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Rosuvastatin

Medically reviewed by Drugs.com. Last updated on Sep 1, 2020.

Pronunciation

(roe soo va STAT in)

Index Terms

  • Ezallor
  • Rosuvastatin Calcium

Dosage Forms

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

Capsule Sprinkle, Oral:

Ezallor Sprinkle: 5 mg [contains brilliant blue fcf (fd&c blue #1), fd&c red #40]

Ezallor Sprinkle: 10 mg, 20 mg [contains brilliant blue fcf (fd&c blue #1)]

Ezallor Sprinkle: 40 mg

Tablet, Oral:

Crestor: 5 mg, 10 mg, 20 mg, 40 mg

Generic: 5 mg, 10 mg, 20 mg, 40 mg

Brand Names: U.S.

  • Crestor
  • Ezallor Sprinkle

Pharmacologic Category

  • Antilipemic Agent, HMG-CoA Reductase Inhibitor

Pharmacology

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).

Distribution

Vd: 134 L

Metabolism

Hepatic (10%), via CYP2C9 (1 active metabolite identified: N-desmethyl rosuvastatin, one-sixth to one-half the HMG-CoA reductase activity of the parent compound)

Excretion

Feces (90%), primarily as unchanged drug

Onset of Action

Within 1 week; maximal at 4 weeks

Time to Peak

Plasma: 3 to 5 hours

Half-Life Elimination

19 hours

Protein Binding

88%

Special Populations: Renal Function Impairment

Plasma concentrations increase about 3-fold in patients with severe renal impairment (CrCl <30 mL/minute/1.73 m2) not requiring hemodialysis. Steady-state plasma concentrations in patients on chronic hemodialysis are ~50% higher compared with patients with normal renal function.

Special Populations: Hepatic Function Impairment

Cmax and AUC are increased in patients with Child-Pugh class A or Child-Pugh class B hepatic impairment.

Special Populations: Race

Asian patients have ~2-fold elevation in exposure (AUC and Cmax).

Use: Labeled Indications

Familial hypercholesterolemia:

Pediatric (excluding Ezallor): Adjunct to diet to reduce total cholesterol, LDL-C, and apoB levels in children and adolescents 8 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) if after an adequate trial of diet therapy the following findings are present: LDL-C greater than 190 mg/dL or greater than 160 mg/dL and there is a positive family history of premature cardiovascular disease or 2 or more other cardiovascular disease risk factors; adjunct to diet to reduce LDL-C, total cholesterol, nonHDL-C, and apoB in children and adolescents 7 to 17 years of age with homozygous familial hypercholesterolemia (HoFH), either alone or with other lipid-lowering treatments (eg, LDL apheresis).

Adult: To reduce LDL-C, total cholesterol, and apoB in adults with familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (eg, LDL apheresis) or alone if such treatments are unavailable.

Prevention of cardiovascular disease (Crestor only):

Primary prevention of atherosclerotic cardiovascular disease: To reduce the risk of myocardial infarction (MI), stroke, revascularization procedures, and angina in adults without a history of coronary heart disease (CHD) but who have multiple CHD risk factors.

Secondary prevention in patients with established atherosclerotic cardiovascular disease: To reduce the risk of MI, stroke, revascularization procedures, and angina in adults with a history of CHD.

Off Label Uses

Transplantation, post heart or post kidney

Based on the 2010 International Society of Heart and Lung Transplantation guidelines for the care of heart transplant recipients, rosuvastatin is effective and recommended following heart transplant, regardless of cholesterol levels, to reduce cardiac allograft vasculopathy and improve long-term outcomes [ISHLT [Costanzo 2010]].

Based on the 2013 Kidney Disease: Improving Global Outcomes clinical practice guideline for lipid management in chronic kidney disease, rosuvastatin is suggested following kidney transplant to reduce cardiovascular events (eg, myocardial infarction, stroke, cardiovascular death) [KDIGO [Tonelli 2014]].

