Fluvastatin Sodium

Class: HMG-CoA Reductase Inhibitors
VA Class: CV350
Chemical Name: [R*,S*-(E)]-(±)-7-[3-(4-Fluo rophenyl)-1-(1-methylethyl)-1H-indol-2-yl]-3,5-dihydroxy-6-heptenoic acid monosodium salt
Molecular Formula: C₂₄H₂₆FNO₄•Na
CAS Number: 93957-55-2
Brands: Lescol

Special Alerts:

[Posted 09/30/2008] An FDA analysis provides new evidence that the use of statins does not increase incidence of amyotrophic lateral sclerosis (ALS), a neurodegenerative disease often referred to as “Lou Gehrig’s Disease.” The FDA analysis, undertaken after the agency received a higher than expected number of reports of ALS in patients on statins, is based on data from 41 long-term controlled clinical trials. The results showed no increased incidence of the disease in patients treated with a statin compared with placebo.

The FDA is anticipating the completion of a case-control or epidemiological study of ALS and statin use. Results from this study should be available within 6-9 months. FDA is also examining the feasibility of conducting additional epidemiologic studies to examine the incidence and clinical course of ALS in patients taking statins.

Based on currently available information, health care professionals should not change their prescribing practices for statins and patients should not change their use of statins. For more information visit the FDA website at: and .

Introduction

Antilipemic agent; hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor (i.e., statin).^{1 4 5}

Uses for Fluvastatin Sodium

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

Prevention of Cardiovascular Events

Adjunct to dietary therapy to reduce the risk of undergoing coronary revascularization procedures in patients with CHD.

Adjunct to dietary therapy to slow the progression of coronary atherosclerosis in patients with CHD as part of a treatment strategy to lower total and LDL-cholesterol concentrations to target levels.¹

Dyslipidemias

Adjunct to dietary therapy 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 and mixed dyslipidemia, including heterozygous familial hypercholesterolemia and other causes of hypercholesterolemia (e.g., polygenic hypercholesterolemia).¹

Adjunct to dietary therapy to decrease elevated serum total cholesterol, LDL-cholesterol, and apo B concentrations in the management of heterozygous familial hypercholesterolemia in boys and girls (≥1 year postmenarchal) 10–16 years of age who have a serum LDL-cholesterol concentration of ≥190 mg/dL or in those who have a serum LDL-cholesterol concentration of ≥160 mg/dL and either a family history of premature cardiovascular disease or multiple cardiovascular risk factors despite an adequate trial of dietary management.¹

Reduction of total and LDL-cholesterol concentrations in patients with hypercholesterolemia associated with or exacerbated by diabetes mellitus† (diabetic dyslipidemia),⁵⁴ renal insufficiency†,⁶³ cardiac† or renal transplantation†,^{20 21 22 21 27 55 57 64} or nephrotic syndrome† (nephrotic hyperlipidemia).^{24 65}

Fluvastatin Sodium Dosage and Administration

General

• 
  

  Patients should be placed on a standard lipid-lowering diet before initiation of fluvastatin therapy and should remain on this diet during treatment with the drug.^{1 60}

  
  

Monitoring during Antilipemic Therapy

• 
  

  Monitor lipoprotein concentrations periodically to ensure that target LDL-cholesterol goals are achieved and maintained at <100 mg/dL (optional goal: <70 mg/dL) for patients with CHD or CHD risk equivalents; <130 mg/dL (optional goal: <100 mg/dL) for patients with ≥2 risk factors and 10-year risk of 10–20%; <130 mg/dL for patients with ≥2 risk factors and 10-year risk <10%; or <160 mg/dL for patients with 0–1 risk factor.

