(prav a STAT in)
- Pravastatin Sodium
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as sodium:
Pravachol: 20 mg
Pravachol: 40 mg [contains fd&c blue #1 aluminum lake, fd&c yellow #10 aluminum lake]
Pravachol: 80 mg
Generic: 10 mg, 20 mg, 40 mg, 80 mg
Brand Names: U.S.
- Antilipemic Agent, HMG-CoA Reductase Inhibitor
Pravastatin is a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is the rate-limiting enzyme involved in de novo cholesterol synthesis. 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).
Rapidly absorbed; average absorption 34%
Vd: 0.46 L/kg
Hepatic multiple metabolites; primary metabolite is 3 alpha-hydroxy-iso-pravastatin (2.5% to 10% activity of parent drug); extensive first-pass metabolism
Feces (70%); urine (~20%, 8% as unchanged drug)
Onset of Action
Several days; Peak effect: 4 weeks; LDL-reduction: 40 mg/day: 34% (for each doubling of this dose, LDL-C is lowered by ~6%)
Time to Peak
Serum: 1-1.5 hours
Children and Adolescents (4.9-15.6 years): 1.6 hours; range: 0.85 to 4.2 hours (Hedman 2003)
Adults: 77 hours (including all metabolites); Pravastatin: ~2 to 3 hours (Pan 1990); 3 alpha hydroxy-iso-pravastatin: ~1.5 hours (Gustavson 2005)
Special Populations: Elderly
Mean AUC was approximately 27% greater and mean cumulative urinary excretion was approximately 19% lower in elderly men. Mean AUC was approximately 46%higher and mean cumulative urinary excretion was approximately 18% lower in elderly women.
Use: Labeled Indications
Dysbetalipoproteinemia: Treatment of primary dysbetalipoproteinemia (Fredrickson type III) in patients who do not respond adequately to diet.
Heterozygous familial hypercholesterolemia: Adjunct to diet in children ≥8 years and adolescents with heterozygous familial hypercholesterolemia (HeFH) if after an adequate trial of diet therapy the following findings are present: LDL-C ≥190 mg/dL or LDL ≥160 mg/dL with positive family history of premature cardiovascular disease (CVD), or with 2 or more other CVD risk factors.
Hypercholesterolemia and mixed dyslipidemia: Adjunct to diet to reduce elevated total cholesterol, LDL-C, apo B, and triglyceride (TG) levels and to increase HDL-C in patients with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson Types IIa and IIb).
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
Primary prevention of cardiovascular disease: To reduce the risk of myocardial infarction, revascularization procedures and cardiovascular mortality in hypercholesterolemic patients without established coronary heart disease (CHD).
Secondary prevention of cardiovascular disease: To slow the progression of coronary atherosclerosis; to reduce the risk of myocardial infarction, revascularization procedures, and total mortality; and to reduce the risk of stroke and transient ischemic attacks (TIA) in patients with established CHD.
Guideline recommendations: Primary and secondary prevention of atherosclerotic cardiovascular disease (ASCVD) to reduce the risk of ASCVD in select adult patients (ACC/AHA [Stone 2013]; NLA [Jacobson 2015]). Refer to respective guideline for specific recommendations.
Hypersensitivity to pravastatin or any component of the formulation; active liver disease; unexplained persistent elevations of serum transaminases; pregnancy; breast-feeding
Note: Doses should be individualized according to the baseline LDL-cholesterol levels, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks or more; doses may need adjusted based on concomitant medications.
Hyperlipidemias, primary prevention of coronary events, secondary prevention of cardiovascular events (also see ACC/AHA Blood Cholesterol Guideline recommendations): Oral: Initial: 40 mg once daily; titrate dosage to response (maximum dose: 80 mg/day)
Prevention of cardiovascular disease/reduce the risk of ASCVD:
ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Stone 2013]): Adults ≥21 years:
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: 40 to 80 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: 40 to 80 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: 40 to 80 mg once daily
NLA Dyslipidemia Guideline recommendations (NLA [Jacobson 2015]): Adults ≥20 years:
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): 40 to 80 mg once daily
High-intensity therapy (≥50% reduction of LDL-C generally): Use alternate statin therapy (eg, atorvastatin or rosuvastatin)
Dosage adjustment for pravastatin with concomitant medications:
Clarithromycin: Maximum pravastatin dose: 40 mg/day.