Contraindications

Hypersensitivity to rosuvastatin 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): Concomitant administration of cyclosporine or sofosbuvir/velpatasvir/voxilaprevir; use of 40 mg dose in Asian patients, patients with predisposing risk factors for myopathy/rhabdomyolysis (eg, hereditary muscle disorders, history of myotoxicity with other HMG-CoA reductase inhibitors, concomitant use with fibrates or niacin, severe hepatic impairment, severe renal impairment [CrCl <30 mL/minute/1.73 m2], hypothyroidism, alcohol abuse, situations where an increase in rosuvastatin plasma levels may occur).

Dosing: Adult

Note: Use in conjunction with lifestyle modification (eg, diet, exercise). When choosing to initiate therapy and selecting dose intensity, consider the following: age, baseline LDL-C, 10-year atherosclerotic cardiovascular disease (ASCVD) risk, risk-enhancing factors, potential adverse effects, and drug interactions. High-intensity statin therapy (rosuvastatin 20 to 40 mg/day) generally reduces LDL-C by ≥50%. Moderate-intensity statin therapy (rosuvastatin 5 to 10 mg/day) generally reduces LDL-C by ~30% to 49%. Assess response ~1 to 3 months after initiation of therapy or dose adjustment and every 3 to 12 months thereafter (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Heterozygous familial hypercholesterolemia:

Note: Multiple lipid-lowering therapies may be needed if statin monotherapy is not effective. Referral to a lipid specialist should be considered if treatment goals are not met (ACC/AHA [Grundy 2019]; Rosenson 2020a; Stein 2003).

High-intensity therapy: Oral: Initial: 20 or 40 mg once daily; if 20 mg once daily is initiated and tolerated, increase to 40 mg once daily (ACC/AHA [Grundy 2019]; Rosenson 2020a).

Homozygous familial hypercholesterolemia:

Note: Multiple lipid-lowering therapies are usually needed to achieve treatment goals; treatment should be guided by an experienced lipid specialist (Rosenson 2020a).

High-intensity therapy: Oral: 40 mg once daily (Rosenson 2020a).

Prevention of atherosclerotic cardiovascular disease:

Note: If LDL-C goal (eg, percent reduction or absolute goal) is not met with the initial dose, may consider up-titration based on estimated 10-year ASCVD risk (see American College of Cardiology ASCVD Risk Estimator Plus online), LDL-C response, and tolerability. If LDL-C goal is not met with maximally tolerated dose, additional lipid-lowering therapy may be warranted (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Primary prevention:

Patients without diabetes, 40 to 75 years of age, and with LDL-C 70 to 189 mg/dL:

ASCVD 10-year risk 5% to <7.5%:

Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest shared decision-making if ASCVD 10-year risk is 5% to 10%; however, in patients with a baseline LDL-C >160 mg/dL, statin therapy is usually recommended (Pignone 2020).

Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49% (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

ASCVD 10-year risk ≥7.5% to <20%:

Note: Depending on baseline LDL-C and presence of risk-enhancing factors, consider statin therapy after shared decision-making with patient. Some experts suggest initiating moderate-intensity statin therapy in most patients if ASCVD 10-year risk is >10% to <20% and LDL-C is >100 mg/dL (Pignone 2020).

Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49%; higher risk patients with multiple risk-enhancing factors may benefit from higher doses to reduce LDL-C by ≥50% (ACC/AHA [Grundy 2019]).

ASCVD 10-year risk ≥20%:

High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Patients with diabetes:

40 to 75 years of age without additional ASCVD risk factors:

Moderate-intensity therapy: Oral: 5 to 10 mg once daily to reduce LDL-C by 30% to 49% (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

ASCVD risk ≥20% or multiple ASCVD risk factors:

High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Patients with LDL-C ≥190 mg/dL and 20 to 75 years of age:

Note: High-intensity therapy is indicated regardless of ASCVD risk calculation or coexisting diabetes mellitus.

High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated.

Note: Consider familial hypercholesterolemia, which is preferably managed by an experienced lipid specialist (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Secondary prevention in patients with established ASCVD (eg, coronary heart disease, cerebrovascular disease [ischemic stroke or transient ischemic attack], peripheral arterial disease):

Note: Patients with high-risk ASCVD may require additional therapies to achieve LDL-C goal (eg, <70 mg/dL or <50 mg/dL if very high risk) (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]; Rosenson 2020b).