  
  

Administration

Oral Administration

Administer orally without regard to meals.¹

Administer conventional capsules once (in the evening) or twice daily.¹ Do not open capsules prior to administration.¹

Administer extended-release tablets as a single dose at any time of day.¹ Do not break, crush, or chew tablets prior to administration.¹

Dosage

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

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

Pediatric Patients

Dyslipidemias

Oral

Children 10–16 years of age: Initially, 20 mg once daily.¹

Adjust dosage at 6-week intervals until the desired effect on lipoprotein concentrations is observed or a daily dosage of 80 mg is reached.¹

Adults

Prevention of Cardiovascular Events or Dyslipidemias

Oral

Initially, 20 mg once daily in the evening in patients who require reductions in LDL-cholesterol concentrations of <25% to achieve their goal.¹

In patients who require larger reductions in LDL-cholesterol concentrations (i.e., >25%), initiate therapy at a dosage of 40 mg (as conventional capsules) once daily in the evening, 80 mg (as extended-release tablets) once daily at any time of day, or 40 mg (as conventional capsules) twice daily.¹

Adjust dosage at intervals of ≥4 weeks until the desired effect on lipoprotein concentrations is observed.¹

Usual maintenance dosage is 20–80 mg daily.¹

Prescribing Limits

Pediatric Patients

Oral

Children 10–16 years of age: Maximum 80 mg daily.¹

Special Populations

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease; monitor such patients closely.¹

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

Renal Impairment

Dosage modification is not necessary in patients with mild to moderate renal impairment.¹

Dosages >40 mg daily have not been studied in patients with severe renal impairment; caution is advised when administering higher dosages to such patients.¹

Cautions for Fluvastatin Sodium

Contraindications

• 
  

  Active liver disease or unexplained, persistent elevations of serum aminotransferases.¹

  
  


• 
  

  Pregnancy or lactation.¹ Administer to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards.¹

  
  


• 
  

  Known hypersensitivity to fluvastatin or any ingredient in the formulation.¹

  
  

Warnings/Precautions

Warnings

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

Fetal/Neonatal Morbidity and Mortality

Suppression of cholesterol biosynthesis could cause fetal harm.¹ Congenital anomalies following intrauterine exposure to statins reported rarely.¹

Administer to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential hazards.¹ If the patient becomes pregnant while taking the drug, discontinue therapy and apprise the patient of the potential hazard to the fetus.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,¹ increased serum alkaline phosphatase concentrations,¹ increased serum γ-glutamyl transpeptidase concentrations,¹ increased bilirubin concentrations,¹ and, rarely, cirrhosis,¹ fulminant hepatic necrosis,¹ and hepatoma¹ have been reported.¹

Perform liver function tests before and at 12 weeks after initiation of therapy or any increase in dosage.¹

Patients who develop increased serum AST/ALT concentrations or manifestations of liver disease should be monitored to confirm the finding and should receive frequent liver function tests thereafter until the abnormalities return to normal.¹ If increases in AST or ALT concentrations of ≥3 times the ULN persist (i.e., found on 2 consecutive occasions), discontinue therapy.¹

The National Lipid Association (NLA) statin safety assessment task force recommends that clinicians be alert to signs and symptoms of hepatotoxicity (e.g., jaundice, malaise, fatigue, lethargy, hepatomegaly, increased indirect bilirubin concentrations, elevated PT). If substantial hepatotoxicity is suspected, discontinue therapy, determine etiology, and refer patient to a gastroenterologist or hepatologist if indicated.

Musculoskeletal Effects

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

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

Risk of myopathy increased in patients receiving higher doses of statins; in patients with multisystem disease (e.g., renal or hepatic impairment); in patients with concurrent serious infections or hypothyroidism; in patients (particularly women) of advanced age (especially >80 years of age); in patients with small body frame and frailty; and in patients undergoing surgery (i.e., during perioperative periods).

Risk also may be increased with concomitant administration of cyclosporine, erythromycin, gemfibrozil, or niacin.¹ Myopathy was not observed in some patients receiving fluvastatin concomitantly with niacin.¹

Measure baseline serum CK concentrations prior to initiation of therapy, particularly in patients at high risk of developing musculoskeletal toxicity (e.g., geriatric patients, black men, patients receiving concomitant therapy with myotoxic drugs).

