Pitavastatin (Monograph)
Brand names: Livalo, Zypitamag
Drug class: HMG-CoA Reductase Inhibitors
- Statins
VA class: CV350
Chemical name: bis[(3R,5S,6E)-7-[2-Cyclopropyl-4-(p-fluorophenyl)-3-quinolyl]-3,5-dihydroxy-6-heptenoic acid] monocalcium
Molecular formula: C50H46CaF2N2O8C50H46MgF2N2O8
CAS number: 147526-32-7
Introduction
Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).1 36
Uses for Pitavastatin
Available as pitavastatin calcium (e.g., Livalo) and pitavastatin magnesium (i.e., Zypitamag).1 36 FDA considers pitavastatin magnesium tablets to be a pharmaceutical alternative (as described in section 505[b][2] of the Federal Food, Drug, and Cosmetic Act) and not a pharmaceutical (generic) equivalent to pitavastatin calcium tablets, since both contain the same active moiety (pitavastatin) but have different salts.1 36 38 39 40 41 Clinical efficacy and safety expected to be similar between the 2 salt forms of the drug.1 36 38 41 42
Dyslipidemias
Adjunct to nondrug therapies (e.g., dietary management) to decrease elevated serum total cholesterol, LDL-cholesterol, apolipoprotein B (apo B), and triglyceride concentrations, and to increase HDL-cholesterol concentrations in the management of primary hypercholesterolemia or mixed dyslipidemia.1 36 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.35 353
Reductions in LDL-cholesterol concentrations achieved with usual dosages (1–4 mg daily) of pitavastatin are similar to or greater than those achieved with low to medium dosages of certain other statins (i.e., atorvastatin, pravastatin, simvastatin).1 3 4 5 9
Safety and efficacy not established in patients with Fredrickson type I, III, or V dyslipidemia.1 36 Effect on cardiovascular morbidity and mortality not established.1 36
Reduction in Risk of Cardiovascular Events
Also may be used for reduction in the risk of atherosclerotic cardiovascular disease (ASCVD)† [off-label].400
Extensive evidence demonstrates that statins can substantially reduce LDL-cholesterol concentrations and associated risk of ASCVD; may be 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 pitavastatin 1–4 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
Related/similar drugs
Leqvio, atorvastatin, rosuvastatin, simvastatin, ezetimibe, Crestor, Zetia
Pitavastatin Dosage and Administration
General
Patient Monitoring
- Antilipemic Therapy
-
Manufacturers recommend obtaining lipoprotein concentrations within 4 weeks following initiation and/or titration of pitavastatin and adjusting dosage accordingly.1 36 AHA/ACC cholesterol management guideline recommends obtaining lipoprotein concentrations within 4–12 weeks following initiation of statin therapy and after dosage changes (to assess response and adherence); monitoring should continue every 3–12 months thereafter as clinically indicated.400
-
Periodically reinforce adherence to lifestyle modifications during statin therapy.400 Antilipemic therapy is an adjunct to, not a substitute for, lifestyle modification therapies that reduce the risk of ASCVD.400
Administration
Oral Administration
Administer orally once daily at any time of day, without regard to food.1 36
Dosage
Available as pitavastatin calcium (e.g., Livalo) and pitavastatin magnesium (i.e., Zypitamag); dosages expressed in terms of pitavastatin.1 36 Commercially available tablets of Livalo and Zypitamag are considered bioequivalent.37 42
Dosage modifications may be necessary when used concomitantly with certain drugs (see Specific Drugs and Foods under Interactions).1
Adults
Reduction in Risk of Cardiovascular Events† [off-label]
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 a moderate-intensity statin (defined as reducing LDL-cholesterol concentrations by 30–49%).400
The AHA/ACC guideline panel considers pitavastatin 1–4 mg daily to be a moderate-intensity statin.400
Dyslipidemias
Primary Hypercholesterolemia or Mixed Dyslipidemia
OralInitially, 2 mg once daily.1 36 Usual maintenance dosage is 1–4 mg once daily.1 36
Prescribing Limits
Adults
Dyslipidemias
Primary Hypercholesterolemia or Mixed Dyslipidemia
OralSpecial Populations
Hepatic Impairment
No specific dosage recommendations at this time.1 36 (See Contraindications under Cautions, and also see Absorption: Special Populations and see Elimination: Special Populations under Pharmacokinetics.)
