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Editor: Amit Sapra Updated: 6/21/2023 7:28:28 PM

Pravastatin is an FDA-approved HMG Co-A reductase inhibitor indicated for the treatment of primary hypercholesterolemia, hyperlipidemia, and mixed dyslipidemia.[1] Indications also include the prevention of cardiovascular events in patients diagnosed with coronary artery disease. Pravastatin can improve total mortality by decreasing the risk of coronary death myocardial infarction and slowing the progression of coronary atherosclerosis. Pravastatin is most beneficial when prescribed as adjunctive therapy with a low-fat diet (i.e., a strict cholesterol-lowering diet including food such as fruits, vegetables, fish, beans, and nuts) and regular exercise. The medication is also safe and effective for the geriatrics population and children over the age of seven. However, drug safety and efficacy remain unestablished in infants, and it is highly contraindicated in pregnant women. The medication is also effective management for individuals with familial heterozygous hypercholesterolemia. Off-label, pravastatin may be used for cerebral vasospasm prophylaxis after subarachnoid hemorrhage in adults.[2]

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Pravastatin falls under the class of competitive hydroxymethylglutaryl Coenzyme-A (HMG Co-A) reductase inhibitors. It is readily absorbed and less potent in comparison to atorvastatin and rosuvastatin. The drug selectively acts on the rate-limiting step in cholesterol biosynthesis by inhibiting HMG Co-A reductase; this results in the upregulation of hepatic LDL (low-density lipoprotein) receptors enhancing LDL metabolism and clearance, which subsequently lowers the total plasma cholesterol in circulation. It also causes a reduction in VLDL, triglycerides, and apolipoprotein B and increases HDL (high-density lipoprotein)-cholesterol levels.[3]

Statins such as pravastatin get metabolized in the liver via the extensive first-pass extraction path, and elimination is primarily through feces. When administered orally, pravastatin has a bioavailability of 17% and a half-life of between 2.6 to 3.2 hours.[4]

Some limited studies have shown when coadministering pravastatin with cholestyramine (bile-binding resin), the drug may decrease LDL levels to half and further slow the progression of atherosclerosis and reduce the risk of coronary death.[5]

Pravastatin is available as an oral tablet and is administered once daily with or without food. It is available in 10 mg, 20 mg, 40 mg, and 80 mg strength tablets. HMG Co-A inhibitors are most effective when taken at bedtime due to their effect on hepatic cholesterol synthesis. The drug should be swallowed whole with water and not crushed. The clinician can make dose adjustments at 4-week intervals based on individual patient responses to the drug.[6]

Hyperlipidemia, hypercholesterolemia, and mixed dyslipidemia:

  • In the adults and geriatrics population: 40 mg orally once daily (do not exceed 80 mg per day)
  • In children eight to thirteen years age: 20 mg orally once daily (do not exceed 60 mg per day)
  • In adolescents fourteen to eighteen years age: 40 mg orally once daily (doses higher than 40 mg are not studied in this population)

Stroke or myocardial infarction prophylaxis and secondary prevention of cardiovascular mortality and acute coronary events:

  • In adults: 40 mg orally once daily (do not exceed 80 mg per day)

Special Population

Patients with Renal Impairment: A starting dose of 10 mg pravastatin once daily is recommended in patients with severe renal impairment.

Patients with Liver Impairment: Liver function tests are recommended to be performed before the initiation of pravastatin therapy and when clinically indicated. Patients with hepatic impairment should avoid HMG Co-A inhibitors.

Pregnancy Implications: After a comprehensive review of all available data, the U.S. Food and Drug Administration (FDA) has removed the strongest warning against using HMG-co-A Reductase Inhibitors in pregnant women. However, most women should stop taking pravastatin once they become pregnant. Assess the risk vs. benefits to the pregnant patient.

Breastfeeding Considerations: Pravastatin is excreted in low levels in human milk. Maternal exposure to statins can have serious adverse reactions in nursing infants. It can disrupt infant lipid metabolism, so women who require treatment with pravastatin should refrain from breastfeeding their infants. Pravastatin has low oral bioavailability and has a lower risk to infants. Children with homozygous familial hypercholesterolemia can be treated with statins beginning at 12 months of age. There is a lack of data, and hence alternative medicines are preferred especially when nursing preterm or newborn infants.[7]

Some common adverse effects associated with pravastatin therapy include nausea and vomiting, dizziness, arthralgia, myalgia, headache, constipation, diarrhea, abdominal pain, flushing, dyspepsia, insomnia, increased creatine phosphokinase, and urinary tract infection. In addition, fatigue, pruritus, rash, cough, heartburn, and flu-like symptoms may also present in patients taking pravastatin. Some potentially serious adverse effects that require adjustment of dose or frequency of administration may include chest pain, edema, hepatitis, jaundice, renal impairment, blurred vision, and confusion.[8]

Drug Interactions

Bile acid-binding resins: Pravastatin may be used concomitantly with bile acid resins like cholestyramine colestipol. When administering pravastatin and resins, pravastatin should be given either 1 hour before or at least 4 hours after the bile-acid-binding resin.