High-intensity therapy: Oral: 20 to 40 mg once daily to reduce LDL-C by ≥50%; if unable to tolerate due to adverse effects, may reduce dose to maximum tolerated (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]).

Transplantation, post heart or post kidney (off-label use):

Note: Initiate after transplant regardless of baseline cholesterol levels. Certain immunosuppressive drugs can induce or exacerbate hypercholesterolemia. Significant drug interactions between statins and immunosuppressant drugs are frequent; some interactions can increase statin serum concentrations and risk of toxicity (eg, myopathy) (AHA [Wiggins 2016]; Brennan 2020; Eisen 2020; ISHLT [Costanzo 2010]; KDIGO [Tonelli 2014]). Consult Drug Interactions Database for more detailed information.

Oral: Initial: 5 mg once daily starting 1 to 2 weeks after transplant; increase dose based on response, tolerability, and use of concomitant medications (AHA [Wiggins 2016]; Brennan 2020; ISHLT [Costanzo 2010]).

Note: In heart transplant recipients, maximum dose is 20 mg/day (ISHLT [Costanzo 2010]). In kidney transplant recipients, some experts use a maximum dose of 10 mg/day (Brennan 2020).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult Drug Interactions Database for more information.

Dosing: Geriatric

Refer to adult dosing.

Dosing: Pediatric

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. A lower, conservative dosing regimen may be necessary in patient populations predisposed to myopathy, including patients of Asian descent or concurrently receiving other lipid-lowering agents (eg, gemfibrozil, niacin, fibric acid derivatives), amiodarone, atazanavir/ritonavir, cyclosporine, lopinavir/ritonavir, or indinavir (see conservative, maximum adult doses below).

Heterozygous familial hypercholesterolemia:

Children 8 to <10 years (females >1 year postmenarche): Oral: 5 to 10 mg once daily; maximum daily dose: 10 mg/day.

Children ≥10 years and Adolescents (females >1 year postmenarche): Oral: 5 to 20 mg once daily; maximum daily dose: 20 mg/day.

Homozygous familial hypercholesterolemia: Children ≥7 years and Adolescents: Oral: Initial dose: 20 mg once daily. Maximum daily dose in adults is 40 mg/day. Although higher doses have been used (ie, 80 mg/day), additional benefit has not been reported (Marais 2008). Note: Patients on a 40 mg daily dose who develop hematuria and/or persistent, unexplained proteinuria should have a dose reduction and diagnostic work-up for causes.

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing adjustment for toxicity: Muscle symptoms (potential myopathy): Children ≥7 years and Adolescents: Discontinue use until symptoms can be evaluated; check creatine phosphokinase (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 rosuvastatin and retitrate. If muscle symptoms recur, discontinue rosuvastatin 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: Adjustment for Toxicity

Severe muscle symptoms or fatigue: Promptly discontinue use; evaluate CPK, creatinine, and urinalysis for myoglobinuria (ACC/AHA [Stone 2014]).

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 rosuvastatin. If muscle symptoms recur, discontinue rosuvastatin 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 2014]).

Administration

Capsule:

Oral: Administer with or without food. May be taken at any time of the day. Swallow capsule whole; do not crush or chew. Capsule may be opened and contents sprinkled over a small amount (teaspoonful) of soft food (eg, applesauce, chocolate/vanilla flavored pudding); swallow mixture within 60 minutes without chewing.

Nasogastric tube: Capsule may be opened and contents emptied into a 60 mL catheter tipped syringe. Add 40 mL of water, then replace plunger and shake syringe vigorously for 15 seconds. Attach syringe to a ≥16-French NG tube and administer contents; flush NG tube with additional 20 mL of water. Mixture must be used immediately after preparation.

Tablet: Administer with or without food. May be taken at any time of the day; swallow tablet whole.

Dietary Considerations

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

Capsule: Store between 20°C to 25°C (68°F to 77°F); excursions permitted between 15°C and 30°C (59°F and 86°F). Protect from moisture.

Tablet: Store between 20°C and 25°C (68°F to 77°F). Protect from moisture.