Cyclosporine: Initial pravastatin dose: 10 mg once daily, titrate with caution (maximum dose: 20 mg/day)
Refer to adult dosing.
Heterozygous familial hypercholesterolemia (HeFH): Oral:
Children and Adolescents 8 to 13 years: 20 mg once daily
Adolescents 14 to 18 years: 40 mg once daily
Dosage adjustment for pravastatin with concomitant medications (clarithromycin, cyclosporine): Refer to adult dosing.
Note: Doses should be individualized according to the baseline LDL-cholesterol levels, the recommended goal of therapy, and patient response; adjustments should be made at intervals of 4 weeks or more; doses may need adjusted based on concomitant medications.
Dosing: Renal Impairment
Mild to moderate impairment: There are no dosage adjustments provided in the manufacturer’s labeling; use with caution.
Severe impairment: Initial: 10 mg once daily
Dosing: Hepatic Impairment
Active hepatic disease or unexplained persistent elevations of serum transaminases: Use is contraindicated.
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, primary muscle diseases). Upon resolution, resume the original or lower dose of pravastatin. If muscle symptoms recur, discontinue pravastatin 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 without regard to meals.
Before initiation of therapy, patients should be placed on a standard cholesterol-lowering diet for 6 weeks and the diet should be continued during drug therapy.
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 25°C (77°F); excursions permitted to 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. Monitor therapy
Antacids: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Monitor therapy
Antihepaciviral Combination Products: May increase the serum concentration of Pravastatin. Management: Limit the pravastatin dose to a maximum of 40 mg per day when used with antihepaciviral combination products and monitor patients for evidence of pravastatin toxicities (eg, myopathy). Consider therapy modification
Asunaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Monitor therapy
Bezafibrate: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors. Bezafibrate may increase the serum concentration of HMG-CoA Reductase Inhibitors. 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
Bile Acid Sequestrants: May decrease the serum concentration of Pravastatin. Management: Administer pravastatin at least 1 hour before or 4 hours after administration of bile-acid resins (eg, cholestyramine, colestipol, colesevelam) to minimize the risk for any significant interaction. Consider therapy modification
Boceprevir: May increase the serum concentration of Pravastatin. Monitor therapy
Ciprofibrate: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. 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 Pravastatin. Management: Limit pravastatin to a maximum of 40 mg/day (for adults) when used in combination with clarithromycin. If this combination is used, monitor patients more closely for evidence of pravastatin toxicity. Consider therapy modification
Colchicine: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors. Colchicine may increase the serum concentration of HMG-CoA Reductase Inhibitors. Consider therapy modification
CycloSPORINE (Systemic): May increase the serum concentration of Pravastatin. Pravastatin may increase the serum concentration of CycloSPORINE (Systemic). Management: Limit pravastatin to 20 mg/day in patients who are also receiving cyclosporine. Consider therapy modification
Daclatasvir: May increase the serum concentration of HMG-CoA Reductase Inhibitors. Monitor therapy
DAPTOmycin: HMG-CoA Reductase Inhibitors 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
Darunavir: May increase the serum concentration of Pravastatin. This effect has only been demonstrated with darunavir/ritonavir. The individual contributions of darunavir and ritonavir are unknown. Monitor therapy
Efavirenz: May decrease the serum concentration of Pravastatin. Monitor therapy
Eltrombopag: May increase the serum concentration of OATP1B1/SLCO1B1 Substrates. Monitor therapy
Erythromycin (Systemic): May increase the serum concentration of Pravastatin. Monitor therapy
Fenofibrate and Derivatives: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Monitor therapy
Fosphenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Consider therapy modification
Fusidic Acid (Systemic): May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. 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 Pravastatin. Gemfibrozil may increase the serum concentration of Pravastatin. Avoid combination
Itraconazole: May increase the serum concentration of Pravastatin. Monitor therapy
Lanthanum: HMG-CoA Reductase Inhibitors may decrease the serum concentration of Lanthanum. Management: Administer HMG-CoA reductase inhibitors at least two hours before or after lanthanum. Consider therapy modification
Nelfinavir: May decrease the serum concentration of Pravastatin. Monitor therapy
Niacin: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Monitor therapy
Niacinamide: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Monitor therapy
PARoxetine: Pravastatin may enhance the adverse/toxic effect of PARoxetine. Specifically, blood glucose elevations may occur with the combination. Monitor therapy
PAZOPanib: HMG-CoA Reductase Inhibitors 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
Phenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. Consider therapy modification
Raltegravir: May enhance the myopathic (rhabdomyolysis) effect of HMG-CoA Reductase Inhibitors. Monitor therapy
Red Yeast Rice: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Avoid combination
Repaglinide: HMG-CoA Reductase Inhibitors may increase the serum concentration of Repaglinide. Monitor therapy
Rifamycin Derivatives: May decrease the serum concentration of HMG-CoA Reductase Inhibitors. 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. Consider therapy modification
Rupatadine: May enhance the adverse/toxic effect of HMG-CoA Reductase Inhibitors. Specifically, the risk for increased CPK and/or other muscle toxicities may be increased. Monitor therapy
Saquinavir: May decrease the serum concentration of Pravastatin. This effect has only been demonstrated with saquinavir/ritonavir. The individual contributions of saquinavir and ritonavir are unknown. Monitor therapy
Simeprevir: May increase the serum concentration of Pravastatin. Monitor therapy
Telaprevir: May increase the serum concentration of Pravastatin. Monitor therapy
Telithromycin: May increase the serum concentration of Pravastatin. Monitor therapy
Teriflunomide: May increase the serum concentration of OATP1B1/SLCO1B1 Substrates. Monitor therapy
Trabectedin: HMG-CoA Reductase Inhibitors may enhance the myopathic (rhabdomyolysis) effect of Trabectedin. Monitor therapy
Vitamin K Antagonists (eg, warfarin): HMG-CoA Reductase Inhibitors may enhance the anticoagulant effect of Vitamin K Antagonists. Monitor therapy
As reported in short-term trials; safety and tolerability with long-term use were similar to placebo.
1% to 10%:
Cardiovascular: Chest pain (4%)
Central nervous system: Headache (2% to 6%), fatigue (4%), dizziness (1% to 3%)
Dermatologic: Skin rash (4%)
Gastrointestinal: Nausea (≤7%), vomiting (≤7%), diarrhea (6%), heartburn (3%)
Genitourinary: Cystitis (interstitial; Huang 2015)
Hepatic: Increased serum transaminases (>3x normal on 2 occasions: 1%)
Infection: Influenza (2%)
Neuromuscular & skeletal: Myalgia (2%)
Respiratory: Cough (3%)
<1% (Limited to important or life-threatening): Amnesia (reversible), anaphylaxis, angioedema, cataract, change in libido, cholestatic jaundice, cognitive dysfunction (reversible), confusion (reversible), cranial nerve dysfunction, dermatomyositis, dysgeusia, erythema multiforme, fulminant hepatic necrosis, gynecomastia, hemolytic anemia, hepatic cirrhosis, hepatic neoplasm, hepatitis, hypersensitivity reaction, increased erythrocyte sedimentation rate, lupus-like syndrome, memory impairment (reversible), myasthenia, myopathy, neuropathy, pancreatitis, paresthesia, peripheral nerve palsy, polymyalgia rheumatica, positive ANA titer, purpura, rhabdomyolysis, Stevens-Johnson syndrome, tremor, vasculitis, vertigo
Concerns related to adverse effects:
• Diabetes mellitus: Increases in HbA1c and fasting blood glucose have been reported with HMG-CoA reductase inhibitors; however, the benefits of statin therapy far outweigh the risk of dysglycemia.
