after a brief interruption in therapy in most cases. 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 pitavastatin. Liver enzyme tests should be obtained at baseline and as clinically indicated. Ethanol may enhance the potential of adverse hepatic effects; instruct patients to avoid excessive ethanol consumption.
• Hypersensitivity: Hypersensitivity reactions, including rash, pruritus, and urticaria, have been reported.
• 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 (doses >4 mg) and is increased with concurrent use of erythromycin, protease inhibitors, fibric acid derivatives (eg, gemfibrozil), or niacin (doses ≥1 g/day). If concurrent use is warranted, consider lower starting and maintenance doses of pitavastatin. 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 rarely. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine, particularly if accompanied by malaise or fever or if muscle signs and symptoms persist after discontinuing pitavastatin. Temporarily withhold therapy in any patient with an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis, hypotension, dehydration, major surgery, trauma, severe metabolic, endocrine, electrolyte disorders, and uncontrolled seizures). Discontinue therapy if markedly elevated CPK levels occur or myopathy is diagnosed/suspected.
• Hepatic impairment: Use is contraindicated in patients with active liver disease or unexplained persistent elevations of serum transaminases; use with caution in patients who consume large amounts of ethanol or have a history of liver disease.
• Renal impairment: Use with caution in patients with renal impairment; these patients are predisposed to myopathy. Dosage adjustment required in patients with GFR <60 mL/minute/1.73 m2 including end-stage renal disease receiving hemodialysis.
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.
• 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 or serious condition predisposing to renal failure (eg, sepsis, hypotension, trauma, uncontrolled seizures). 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.
• Appropriate use: Has not been studied in Fredrickson types I, III, and V dyslipidemias. The effect on cardiovascular morbidity and mortality has not been determined.
• Hyperlipidemia: Secondary causes of hyperlipidemia should be ruled out prior to therapy.
2013 ACC/AHA Blood Cholesterol Guideline recommendations (Stone 2013):
Lipid panel (total cholesterol, HDL, LDL, triglycerides): Baseline lipid panel; fasting lipid profile within 4 to 12 weeks after initiation or dose adjustment and every 3 to 12 months (as clinically indicated) thereafter. If 2 consecutive LDL levels are <40 mg/dL, consider decreasing the dose.
Hepatic transaminase levels: Baseline measurement of hepatic transaminase levels (ie, ALT); measure hepatic function 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.
Manufacturer's labeling: Liver enzyme tests at baseline and repeated when clinically indicated. Upon initiation or titration, lipid panel should be analyzed after 4 weeks of therapy.
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.
Use of pitavastatin is contraindicated in pregnancy. Because they are potentially teratogenic, the ADA Diabetes guidelines recommends avoiding use of HMG-CoA reductase inhibitors in sexually active women of childbearing age who are not using reliable contraception (ADA 2018a). If treatment of dyslipidemias is needed in pregnant women or in women of reproductive age, other agents are preferred (Berglund 2012; Stone 2013). The manufacturer recommends administration to women of childbearing potential only when conception is highly unlikely and patients have been informed of potential hazards.
• 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 back pain, constipation, or diarrhea. Have patient report immediately to prescriber urinary retention, change in amount of urine passed, muscle pain, muscle tenderness, muscle weakness, or signs of liver problems (dark urine, feeling tired, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or yellow skin or eyes) (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 health care 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.
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- Drug class: statins
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