Obtain serum CK concentrations and compare with baseline concentrations in patients presenting with musculoskeletal symptoms suggestive of myopathy; because hypothyroidism may be a predisposing factor, TSH concentrations also should be obtained in such patients.

Discontinue therapy if serum CK concentrations become markedly elevated or if myopathy is diagnosed or suspected.¹

Monitor patients weekly if myalgia (muscle pain, tenderness) is present with either no CK elevation or a moderate elevation (3–10 times the ULN) until manifestations improve; discontinue if manifestations worsen.

Dosage reduction or temporary discontinuance may be prudent in patients with muscle discomfort and/or weakness in the presence of progressive elevation of CK concentrations on serial measurements.

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

General Precautions

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

Renal Effects

NLA recommends performing renal function tests prior to initiating statin therapy; routine monitoring of S_cr and proteinuria is not necessary.

If S_cr is elevated in the absence of rhabdomyolysis, may continue therapy but dosage adjustment may be necessary per labeling recommendations.

If unexpected proteinuria develops, determine etiology; may continue therapy but dosage adjustment may be necessary per labeling recommendations.

Peripheral Neuropathy

If manifestations of peripheral neuropathy occur, NLA recommends evaluating patient to rule out secondary causes (e.g., diabetes mellitus, renal impairment, alcohol abuse, vitamin B₁₂ deficiency, cancer, hypothyroidism, acquired immunodeficiency syndrome [AIDS], Lyme disease, heavy metal intoxication). If a secondary cause is not identified, discontinue statin therapy for 3–6 months.

If neurologic manifestations improve over this period, a presumptive diagnosis of statin-induced peripheral neuropathy may be made; however, consider reinitiating therapy with a different statin and dosage.

If neurologic manifestations do not improve during period of discontinuance, reinitiate statin therapy, taking into consideration the risks and benefits of such therapy.

CNS Effects

CNS vascular lesions, characterized by perivascular hemorrhage, edema, and mononuclear cell infiltration of perivascular spaces, observed in animals.¹

If manifestations of impaired cognition occur, NLA recommends evaluating patient to rule out secondary causes. If a secondary cause is not identified, discontinue statin therapy for 1–3 months. If no improvement, reinitiate statin therapy, taking into consideration the risks and benefits of such therapy.

Ocular Effects

Cataracts¹ and optic nerve degeneration observed in animals receiving other statins.

Specific Populations

Pregnancy

Category X.¹ (See Contraindications and also Fetal/Neonatal Morbidity and Mortality, under Cautions.)

Lactation

Distributed into milk.¹ Use is contraindicated.¹

Pediatric Use

Safety and efficacy not established in children <10 years of age or in premenarchal girls.¹

Geriatric Use

Possible increased treatment response with respect to total cholesterol, LDL-cholesterol, and LDL-/HDL-cholesterol ratio in patients ≥65 years of age compared to younger adults.¹

Caution in patients (particularly women) of advanced age (especially >80 years of age) and in those with small body frame and frailty.

Hepatic Impairment

Use with caution in patients who consume substantial amounts of alcohol and/or have a history of liver disease.¹

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

Common Adverse Effects

GI disturbances (e.g., dyspepsia, diarrhea, abdominal pain, nausea, flatulence), myalgia, arthritis, sinusitis, bronchitis, headache, accidental trauma, fatigue, allergy, insomnia, urinary tract infection.¹

Interactions for Fluvastatin Sodium

Metabolized principally by CYP2C9; CYP2C8 and CYP3A4 also contribute to fluvastatin metabolism.¹