Renal Impairment
Moderate to severe renal impairment (GFR 15–59 mL/minute per 1.73 m2, not undergoing hemodialysis): Initially, 1 mg once daily.1 36 Maximum 2 mg once daily.1 36
End-stage renal disease (ESRD) requiring hemodialysis: Initially, 1 mg once daily.1 36 Maximum 2 mg once daily.1 36
Geriatric Patients
No specific dosage recommendations at this time.1 36 (See Geriatric Use under Cautions.)
Cautions for Pitavastatin
Contraindications
-
Active liver disease, including unexplained, persistent elevations of serum aminotransferase concentrations.1 36
-
Known hypersensitivity to pitavastatin or any ingredient in the formulation.1 36
Warnings/Precautions
Musculoskeletal Effects
Myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria reported.1 May occur at any dosage, but risk increases with increasing dosage; in clinical studies, risk of severe myopathy increased with dosages >4 mg daily.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
Use with caution in patients with predisposing factors for myopathy (e.g., age ≥65 years, renal impairment, inadequately treated hypothyroidism) and in patients receiving concomitant therapy with certain antilipemic agents (i.e., fibric acid derivatives, niacin).1 36 (See Interactions.)
AHA/ACC recommends measurement of CK levels in patients with severe statin-associated muscle symptoms; however, routine monitoring is not useful.400
Discontinue if CK concentrations become markedly elevated or if myopathy is diagnosed or suspected.1 36
Temporarily withhold therapy in patients experiencing an acute, serious condition suggestive of myopathy or predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., sepsis; hypotension; dehydration; major surgery; trauma; severe metabolic, endocrine, or electrolyte disorders; uncontrolled seizures).1 36 (See Advice to Patients.)
Hepatic Effects
Increases in serum aminotransferase (i.e., AST, ALT) concentrations reported.1 Increases usually transient and resolve or improve with continued therapy or after temporary interruption of therapy.1 Increases in alkaline phosphatase and bilirubin concentrations also reported.1
Fatal and nonfatal hepatic failure reported rarely.1
Perform liver function tests prior to initiation of therapy and as clinically indicated (e.g., presence of manifestations suggestive of liver damage).1 36 201 Serious statin-related liver injury with statins 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 pitavastatin therapy.1 36 If an alternate etiology is not found, do not restart pitavastatin.1 36 (See Hepatic Impairment under Cautions.)
Use with caution in patients who consume substantial amounts of alcohol.1 36 Contraindicated in patients with active liver disease.1 36
Endocrine Effects
Increases in HbA1c and fasting serum glucose concentrations reported.1 200 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
Cognitive Impairment
Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) reported rarely.1 36
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 36 200 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
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
Not known whether distributed into human milk; however, another statin has been shown to distribute into human milk.1 36 Use of pitavastatin is contraindicated.1 36 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 pediatric patients <18 years of age.1 29 36
Geriatric Use
No substantial differences in safety or efficacy relative to younger adults, but increased sensitivity cannot be ruled out.1 36
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
Contraindicated in patients with active liver disease, including unexplained, persistent elevations in serum aminotransferase concentrations.1 36
Renal Impairment
Dosage adjustments necessary in patients with moderate or severe renal impairment and patients with ESRD undergoing hemodialysis.1 36 (See Renal Impairment under Dosage and Administration.)