Drug Interactions

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

Antacids: May decrease the serum concentration of Rosuvastatin. Monitor therapy

Apalutamide: May decrease the serum concentration of Rosuvastatin. Monitor therapy

Asunaprevir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). 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 Consider therapy modification

Capmatinib: May increase the serum concentration of Rosuvastatin. Monitor therapy

CarBAMazepine: May decrease the serum concentration of Rosuvastatin. 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

Clopidogrel: May increase the serum concentration of Rosuvastatin. Monitor therapy

Cobicistat: May increase the serum concentration of Rosuvastatin. Management: If coadministeed with cobicistat/atazanavir or cobicistat/darunavir, initiate rosuvastatin at the lowest dose. Do not exceed rosuvastatin 10 mg/day with concurrent use of atazanavir/cobicistat or 20 mg/day with concurrent use of darunavir/cobicistat. 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). Monitor therapy

CycloSPORINE (Systemic): May increase the serum concentration of Rosuvastatin. Management: Limit rosuvastatin to 5 mg daily in patients who are also receiving cyclosporine, and monitor patients for increased rosuvastatin toxicities. Canadian labeling contraindicates concomitant use of rosuvastatin with cyclosporine. Consider therapy modification

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

Darolutamide: May increase the serum concentration of Rosuvastatin. Management: Limit the dose of rosuvastatin to 5 mg daily when combined with darolutamide. Monitor closely for increased rosuvastatin effects/toxicities (eg, myalgias, rhabdomyolysis) when these agents are combined. Consider therapy modification

Dasabuvir: May increase the serum concentration of Rosuvastatin. Management: Limit the rosuvastatin dose to a maximum of 10 mg per day when used with the ombitasvir/paritaprevir/ritonavir/dasabuvir combination product. Labeling outside of the US recommends limiting the rosuvastatin dose to 5 mg per day. Consider therapy modification

Dronedarone: May increase the serum concentration of Rosuvastatin. Monitor therapy

Elagolix: May decrease the serum concentration of Rosuvastatin. Monitor therapy

Elagolix, Estradiol, and Norethindrone: May decrease the serum concentration of Rosuvastatin. Monitor therapy

Elbasvir: May increase the serum concentration of Rosuvastatin. Management: Initiate rosuvastatin at 5 mg daily and limit the rosuvastatin dose to a maximum of 10 mg per day during coadministration with elbasvir/grazoprevir. Monitor closely for evidence of rosuvastatin toxicities (eg, myopathy, rhabdomyolysis). Consider therapy modification

Eltrombopag: May increase the serum concentration of Rosuvastatin. Management: Consideration a preventive 50% reduction in rosuvastatin adult dose when starting this combination. Consider therapy modification

Eluxadoline: May increase the serum concentration of Rosuvastatin. Management: Use the lowest effective dose of rosuvastatin if combined with eluxadoline. Consider therapy modification

Eslicarbazepine: May decrease the serum concentration of Rosuvastatin. Monitor therapy

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

Fosphenytoin-Phenytoin: May decrease the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Consider avoiding coadministration of fosphenytoin/phenytoin and statins. If combined, monitor for decreased therapeutic effects of statins if fosphenytoin/phenytoin is initiated/dose increased. Consider therapy modification

Fostamatinib: May increase the serum concentration of Rosuvastatin. Monitor therapy

Fostemsavir: May increase the serum concentration of HMG-CoA Reductase Inhibitors (Statins). Management: Use the lowest possible starting statin dose and monitor patients closely for statin-related adverse effects (eg, muscle aches and pains) during coadministration with fostemsavir. 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. Avoid combination

Gemfibrozil: May enhance the myopathic (rhabdomyolysis) effect of Rosuvastatin. Gemfibrozil may increase the serum concentration of Rosuvastatin. Management: Avoid combination is possible. If combination cannot be avoided, initiate rosuvastatin at 5 mg/day and limit rosuvastatin to 10 mg/day. Monitor for signs/symptoms of rhabdomyolysis. Consider therapy modification

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

Grazoprevir: May increase the serum concentration of Rosuvastatin. Management: Initiate rosuvastatin at 5 mg daily and limit the rosuvastatin dose to a maximum of 10 mg per day during coadministration with sofosbuvir/velpatasvir. Monitor closely for evidence of rosuvastatin toxicities (eg, myopathy, rhabdomyolysis). Consider therapy modification

