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Pravastatin (Monograph)

Brand name: Pravachol
Drug class: HMG-CoA Reductase Inhibitors
- Statins
VA class: CV350
Chemical name: [1S-[1α(βS*,δS*),2α,6α,8β(R*),8aα]]-1,2,6,7,8,8a-Hexahydro-β,δ,6-trihydroxy-2-methyl-8-(2-methyl-1-oxobutoxy)-1-naphthalene-heptanoic acid monosodium salt
CAS number: 81131-70-6

Medically reviewed by Drugs.com on Dec 4, 2023. Written by ASHP.

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).1 2 3 4 5 6

Uses for Pravastatin

Reduction in Risk of Cardiovascular Events

Adjunct to nondrug therapies (i.e., lifestyle modifications) in patients with hypercholesterolemia without clinical evidence of CHD to reduce the risk of MI, to reduce the risk of undergoing myocardial revascularization procedures, and to reduce the risk of cardiovascular mortality (with no increase in death from noncardiovascular causes).1 12

Adjunct to diet and lifestyle modifications400 in patients with clinical evidence of CHD to reduce the risk of total mortality by reducing coronary death, to reduce the risk of MI, to reduce the risk of undergoing myocardial revascularization procedures, and to reduce the risk of stroke or TIA.1 17 29 48 54 65 69

Adjunct to diet and lifestyle modifications400 in patients with clinical evidence of CHD to slow the progression of coronary atherosclerosis.1 13 14 16

Extensive evidence demonstrates that statins can substantially reduce LDL-cholesterol concentrations and associated risk of atherosclerotic cardiovascular disease (ASCVD) when used for secondary prevention or primary prevention in high-risk patients.336 337 338 350 400

AHA/ACC cholesterol management guideline states that lifestyle modification is the foundation of ASCVD risk reduction.400 Patients with established ASCVD or high risk of ASCVD should also be treated with a statin.400

Because relative ASCVD risk reduction is correlated with degree of LDL-cholesterol lowering, use maximum tolerated intensity of a statin to achieve greatest benefit.400 High-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by ≥50%) is recommended; if high-intensity statin therapy not possible (e.g., because of a contraindication or intolerable adverse effect), may consider moderate-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by 30–49%).400 AHA/ACC considers pravastatin 40–80 mg daily to be a moderate-intensity statin.400

The addition of a nonstatin drug (e.g., ezetimibe, PCSK9 inhibitor) to statin therapy may be considered in certain high-risk patients who require further reduction in LDL-cholesterol concentrations, particularly if there is evidence from randomized controlled studies suggesting that the addition of the nonstatin drug further reduces ASCVD events.400

When considering whether to initiate statin therapy for primary prevention, AHA/ACC recommends an individualized approach and shared decision making between patient and clinician.400 According to the guidelines, statin therapy may be considered in certain high-risk groups such as adults 20–75 years of age with LDL cholesterol ≥190 mg/dL, adults 40–75 years of age with diabetes mellitus, adults 40–75 years of age without diabetes mellitus but with LDL-cholesterol levels ≥70 mg/dL and an estimated 10-year ASCVD risk ≥7.5%, and adults 40–75 years of age with chronic kidney disease (not treated with dialysis or transplantation) and LDL-cholesterol concentrations of 70–189 mg/dL who have a 10-year ASCVD risk ≥7.5%.400

Dyslipidemias

Adjunct to nondrug therapies (e.g., dietary management) in adults to decrease elevated serum total and LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia (Fredrickson type IIa or IIb).1 2 3 5 17 Also used in combination with fenofibrate to decrease triglyceride concentrations and increase HDL-cholesterol concentrations in patients with mixed dyslipidemia and CHD (or CHD risk equivalents) who are on optimal statin therapy; however, no incremental benefit on cardiovascular morbidity and mortality beyond that provided by statin monotherapy.74 353

Adjunct to dietary therapy and lifestyle modification in the management of heterozygous familial hypercholesterolemia in children ≥8 years of age who, despite an adequate trial of dietary management, have a serum LDL-cholesterol concentration of ≥190 mg/dL or a serum LDL-cholesterol concentration of ≥160 mg/dL and either a family history of premature cardiovascular disease or ≥2 other cardiovascular risk factors.1

Adjunct to nondrug therapies (e.g., dietary management) in the treatment of primary dysbetalipoproteinemia (Fredrickson type III) in patients who do not respond adequately to diet.1

Adjunct to nondrug therapies (e.g., dietary management) in the treatment of elevated serum triglyceride concentrations (Fredrickson type IV).1

Reduction of total and LDL-cholesterol concentrations in patients with hypercholesterolemia associated with or exacerbated by diabetes mellitus† [off-label] (diabetic dyslipidemia),51 62 cardiac† [off-label] or liver† [off-label] transplantation,19 63 or nephrotic syndrome† [off-label] (nephrotic hyperlipidemia).20