Common Adverse Effects
Myalgia, back pain, diarrhea, constipation, pain in extremity.1
Drug Interactions
Minimally metabolized by CYP2C9 and, to a lesser extent, by CYP2C8.1 7 8
Substrate of organic anionic transport polypeptide (OATP) 1B1 (OATP2) (see Extent under Pharmacokinetics);7 8 30 pharmacokinetic interactions observed with drugs that inhibit OATP1B1.1 7 9 30
Specific Drugs and Foods
Drug or Food |
Interaction |
Comments |
---|---|---|
Colchicine |
Myopathy, including rhabdomyolysis, reported1 |
|
Digoxin |
Slight decrease in peak plasma concentrations and increase in AUC of pitavastatin1 Slight decrease in peak plasma concentrations and AUC of digoxin1 |
Not considered clinically important29 |
Diltiazem |
Slight increases in peak plasma concentration and AUC of pitavastatin; slight decreases in peak plasma concentration and AUC of diltiazem1 |
|
Enalapril |
Decreased peak plasma concentrations and increased AUC of pitavastatin1 Increased peak plasma concentrations and AUC of enalapril1 |
Not considered clinically important29 |
Erythromycin |
Substantially increased peak plasma concentrations and AUC of pitavastatin1 |
|
Ezetimibe |
Negligible decreases in peak plasma concentrations and AUC of pitavastatin1 Increased peak plasma concentrations and AUC of ezetimibe1 |
Not considered clinically important29 |
Fibric acid derivatives (e.g., fenofibrate, gemfibrozil) |
Increased risk of myopathy or rhabdomyolysis1 36 Increased peak plasma concentration and AUC of pitavastatin; increases more pronounced when used concomitantly with gemfibrozil than with fenofibrate1 |
Gemfibrozil: Avoid concomitant use1 36 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 36 350 |
Grapefruit juice |
Decreased peak plasma concentrations and increased AUC of pitavastatin1 |
Not considered clinically important29 |
HIV protease inhibitors |
Atazanavir: Increased peak plasma concentration and AUC of pitavastatin and atazanavir1 31 Ritonavir-boosted darunavir: Decreased peak plasma concentration and AUC of pitavastatin; increased peak plasma concentration and AUC of darunavir and ritonavir1 31 Lopinavir/ritonavir: Decreased peak plasma concentration and AUC of pitavastatin, lopinavir, and ritonavir1 31 |
Atazanavir: Not considered clinically important;29 dosage adjustment not necessary31 Ritonavir-boosted darunavir: Dosage adjustment not necessary31 Lopinavir/ritonavir: Dosage adjustment not necessary31 |
Immunosuppressive agents (i.e., cyclosporine, everolimus, sirolimus, tacrolimus) |
Cyclosporine: Substantially increased peak plasma concentrations and AUC of pitavastatin1 Everolimus, sirolimus, tacrolimus: Data more limited, but interaction potential expected to be similar to cyclosporine because of similar metabolism339 |
Cyclosporine: Concomitant use contraindicated1 36 Everolimus, sirolimus, tacrolimus: Some experts recommend avoiding concomitant use339 |
Itraconazole |
Decreased peak plasma concentration and AUC of pitavastatin1 |
Not considered clinically important29 |
Niacin (antilipemic dosages29 [≥1 g daily]) |
Possible increased risk of myopathy1 36 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 pitavastatin dosage1 36 |
Rifampin |
Substantially increased peak plasma concentration and AUC of pitavastatin; decreased peak plasma concentration and AUC of rifampin1 |
|
Warfarin |
No clinically important pharmacokinetic interaction with R- and S-warfarin1 No clinically important effect on PT and INR in patients receiving long-term warfarin therapy1 |
Monitor PT and INR when pitavastatin is initiated and when dosage is changed in patients receiving warfarin1 36 339 |
Pitavastatin Pharmacokinetics
Absorption
Bioavailability
Absorbed from GI tract, principally from small intestine, with very small amounts absorbed from colon.1
Absolute bioavailability of oral solution (not commercially available in the US) is 51%.1
Peak plasma concentrations attained approximately 1 hour after administration of tablets.1 29
Peak plasma concentrations and AUC increase in an approximately dose-proportional manner for single pitavastatin dosages of 1–24 mg once daily.1
Peak plasma concentrations and AUC reportedly not different following evening or morning administration; however, reductions in LDL-cholesterol concentrations achieved with 4-mg tablets slightly higher following evening administration compared with morning administration in healthy individuals.1
Pitavastatin calcium tablets (Livalo) are bioequivalent to pitavastatin magnesium tablets (Zypitamag) under fasting conditions.37 42
Onset
Therapeutic response observed within one week; maximal response occurs within 2–4 weeks.29
Food
High-fat meal (50% fat content) reduces peak plasma concentrations of pitavastatin by 43% when administered as the calcium salt;1 high-fat meal (50% fat content) reduced peak plasma concentrations of pitavastatin by 39% when administered as the magnesium salt.36 37 Extent of absorption (i.e., AUC) not substantially reduced when either formulation was administered with a high-fat meal.1 36 37
Special Populations
Race: Peak plasma concentrations or AUC are 21 or 5% lower, respectively, in black individuals compared with white individuals; no substantial differences in peak plasma concentrations and AUC observed among Japanese and white individuals.1
Gender: Peak plasma concentrations or AUC are 60 or 54% higher, respectively, in healthy women compared with healthy men; however, no difference in safety or efficacy observed in clinical trials.1
Geriatric patients: Peak plasma concentrations or AUC are 10 or 30% higher, respectively, in geriatric individuals (≥65 years of age) compared with younger adults.1 (See Geriatric Use under Cautions.)