Itraconazole: May increase the serum concentration of Rosuvastatin. Monitor therapy

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

Lasmiditan: May increase the serum concentration of BCRP/ABCG2 Substrates. Avoid combination

Ledipasvir: May increase the serum concentration of Rosuvastatin. Avoid combination

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

Niacin: May enhance the myopathic (rhabdomyolysis) effect of Rosuvastatin. 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 Rosuvastatin. Management: Initiate rosuvastatin at 5 mg daily and limit the rosuvastatin dose to a maximum of 10 mg per day when used with the ombitasvir/paritaprevir/ritonavir/dasabuvir combination product. Monitor for rosuvastatin toxicities (eg, myopathy, rhabdomyolysis). Consider therapy modification

Osimertinib: May increase the serum concentration of BCRP/ABCG2 Substrates. Monitor therapy

Protease Inhibitors: May increase the serum concentration of Rosuvastatin. Management: Limit rosuvastatin to 10 mg daily in patients receiving atazanavir/ritonavir or lopinavir/ritonavir. Patients receiving fosamprenavir/ritonavir or tipranavir/ritonavir do not require dose adjustments if rosuvastatin is used concomitantly. Consider therapy modification

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

Regorafenib: May increase the serum concentration of Rosuvastatin. Management: Limit the dose of rosuvastatin to 10 mg daily when combined with regorafenib. Monitor closely for increased rosuvastatin effects/toxicities (eg, myalgias, rhabdomyolysis) when these agents are combined. Consider therapy modification

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

RifAMPin: May decrease the serum concentration of Rosuvastatin. Monitor therapy

Rolapitant: May increase the serum concentration of BCRP/ABCG2 Substrates. Management: Monitor patients receiving rolapitant for increased exposure to and/or effects of BCRP/ABCG2 substrates. Use the lowest effective rosuvastatin dose when used in combination with rolapitant. Monitor therapy

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 Rosuvastatin. Management: Limit initial rosuvastatin dose to 5 mg/day when being started in a patient who is also being treated with simeprevir. The maximum rosuvastatin dose should not exceed 10 mg/day with concurrent use of simeprevir. Consider therapy modification

Tafamidis: May increase the serum concentration of BCRP/ABCG2 Substrates. Monitor therapy

Tedizolid: May increase the serum concentration of BCRP/ABCG2 Substrates. Monitor therapy

Teriflunomide: May increase the serum concentration of Rosuvastatin. Management: Limit the maximum adult rosuvastatin dose to 10 mg/day in patients receiving teriflunomide, and monitor for evidence of rosuvastatin toxicity (eg, muscle toxicity, elevated transaminase concentrations). Consider therapy modification

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

Velpatasvir: May increase the serum concentration of Rosuvastatin. Management: Initiate rosuvastatin at 5 mg daily and limit the rosuvastatin dose to a maximum of 10 mg per day during coadministration with sofosbuvir/velpatasvir. Monitor closely for evidence of rosuvastatin toxicities (eg, myopathy, rhabdomyolysis). Consider therapy modification

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 Rosuvastatin. Avoid combination

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.

>10%: Neuromuscular & skeletal: Myalgia (2% to 13%)

1% to 10%:

Central nervous system: Headache (6% to 9%), dizziness (4%)

Endocrine & metabolic: Diabetes mellitus (new onset: 3%)

Gastrointestinal: Nausea (4% to 6%), constipation (3% to 5%)

Genitourinary: Cystitis (interstitial; Huang 2015)

Hepatic: Increased serum ALT (2%; >3 times ULN)

Neuromuscular & skeletal: Arthralgia (4% to 10%), increased creatine phosphokinase (3%; >10 x ULN: Children 3%), weakness (5%)