Pravastatin Dosage and Administration

General

Patient Monitoring

Administration

Oral Administration

Administer orally at any time of day without regard to meals.1

Dosage

Available as pravastatin sodium; dosage expressed in terms of pravastatin.1

Dosage modifications may be necessary when used concomitantly with certain drugs (see Specific Drugs under Interactions).1

Pediatric Patients

Dyslipidemias
Oral

Children 8–13 years of age: 20 mg once daily.1 Dosages >20 mg daily have not been evaluated.1

Adolescents 14–18 years of age: 40 mg once daily.1 Dosages >40 mg daily have not been evaluated.1

Re-evaluate in adulthood and modify therapy appropriately.1

Adults

Reduction in Risk of Cardiovascular Events
Oral

Use maximally tolerated statin intensity to achieve optimal ASCVD risk reduction.400 High-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by ≥50%) is preferred; if high-intensity statin therapy not possible (e.g., because of a contraindication or intolerable adverse effect), may consider moderate-intensity statin therapy (defined as reducing LDL-cholesterol concentrations by 30–49%).400

The AHA/ACC guideline panel considers pravastatin 40–80 mg daily to be a moderate-intensity statin.400

Dyslipidemias
Oral

Initially, 40 mg once daily.1 If antilipemic response is inadequate, increase dosage to 80 mg daily.1 Adjust dosage at intervals of ≥4 weeks until the desired effect on lipoprotein concentrations is observed.1

Special Populations

Hepatic Impairment

No specific dosage recommendations at this time.1

Use with caution in patients who consume substantial amounts of alcohol, have a recent (<6 months) history of liver disease, or exhibit manifestations of liver disease (e.g., unexplained increases in aminotransferase concentrations, jaundice).1

Contraindicated in patients with active liver disease or unexplained, persistent increases in serum aminotransferase concentrations.1

Renal Impairment

Initially, 10 mg once daily in patients with severe renal impairment.1

Detailed Pravastatin dosage information

Cautions for Pravastatin

Contraindications

Warnings/Precautions

Musculoskeletal Effects

Myopathy (manifested as muscle pain, tenderness, or weakness and serum creatine kinase [CK, creatine phosphokinase, CPK] concentration increases >10 times the ULN) reported occasionally.1

Rhabdomyolysis (characterized by muscle pain or weakness with marked increases [>10 times the ULN] in serum CK concentrations and increases in Scr [usually accompanied by brown urine and urinary myoglobinuria])138 with acute renal failure secondary to myoglobinuria has been reported.1

Immune-mediated necrotizing myopathy (IMNM), an autoimmune myopathy, reported rarely in patients receiving statins.1 Characterized by proximal muscle weakness and elevated CK concentrations that persist despite discontinuance of statin therapy, necrotizing myopathy without substantial inflammation, and improvement following therapy with immunosuppressive agents.1

Risk of myopathy is increased in patients receiving higher dosages of statins; risk also may be increased in geriatric patients (≥65 years of age) and patients with renal impairment or uncontrolled hypothyroidism.1

Certain drug interactions also may increase risk of myopathy and/or rhabdomyolysis.1 (See Specific Drugs under Interactions.)

AHA/ACC recommends measurement of CK levels in patients with severe statin-associated muscle symptoms; however, routine monitoring not useful.400

Consider myopathy in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation in CK.1 Discontinue if serum CK concentrations increase markedly or if myopathy is diagnosed or suspected.1

Temporarily withhold therapy in any patient experiencing an acute or serious condition predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).1

Hepatic Effects

Associated with increases in serum aminotransferase (AST, ALT) concentrations.1

Pancreatitis,1 hepatitis (including chronic active hepatitis),1 cholestatic jaundice,1 fatty change in liver, cirrhosis,1 fulminant hepatic necrosis,1 hepatoma,1 and fatal and nonfatal hepatic failure1 have been reported.1

Perform liver function tests before initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage201 ).1 Serious statin-related liver injury is rare and unpredictable, and routine periodic monitoring of liver enzymes does not appear to be effective in detecting or preventing serious liver injury.200 AHA/ACC cholesterol management guideline states that it is reasonable to obtain liver function tests in patients with symptoms of hepatotoxicity (e.g., unusual fatigue or weakness, loss of appetite, abdominal pain, dark colored urine, yellowing of skin or sclera); however, routine monitoring not recommended.350 400

If serious liver injury with clinical manifestations and/or hyperbilirubinemia or jaundice occurs, promptly interrupt pravastatin therapy.1 If an alternate etiology is not found, do not restart pravastatin.1