Mild hepatic impairment (Child-Pugh class A): Peak plasma concentrations and AUC are 1.3- and 1.6-fold higher, respectively, than values in healthy individuals.1
Moderate hepatic impairment (Child-Pugh class B): Peak plasma concentrations and AUC are 2.7- and 3.8-fold higher, respectively, than values in healthy individuals.1
Patients with aminotransferase (AST, ALT) concentrations >1.5 times the ULN were excluded from phase 3 clinical studies.3 4 29
Mild renal impairment: Effects on pitavastatin exposure are unknown.1
Moderate renal impairment (GFR 30–59 mL/minute per 1.73 m2): Peak plasma concentrations and AUC are 60 and 102% higher, respectively, than values in healthy individuals.1
Severe renal impairment (GFR 15–29 mL/minute per 1.73 m2, not requiring hemodialysis): Peak plasma concentrations and AUC are 18 and 36% higher, respectively, than values in healthy individuals.1
ESRD requiring hemodialysis: Peak plasma concentrations and AUC are 40 and 86% higher, respectively, than values in healthy individuals.1
Distribution
Extent
Crosses placenta in rats.1 (See Pregnancy.)
Not known whether pitavastatin is distributed into human milk.1 36
Undergoes carrier-mediated uptake into hepatocytes, principally via OATP1B1 (OATP2) and, to a lesser extent, by OATP1B3 and OATP2B1;7 8 29 33 hepatic uptake is required for pharmacologic effects.7
Plasma Protein Binding
>99% (mainly albumin and alpha 1-acid glycoprotein).1
Special Populations
Patients undergoing hemodialysis have a 33 or 36% increase in mean unbound fraction of pitavastatin compared with healthy individuals or patients with moderate renal impairment, respectively.1
Elimination
Metabolism
Principally metabolized by uridine 5′-diphosphate (UDP) glucuronosyltransferase (i.e., UGT1A1, UGT1A3, UGT2B7) to an ester-type pitavastatin glucuronide conjugate, which is further metabolized to the inactive metabolite pitavastatin lactone.1 7 8 36
Minimally metabolized by CYP2C9 and, to a lesser extent, by CYP2C8.1 7 8 36
Elimination Route
Excreted in feces (79%) and in urine (15%) within 7 days following administration of oral solution (not commercially available in the US).1 29
Unlikely to be removed by hemodialysis because of high (>99%) protein binding.1
Half-life
Approximately 12 hours.1
Special Populations
Mean elimination half-life is prolonged in patients with mild (10 hours) or moderate (15 hours) hepatic impairment compared with healthy individuals (8 hours).1
Stability
Storage
Oral
Tablets
Pitavastatin calcium: 15–30°C.1 Protect from light.1
Pitavastatin magnesium: 20–25°C.36 Protect from moisture and light.36
Actions
-
Inhibits HMG-CoA reductase, causing reduction in hepatic cholesterol biosynthesis; this leads to compensatory increase in expression of LDL receptors on hepatic cell surfaces and, subsequently, increased hepatic clearance of LDL-cholesterol from blood.1 7 8 36 Reduces serum concentrations of total cholesterol, LDL-cholesterol, VLDL-cholesterol, apo B, and triglyceride, and increases serum HDL-cholesterol concentrations in patients with primary hypercholesterolemia or mixed dyslipidemia.1 3 4 5 6 36
-
Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries,10 11 12 13 14 15 16 17 18 19 20 21 22 23 28 modulate BP in hypercholesterolemic patients with hypertension,24 25 and possess anti-inflammatory activity.26 27
Advice to Patients
-
Importance of adhering to nondrug therapies and measures, including adherence to a heart-healthy diet, regular exercise, avoidance of tobacco products, and maintenance of a healthy weight.2 350
-
Risk of myopathy and/or rhabdomyolysis; risk is increased with higher dosages or when used concomitantly with certain drugs.1 36 Importance of promptly informing clinicians of any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever, or if manifestations persist after discontinuance of therapy.1 36
-
Risk of adverse hepatic effects.1 36 Importance of promptly reporting any symptoms suggestive of liver injury (e.g., fatigue, anorexia, right upper abdominal discomfort, dark urine, jaundice).1 36
-
Risk of nonserious, reversible cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion).1 36 200
-
Risk of increased glucose concentrations and development of type 2 diabetes;1 36 200 may need to monitor glucose concentrations following initiation of statin therapy.201
-
Importance of advising women to notify their clinician if they become pregnant during therapy.405
-
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.1 36
-
Importance of informing patients of other important precautionary information.1 36 (See Cautions.)