Cyclosporin: In patients taking immunosuppressive medicines such as cyclosporine concomitantly with pravastatin, therapy should begin with 10 mg of pravastatin daily at bedtime. Exercise caution when titrating to higher doses as there is an increased risk of myopathy and rhabdomyolysis. Most patients treated concomitantly receive a maximum of 20 mg of pravastatin.[9]

Clarithromycin: The risk of myopathy/rhabdomyolysis is higher with concomitant administration of pravastatin and clarithromycin. In patients taking clarithromycin, the pravastatin dose should not be more than 40 mg daily. Other macrolides (e.g., erythromycin and azithromycin) can increase statin exposures while used with pravastatin. Therefore, exercise caution when macrolide antibiotics are used with pravastatin.

Colchicine: There is an increased risk of myopathy and/or rhabdomyolysis with concomitant administration of colchicine and pravastatin. 

Gemfibrozil: There is an increased risk of myopathy and/or rhabdomyolysis when gemfibrozil is coadministered with statins. Therefore, concomitant administration of pravastatin and gemfibrozil is contraindicated.[10]

Fibrates: There is a known risk of myopathy during treatment with statins, and it is increased with concurrent administration of other fibrates. Use pravastatin with caution when other fibrates are concomitantly administered.

Niacin: There is an enhanced risk of skeletal muscle adverse reactions when niacin is used in combination with pravastatin; a reduction in pravastatin dosage should be considered in this scenario.

Pravastatin is contraindicated in patients with HMG Co-A reductase inhibitor hypersensitivity or suspected reaction to any component of the medication. Statins such as pravastatin are highly contraindicated in individuals with any active form of liver disease (i.e., hepatitis, hepatic encephalopathy, jaundice, hepatic impairment) or persistently elevated serum transaminase levels. Safety measures are necessary for patients with a recent history of hepatic disease or a history of heavy alcohol use/misuse. These patients should be closely monitored for any signs of liver impairment and treated accordingly. Pravastatin therapy requires discontinuation in patients with signs or symptoms of muscle weakness, myalgias, or suspected rhabdomyolysis.[11] In patients taking fibrates, niacin, or cyclosporine, the risk of myopathy may increase when on statins; thus, prompt dose adjustment is necessary. Diabetic patients should receive counsel to use precaution when on pravastatin therapy due to the increased risk of hyperglycemia.[12]

Pregnant or breastfeeding women should avoid HMG Co-A inhibitors due to the elevated risk of teratogenicity and excretion into breast milk. Caution is necessary for the geriatrics population due to advanced age being a predisposing factor for myopathy. Avoid pravastatin therapy with cytochrome P450 inducers and inhibitors due to its effect on drug absorption.[13]

Patients taking pravastatin should undergo monitoring for the relief of symptoms and any adverse effects pertaining to the medication. A complete list of patient medications should be revised extensively before prescribing the drug. Renal function (UA, BUN, and creatinine) should be regularly monitored in individuals with renal impairment, and dosing can be corrected. It is crucial to monitor the hepatic function (LFTs) to avoid administering the medication in patients with active liver disease or persistently elevated serum transaminases.[14] Creatine phosphokinase (CPK) levels need close monitoring for any signs of myopathy or rhabdomyolysis associated with the medication. The patient's blood pressure and cardiac function (heart rate) should have been routinely checked at each physician visit, and dose adjustments should checking accordingly. A complete lipid panel (total cholesterol, LDL, TGs) is regularly necessary, and dose adjustment can occur at intervals of four weeks. Diet and exercise regimes should also have revisions with the patient at each clinic visit for optimal results.[15] Pravastatin should be stored in a cool, dry place and away from light.


Rhabdomyolysis and other muscle symptoms can be indicative of toxicity. Several studies and case reports have also suggested an association between statin therapy and neuromuscular disorders such as dermatomyositis, polymyositis, and necrotizing myopathies. If rhabdomyolysis is ruled out and other muscle symptom pathologies are suspected, the statin-associated muscle symptoms clinical index (SAMS-CI) must be administered to determine if muscle symptoms are due to statin therapy.[16] Stopping statin use, administration of replacement vitamin D (associated with myopathy), and switching statins are all viable options depending on the etiology of myopathy.[17]

Enhancing Healthcare Team Outcomes

An interprofessional team consisting of physicians, nurses, and pharmacists is needed to successfully manage patients treated with HMG Co-A reductase inhibitors such as pravastatin. Providers must be knowledgeable regarding the symptoms of toxicity. Other specialty physicians, such as nephrologists and toxicologists, may be consulted to ensure the best patient outcome. Patient education is necessary for individuals with hepatic or renal impairment. Clinicians and pharmacists must advise patients to report any signs or symptoms of hepatic injury (abnormal fatigue, weight loss, right upper quadrant pain, jaundice). Pharmacists should also check for drug interactions and inform the prescriber of any concerns. The primary care physician or the nurse practitioner must also counsel the patient on the importance of reading labels to avoid overdosing to prevent any drug-related toxicities. Pravastatin therapy requires a communicative team dynamic, successfully coordinating to manage any adverse effects and provide patient care to obtain the best outcomes. [Level 5]