<1%, postmarketing, and/or case reports: Abnormal thyroid function test, cognitive dysfunction (reversible; includes amnesia, confusion, memory impairment), depression, elevated glycosylated hemoglobin (HbA1c), gynecomastia, hematuria (microscopic), hepatic failure, hepatitis, hypersensitivity reaction (including angioedema, pruritus, skin rash, urticaria), immune-mediated necrotizing myopathy, increased gamma-glutamyl transferase, increased serum alkaline phosphatase, increased serum bilirubin, increased serum glucose, increased serum transaminases, interstitial pulmonary disease, jaundice, myoglobinuria, myopathy, myositis, pancreatitis, peripheral neuropathy, proteinuria (dose related), renal failure, rhabdomyolysis, sleep disorder (including insomnia and nightmares), thrombocytopenia

Warnings/Precautions

Concerns related to adverse effects:

• Diabetes mellitus: Small increases in HbA1c (mean: ~0.1%) and fasting blood glucose have been reported with rosuvastatin; however, the benefits of statin therapy far outweigh the risk of dysglycemia.

• Hematuria/proteinuria: Hematuria (microscopic) and proteinuria have been observed; more commonly reported in adults receiving rosuvastatin 40 mg daily. Typically, transient and not associated with a decrease in renal function. Consider dosage reduction if unexplained hematuria and proteinuria persists.

• 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 rosuvastatin. Liver enzyme tests should be obtained at baseline and as clinically indicated; routine periodic monitoring of liver enzymes is not necessary.

• Hypersensitivity: Hypersensitivity reactions, including rash, pruritus, urticaria, and angioedema, have been reported.

• 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 concomitant use of interacting medications. Consult drug interactions database for more detailed information. If concurrent use is warranted, consider lower starting and maintenance doses of rosuvastatin. Use caution in patients with inadequately treated hypothyroidism, patients taking other drugs associated with myopathy (eg, colchicine), ≥65 years of age, and women; 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; consider treatment with immunosuppressants and additional neuromuscular and serologic testing. Prior to initiating a different HMG-CoA reductase inhibitor, consider risk of IMNM; monitor closely.

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 with active liver disease or unexplained transaminase elevations.

• Renal impairment: Dosage adjustment required in patients with a CrCl <30 mL/minute/1.73 m2 and not receiving hemodialysis.

Special populations:

• Asian population: Increased risk of rosuvastatin-associated myopathy in certain subgroups; dosage adjustment should be considered for patients of Asian descent.

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

• Surgical patients: 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.

Other warnings/precautions:

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

Monitoring Parameters

Manufacturer's labeling:

Consider neuromuscular and serologic testing if immune-mediated necrotizing myopathy is suspected.

ACC/AHA Blood Cholesterol Guideline recommendations (ACC/AHA [Grundy 2019]; ACC/AHA [Stone 2014]):

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 (ie, 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.

Reproductive Considerations

Rosuvastatin is contraindicated in females who may become pregnant.

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 2019]).

Pregnancy Considerations

Rosuvastatin is contraindicated in pregnant females.

Adverse events have been observed in some animal reproduction studies. 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.

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

Patient Education

What is this drug used for?

• 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 is used in some people to lower the chance of heart attack, stroke, and certain heart procedures.

• It may be given to you for other reasons. Talk with the doctor.

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:

• Headache

• Abdominal pain

• Nausea

• Joint pain

• Weakness

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:

• High blood sugar like confusion, fatigue, increased thirst, increased hunger, passing a lot of urine, flushing, fast breathing, or breath that smells like fruit.

• Liver problems like dark urine, feeling tired, lack of appetite, nausea, abdominal pain, light-colored stools, vomiting, or yellow skin or eyes.

• Blood in the urine

• Unable to pass urine

• Change in amount of urine passed

• Muscle pain

• Muscle tenderness

• Muscle weakness

• 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.

Note: This is not a comprehensive list of all side effects. Talk to your doctor if you have questions.

Consumer Information Use and Disclaimer: This information should not be used to decide whether or not to take this medicine or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a limited summary of general information about the medicine's uses from the patient education leaflet and is not intended to be comprehensive. This limited summary does NOT include all information available about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to this medicine. This information is not intended to provide medical advice, diagnosis or treatment and does not replace information you receive from the healthcare provider. For a more detailed summary of information about the risks and benefits of using this medicine, please speak with your healthcare provider and review the entire patient education leaflet.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

Frequently Asked Questions