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
Routes |
Dosage Forms |
Strengths |
Brand Names |
Manufacturer |
---|---|---|---|---|
Oral |
Tablets, film-coated |
1 mg (of pitavastatin)* |
Livalo |
Kowa |
Pitavastatin Calcium Tablets |
||||
2 mg (of pitavastatin)* |
Livalo |
Kowa |
||
Pitavastatin Calcium Tablets |
||||
4 mg (of pitavastatin)* |
Livalo |
Kowa |
||
Pitavastatin Calcium Tablets |
Routes |
Dosage Forms |
Strengths |
Brand Names |
Manufacturer |
---|---|---|---|---|
Oral |
Tablets, film-coated |
1 mg (of pitavastatin) |
Zypitamag |
Medicure |
2 mg (of pitavastatin) |
Zypitamag |
Medicure |
||
4 mg (of pitavastatin) |
Zypitamag |
Medicure |
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
1. Kowa Pharmaceuticals America, Inc. Livalo (pitavastatin calcium) tablets prescribing information. Montgomery, AL; 2016 Nov.
2. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Adult Treatment Panel III Report. From NIH web site. http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3_rpt.htm
3. Budinski D, Arneson V, Hounslow N, Grasiansky N. Pitavastatin compared with atorvastatin in primary hypercholesterolemia or combined dyslipidemia. Clin Lipidol. 2009; 4:291-302.
4. Ose L, Budinski D, Hounslow N et al. Comparison of pitavastatin with simvastatin in primary hypercholesterolaemia or combined dyslipidaemia. Curr Med Res Opin. 2009; 25:2755-64. http://www.ncbi.nlm.nih.gov/pubmed/19785568?dopt=AbstractPlus
5. Stender S, Hounslow N. Robust efficacy of pitavastatin and comparable safety to pravastatin. Atherosclerosis Suppl. 2009; 10:945, abstract P770.
6. Ose L, Budinski D, Hounslow N et al. Long-term treatment with pitavastatin is effective and well tolerated by patients with primary hypercholesterolemia or combined dyslipidemia. Atherosclerosis. 2010; 210:202-8. http://www.ncbi.nlm.nih.gov/pubmed/20080236?dopt=AbstractPlus
7. Wensel TM, Waldrop BA, Wensel B. Pitavastatin: a new HMG-CoA reductase inhibitor. Ann Pharmacother. 2010; 44:507-14. http://www.ncbi.nlm.nih.gov/pubmed/20179258?dopt=AbstractPlus
8. Saito Y. Critical appraisal of the role of pitavastatin in treating dyslipidemias and achieving lipid goals. Vasc Health Risk Manag. 2009; 5:921-36. http://www.pubmedcentral.nih.gov/picrender.fcgi?tool=pmcentrez&artid=2788597&blobtype=pdf http://www.ncbi.nlm.nih.gov/pubmed/19997573?dopt=AbstractPlus
9. Food and Drug Administration. Center for Drug Evaluation and Research: Application number 22-363: Summary Review. From FDA website. 2009 Aug 3. http://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/022363s000_SumR.pdf
10. Merck & Co., Inc. Mevacor (lovastatin) tablets prescribing information. White House Station, NJ; 2005 Nov.
11. Bristol-Myers Squibb Company. Pravachol (pravastatin sodium) tablets prescribing information. Princeton, NJ; 2005 Aug.