Hyperglycemic Effects

Increases in HbA1c and fasting serum glucose concentrations reported.200 Possible increased risk of developing diabetes.200 May need to monitor glucose concentrations following initiation of statin therapy.201

AHA/ACC cholesterol management guideline states that in patients with increased risk of diabetes mellitus or new-onset diabetes mellitus, statin therapy and lifestyle modifications should be continued to reduce risk of ASCVD.400

Endogenous Steroid Production

Statins interfere with cholesterol synthesis and theoretically may blunt adrenal and/or gonadal steroid production.1

Effects of pravastatin on basal steroid hormone levels not established.1 Effects on pituitary-gonadal axis in premenopausal women unknown.1

If clinical evidence of endocrine dysfunction is present, evaluate patients appropriately.1

Caution advised if a statin or another antilipemic agent is used concomitantly with drugs that may decrease concentrations or activity of endogenous steroid hormones (e.g., ketoconazole, spironolactone, cimetidine).1

Cognitive Impairment

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.1

Generally nonserious and reversible, with variable times to symptom onset (1 day to years) and resolution (median of 3 weeks following discontinuance of therapy).1 200 Not associated with fixed or progressive dementia (e.g., Alzheimer’s disease) or clinically important cognitive decline.200 Not associated with any specific statin, patient's age, statin dosage, or concomitant drug therapy.200

FDA states that cardiovascular benefits of statins outweigh the small increased risk of cognitive impairment.200

If manifestations consistent with cognitive impairment occur, National Lipid Association (NLA) statin safety assessment task force recommends evaluating and managing patients appropriately.202

Role as Adjunct Therapy

Prior to institution of antilipemic therapy, vigorously attempt to control serum cholesterol by appropriate dietary regimens, weight reduction, exercise, and treatment of any underlying disorder that might be the cause of lipid abnormality.1

Specific Populations

Pregnancy

All statins were previously contraindicated in pregnant women because fetal risk was thought to outweigh any possible benefit.405 However, the totality of evidence to date indicates limited potential for statins to cause malformations and other adverse embryofetal effects; FDA has therefore requested removal of the contraindication.405 Most pregnant patients should still discontinue statins because of the possibility of fetal harm; however, some patients (e.g., those with homozygous familial hypercholesterolemia or established cardiovascular disease) may benefit from continued therapy.400 405 Consider patient's individual risks and benefits.405

Patients who become pregnant or suspect that they are pregnant while receiving a statin should notify their clinician; clinician should advise patient on the appropriate course of action.405

Increased risk of miscarriage reported in pregnant women exposed to statins; however, not clear whether drug-related or due to other confounding factors.400 405

Lactation

Distributed into milk; effects of drug on breast-fed infants or milk production not known.1 Use contraindicated in nursing women; women who require pravastatin therapy should not breast-feed their infants.1 Many patients can stop statin therapy temporarily until breast-feeding is complete; patients who require ongoing statin treatment should not breast-feed and should use alternatives such as infant formula.400 405

Pediatric Use

Safety and efficacy not established in children <8 years of age.1 Advise adolescent girls to use effective and appropriate contraceptive methods during therapy to reduce the likelihood of unintended pregnancy.1

Geriatric Use

No substantial differences in safety or efficacy relative to younger adults.1

Use with caution, since age ≥65 years is a predisposing factor for myopathy.1

Patients >75 years of age may have a higher risk of adverse effects and lower adherence to therapy; consider expected benefits versus adverse effects before initiating statin therapy in this population.400

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol, have a recent (<6 months) history of liver disease, or exhibit manifestations of liver disease (e.g., unexplained increases in aminotransferase concentrations, jaundice).1

Contraindicated in patients with active liver disease or unexplained, persistent increases in liver function test results.1

Renal Impairment

Monitor closely for adverse musculoskeletal effects, since history of renal impairment may be a risk factor for development of rhabdomyolysis.1

Dosage adjustments necessary in patients with severe renal impairment.1 (See Renal Impairment under Dosage and Administration.)

Common Adverse Effects

Musculoskeletal pain, nausea or vomiting, upper respiratory infection, diarrhea, headache.1

Drug Interactions

Minimally metabolized by CYP3A4; pharmacokinetic interaction unlikely.1

Specific Drugs

Drug

Interaction

Comments

Aspirin

Increased pravastatin peak plasma concentration and AUC1

Bile acid sequestrants (i.e., cholestyramine, colestipol)

Variable effects on pravastatin concentrations1

Administer pravastatin 1 hour before or 4 hours after the resin66

Calcium-channel blocking agents (diltiazem, verapamil)