• Endocrine effects: Reduced cholesterol synthesis as a result of therapy could theoretically lead to reduced adrenal or gonadal steroid hormone production; clinical trial data is inconsistent in regards to the effect on basal steroid hormone levels. Patients with signs/symptoms of endocrine dysfunction should be evaluated as clinically indicated; use caution with concomitant medications (eg, spironolactone, cimetidine, ketoconazole) that may reduce steroid hormone levels/activity.
• Hepatotoxicity: Postmarketing reports of fatal and nonfatal hepatic failure are rare. If serious hepatotoxicity with clinical symptoms and/or hyperbilirubinemia or jaundice occurs during treatment, interrupt therapy. If an alternate etiology is not identified, do not restart pravastatin. Liver enzyme tests should be obtained at baseline and as clinically indicated; routine periodic monitoring of liver enzymes is not necessary. Ethanol may enhance the potential of adverse hepatic effects; instruct patients to avoid excessive ethanol consumption.
• Immune-mediated necrotizing myopathy (IMNM): IMNM, an autoimmune-mediated myopathy, has been reported (rarely) with HMG-CoA reductase inhibitor therapy. IMNM presents as proximal muscle weakness with elevated CPK levels, which persists despite discontinuation of HMG-CoA reductase inhibitor therapy; additionally, muscle biopsy may show necrotizing myopathy with limited inflammation. Immunosuppressive therapy (eg, corticosteroids, azathioprine) may be used for treatment.
• Myopathy/rhabdomyolysis: Rhabdomyolysis with acute renal failure secondary to myoglobinuria and/or myopathy have been reported; patients should be monitored closely. This risk is dose-related and is increased with concurrent use of erythromycin, cyclosporine, fibric acid derivatives (eg, gemfibrozil), or niacin (doses ≥1 g/day). Temporarily withhold therapy in patients experiencing conditions predisposing to the development of renal failure secondary to rhabdomyolysis (eg, sepsis, hypotension, major surgery, trauma, uncontrolled epilepsy; severe metabolic, endocrine, or electrolyte disorders). Discontinue therapy in any patient in which CPK levels are markedly elevated (>10 times ULN) or if myopathy is suspected/diagnosed. Use caution in patients with inadequately treated hypothyroidism, and those taking other drugs associated with myopathy (eg, colchicine); these patients are predisposed to myopathy. Patients should be instructed to report unexplained muscle pain, tenderness, weakness, or brown urine.
• 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 transaminase elevations.
• Renal impairment: Use with caution in patients with renal impairment; these patients are predisposed to myopathy.
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 (Fleisher 2009), HMG-CoA reductase inhibitors should be continued in the perioperative period. Postoperative discontinuation of statin therapy is associated with an increased risk of cardiac morbidity and mortality.
• Appropriate use: Has not been studied in homozygous familial hypercholesterolemia (statins may be less effective due to lack of functional LDL receptors).
• 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 4-12 weeks after initiation or dose adjustment and every 3-12 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 at intervals of 4 weeks or more.
Pregnancy Risk Factor
Use of pravastatin is contraindicated in pregnancy.
Adverse events were observed in some animal reproduction studies. Pravastatin was found to cross the placenta in an ex vivo study using term human placentas (Nanovskaya 2013). 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.
HMG-CoA reductase Inhibitors should be discontinued prior to pregnancy (ADA 2013). 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 headache, dizziness, loss of strength and energy, diarrhea, nausea, vomiting, rhinitis, pharyngitis, cough, or rhinorrhea. Have patient report immediately to prescriber signs of liver problems (dark urine, feeling tired, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or yellow skin or eyes), angina, vision changes, urinary retention, change in amount of urine passed, muscle pain, muscle tenderness, or 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 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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Other brands: Pravachol