12. Merck & Co., Inc. Zocor (simvastatin) tablets prescribing information. Whitehouse Station, NJ; 2008 Jun.
13. Herd JA, Ballantyne CM, Farmer JA et al. Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]). Am J Cardiol. 1997; 80:278-86. http://www.ncbi.nlm.nih.gov/pubmed/9264419?dopt=AbstractPlus
14. MAAS Investigators. Effect of simvastatin on coronary atheroma: the multicentre anti-atheroma study (MAAS). Lancet. 1994; 344:633-8. http://www.ncbi.nlm.nih.gov/pubmed/7864934?dopt=AbstractPlus
15. Pitt B, Mancini GBJ, Ellis SG et al. Pravastatin limitation of atherosclerosis in the coronary arteries (PLAC I): reduction in atherosclerosis progression and clinical events. J Am Coll Cardiol. 1995; 26:1133-9. http://www.ncbi.nlm.nih.gov/pubmed/7594023?dopt=AbstractPlus
16. Crouse JR III, Byington RP, Bond MG et al. Pravastatin, lipids, and atherosclerosis in the carotid arteries (PLAC-II). Am J Cardiol. 1995; 75:455-9. http://www.ncbi.nlm.nih.gov/pubmed/7863988?dopt=AbstractPlus
17. Jukema JW, Bruschke AVG, van Boven AJ et al. Effects of lipid lowering by pravastatin on progression and regression of coronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. The Regression Growth Evaluation Statin Study (REGRESS). Circulation. 1995; 91:2528-40. http://www.ncbi.nlm.nih.gov/pubmed/7743614?dopt=AbstractPlus
18. Salonen R, Nyyssonen K, Porkkala-Sarataho E et al. The Kuopio Atherosclerosis Prevention Study (KAPS): Effect of pravastatin treatment on lipids, oxidation resistance of lipoproteins, and atherosclerotic progression. Am J Cardiol. 1995; 76:34-9C.
19. Blankenhorn DH, Azen SP, Kramsch DM et al. Coronary angiographic changes with lovastatin therapy. The Monitored Atherosclerosis Regression Study (MARS). The MARS Research Group. Ann Intern Med. 1993; 119:969-76.
20. Waters D, Higginson L, Gladstone P et al. Effects of cholesterol lowering on the progression of coronary atherosclerosis in women. A Canadian Coronary Atherosclerosis Intervention Trial (CCAIT) Substudy. Circulation. 1995; 92:2404-10.
21. Brown G, Albers JJ, Fisher LD et al. Regression of coronary artery disease as a result of intensive lipid-lowering therapy in men with high levels of apolipoprotein B. N Engl J Med. 1990; 323:1289-98. http://www.ncbi.nlm.nih.gov/pubmed/2215615?dopt=AbstractPlus
22. Furberg CD, Adams HP, Applegate WB et al for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effect of lovastatin on early carotid atherosclerosis and cardiovascular events. Circulation. 1994; 90:1679-87. http://www.ncbi.nlm.nih.gov/pubmed/7734010?dopt=AbstractPlus
23. DeGroot E, Jukema JW, Montauban AD et al. B-mode ultrasound assessment of pravastatin treatment effect on carotid and femoral artery walls and its correlations with coronary arteriographic findings: a report of the Regression Growth Evaluation Statin Study (REGRESS). J Am Coll Cardiol. 1998; 31:1561-7. http://www.ncbi.nlm.nih.gov/pubmed/9626835?dopt=AbstractPlus
24. Glorioso N, Troffa C, Filigheddu F et al. Effect of the HMG-CoA reductase inhibitors on blood pressure in patients with essential hypertension and primary hypercholesterolemia. Hypertension. 1999; 34:1281-6. http://www.ncbi.nlm.nih.gov/pubmed/10601131?dopt=AbstractPlus
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