Increased pravastatin peak plasma concentration and AUC1

Cimetidine

Increased pravastatin peak plasma concentration and AUC1

Colchicine

Myopathy, including rhabdomyolysis, reported1

Use concomitantly with caution1

Cyclosporine

Substantially increased pravastatin concentrations; possible increased risk of myopathy or rhabdomyolysis1 339

If used concomitantly, initiate pravastatin at 10 mg daily; do not exceed pravastatin dosage of 20 mg daily1

Digoxin

Slight increases in plasma digoxin and pravastatin concentrations1

Fibric acid derivatives (e.g., fenofibrate, gemfibrozil)

Increased risk of myopathy or rhabdomyolysis1

Gemfibrozil: Decreased pravastatin peak plasma concentration and AUC1

Gemfibrozil: Avoid concomitant use1

Other fibric acid derivatives (e.g., fenofibrate): Use concomitantly with caution and only if benefits outweigh risks; consider using only low- or moderate-intensity statin therapy during concomitant therapy1 350

Fluconazole

Decreased pravastatin peak plasma concentration and AUC1

HIV protease inhibitors

Ritonavir-boosted darunavir: Increased pravastatin peak plasma concentration and AUC1

Lopinavir/ritonavir: Increased pravastatin peak plasma concentration and AUC1

Ritonavir-boosted darunavir: Some experts recommend using the lowest necessary dosage of pravastatin and carefully monitoring patients72

Lopinavir/ritonavir: Dosage adjustment not necessary72

Ritonavir-boosted saquinavir: Dosage adjustment not necessary72 73

Itraconazole

Increased pravastatin concentrations1

Macrolides (e.g., azithromycin. clarithromycin, erythromycin)

Azithromycin: Potential increased pravastatin concentrations1

Clarithromycin: Increased pravastatin peak plasma concentration and AUC;1 increased risk of myopathy or rhabdomyolysis1

Erythromycin: Potential increased pravastatin concentrations and increased risk of myopathy1

Azithromycin and erythromycin: Use concomitantly with caution1

Clarithromycin: Use concomitantly with caution; if used concomitantly, do not exceed pravastatin dosage of 40 mg daily1

Niacin (antilipemic dosages [≥1 g daily])

Decreased pravastatin peak plasma concentration and AUC;1 possible increased risk of myopathy1

Increased risk of severe adverse effects (disturbances in glycemic control requiring hospitalization, development of diabetes mellitus, adverse GI effects, myopathy, gout, rash, skin ulceration, infection, bleeding) with concomitant use of niacin (1.5–2 g daily) and simvastatin (40–80 mg daily, with or without ezetimibe)369 371

Use concomitantly with caution; consider reducing pravastatin dosage1

Warfarin

Increased warfarin peak plasma concentration and AUC; increased PT1 339

Monitor INR more closely after initiating or changing dosage of pravastatin339
Pravastatin drug interactions (more detail)

Pravastatin Pharmacokinetics

Absorption

Bioavailability

Rapidly absorbed following oral administration; undergoes extensive first-pass metabolism in the liver.1 129 130 131 132 Mean peak plasma concentrations occur at 1–1.5 hours.1 133

Absolute bioavailability is 17%.1 130

Evening administration of the drug is associated with a decrease in the extent of absorption;1 however, the antilipemic activity remains unchanged and may be superior to the activity achieved with morning administration.1

Onset

A therapeutic response to pravastatin is usually apparent within 1 week after initiating therapy, with a maximal response occurring within 4 weeks.1 37 38 132

Food

Food appears to reduce the systemic bioavailability of pravastatin;1 129 131 however, antilipemic effects are similar whether pravastatin is administered with or 1 hour prior to meals.1

Distribution

Extent

Distributed mainly to the liver.1

Distributed into human milk.1

Plasma Protein Binding

Approximately 50%.1

Elimination

Metabolism

Undergoes enzymatic and nonenzymatic biotransformation independent of the CYP enzyme system.131 136 The principal metabolites are pharmacologically inactive.129 130 131 137

Elimination Route

Excreted in urine (20%) and feces (70%).1 129 130 132

Half-life

1.8 hours.1

Special Populations

Renal impairment may reduce clearance of pravastatin and/or active metabolites.1

Hepatic impairment may reduce clearance of pravastatin and/or active metabolites.1

Stability

Storage

Oral

Tablets

Tight containers at 25°C (may be exposed to 15–30°C); protect from light and moisture.1

Actions

Advice to Patients

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name

Pravastatin Sodium

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets

10 mg (of pravastatin)*

Pravastatin Sodium Tablets

20 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

40 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

80 mg (of pravastatin)*

Pravachol

Bristol-Myers Squibb

Pravastatin Sodium Tablets

AHFS DI Essentials™. © Copyright 2024, Selected Revisions December 13, 2021. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Off-label: Use is not currently included in the labeling approved by the US Food and Drug Administration.

References

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