Pravastatin 2012;     [PubMed PMID: 31643964]


. Statins. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. 2012:():     [PubMed PMID: 31643398]


Expanded table: statins. The Medical letter on drugs and therapeutics. 2019 Sep 23;     [PubMed PMID: 31599870]

Level 3 (low-level) evidence


Wagmann L,Hemmer S,Caspar AT,Meyer MR, Method development for quantitative determination of seven statins including four active metabolites by means of high-resolution tandem mass spectrometry applicable for adherence testing and therapeutic drug monitoring. Clinical chemistry and laboratory medicine. 2019 Oct 30;     [PubMed PMID: 31665111]


Carmena R, Betteridge DJ. Diabetogenic Action of Statins: Mechanisms. Current atherosclerosis reports. 2019 Apr 30:21(6):23. doi: 10.1007/s11883-019-0780-z. Epub 2019 Apr 30     [PubMed PMID: 31037345]


Lipid-lowering drugs. The Medical letter on drugs and therapeutics. 2019 Feb 11;     [PubMed PMID: 30845106]

Level 3 (low-level) evidence


. Pravastatin. Drugs and Lactation Database (LactMed®). 2006:():     [PubMed PMID: 30000416]


Gosho M, Rhabdomyolysis risk from the use of two-drug combination of antidyslipidemic drugs with antihypertensive and antidiabetic medications: a signal detection analysis. Fundamental     [PubMed PMID: 30575126]


Olbricht C,Wanner C,Eisenhauer T,Kliem V,Doll R,Boddaert M,O'Grady P,Krekler M,Mangold B,Christians U, Accumulation of lovastatin, but not pravastatin, in the blood of cyclosporine-treated kidney graft patients after multiple doses. Clinical pharmacology and therapeutics. 1997 Sep     [PubMed PMID: 9333107]


Wiklund O, Angelin B, Bergman M, Berglund L, Bondjers G, Carlsson A, Lindén T, Miettinen T, Odman B, Olofsson SO. Pravastatin and gemfibrozil alone and in combination for the treatment of hypercholesterolemia. The American journal of medicine. 1993 Jan:94(1):13-20     [PubMed PMID: 8420296]


Muhammad ZA,Ahmad T,Baloch N, Can alternate-day Statin regimen minimize its adverse effects on muscle and tendon? A systematic review. JPMA. The Journal of the Pakistan Medical Association. 2019 Jul;     [PubMed PMID: 31308572]

Level 1 (high-level) evidence


Hori E, Kikuchi C, Imaeda K, Okayama N, Suzuki T, Matsunaga T. [Effect of Statins on Glycemic Status and Plasma Adiponectin Concentrations in Patients with Type 2 Diabetes Mellitus and Hypercholesterolemia]. Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan. 2019 May 1:139(5):807-815. doi: 10.1248/yakushi.18-00218. Epub 2019 Feb 15     [PubMed PMID: 30773524]


Andrus MR, East J. Use of statins in patients with chronic hepatitis C. Southern medical journal. 2010 Oct:103(10):1018-22; quiz 1023. doi: 10.1097/SMJ.0b013e3181f0c6b4. Epub     [PubMed PMID: 20818300]


Charlton M, Obesity, hyperlipidemia, and metabolic syndrome. Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society. 2009 Nov;     [PubMed PMID: 19877024]


Ochs-Balcom HM,Nguyen LM,Ma C,Isackson PJ,Luzum JA,Kitzmiller JP,Tarnopolsky M,Weisman M,Christopher-Stine L,Peltier W,Wortmann RL,Vladutiu GD, Clinical features related to statin-associated muscle symptoms. Muscle     [PubMed PMID: 30549046]


Backes JM, Ruisinger JF, Gibson CA, Moriarty PM. Statin-associated muscle symptoms-Managing the highly intolerant. Journal of clinical lipidology. 2017 Jan-Feb:11(1):24-33. doi: 10.1016/j.jacl.2017.01.006. Epub 2017 Jan 18     [PubMed PMID: 28391891]


Ovesjö ML, Skilving I, Bergman P, Rane A, Ekström L, Björkhem-Bergman L. Low Vitamin D Levels and Genetic Polymorphism in the Vitamin D Receptor are Associated with Increased Risk of Statin-Induced Myopathy. Basic & clinical pharmacology & toxicology. 2016 Mar:118(3):214-8. doi: 10.1111/bcpt.12482. Epub 2015 Oct 1     [PubMed PMID: 26423691]