Specific Drugs

Drug	Interaction	Comments
Anticoagulants, oral (e.g., warfarin)	Bleeding and/or increased PT observed with other statins1	Closely monitor PT until stabilized if fluvastatin is initiated or dosage is adjusted in patients receiving coumarin anticoagulants1
Bile acid sequestrants (e.g., cholestyramine)	Decreased fluvastatin concentrations when administered concomitantly with cholestyramine.1 Additive cholesterol-lowering effect when these drugs are administered 4 hours apart1	Administer fluvastatin at least 2 hours after the resin1
Cyclosporine	Increased fluvastatin concentrations.1 Increased risk of myopathy and/or rhabdomyolysis1	Concomitant use with immunosuppressants generally not recommended1
Diclofenac	Increased diclofenac concentrations1
Digoxin	Increased digoxin concentrations and slight increase in digoxin urinary clearance1
Erythromycin	Increased risk of myopathy and/or rhabdomyolysis1	Concomitant use generally not recommended1
Fibric acid derivatives (e.g., gemfibrozil)	Increased risk of myopathy and/or rhabdomyolysis1	Concomitant use generally should be avoided.1 However, use of fibric acid derivatives with moderate dosages of statins appears to have a relatively low incidence of myopathy, especially when used in patients without multisystem disease or multiple-drug therapy
Fluconazole	Increased peak plasma concentrations and AUC of fluvastatin1	Use concomitantly with caution1
Glyburide	Increased fluvastatin and glyburide concentrations.1 No change in glucose, insulin, or C-peptide concentrations1	Monitor appropriately when fluvastatin dosage is increased to 40 mg twice daily1
Histamine H2-receptor antagonists (e.g., cimetidine, ranitidine)	Increased plasma concentrations and decreased clearance of fluvastatin1
Niacin	Increased risk of myopathy and/or rhabdomyolysis1	Concomitant use with antilipemic dosages (≥1 g daily) of niacin generally not recommended1
Phenytoin	Increased fluvastatin and phenytoin concentrations1	Patients receiving phenytoin should be monitored appropriately when fluvastatin is initiated or dosage is adjusted1
Proton-pump inhibitors (e.g., omeprazole)	Increased plasma concentrations and decreased clearance of fluvastatin1
Rifampin	Decreased plasma concentrations and increased clearance of fluvastatin1

Fluvastatin Sodium Pharmacokinetics

Pharmacokinetic data in pediatric patients not available.¹

Absorption

Bioavailability

Rapidly and completely absorbed.¹

Absolute bioavailability of conventional capsules is 24%.¹

The mean relative bioavailability of extended-release tablets is approximately 29% compared with conventional capsules administered under fasting conditions.¹

Mean peak plasma concentrations occur within 1 or 3 hours following oral administration of conventional capsules or extended-release tablets, respectively.¹

Onset

A therapeutic response usually is apparent within 2 weeks after initiating therapy, with a maximal response occurring within 4 weeks.¹

Food

Peak plasma concentration decreased and time to peak plasma concentrations increased following administration of fluvastatin conventional capsules with the evening meal; however, no substantial differences in extent of absorption or lipid-lowering effects following administration with food.¹

Bioavailability increased and absorption delayed following administration of extended-release tablets with a high-fat meal; however, peak plasma concentrations achieved with the extended-release tablets following a high-fat meal are much less than those achieved with a single or twice-daily dose of 40 mg.¹

Distribution

Extent

Distributed mainly to the liver.¹

Distributed into milk (milk to plasma ratio 2:1).¹

Plasma Protein Binding

About 98%.¹

Elimination

Metabolism

Metabolized in the liver, principally by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8.¹

Elimination Route

Excreted in feces (90%) and urine (5%) mainly as metabolites; <2% excreted as unchanged drug.¹

Half-life

<3 hours (conventional capsules) and 9 hours (extended-release tablets).¹

Special Populations

Patients with hepatic impairment may have increased exposure to fluvastatin due to decreased presystemic metabolism.¹

Stability

Storage

Oral

Capsules and Extended-release Tablets

Tight containers at 25°C (may be exposed to 15–30°C).¹ Protect from light.¹

ActionsActions

• 
  

  Inhibits HMG-CoA reductase, causing subsequent reduction in hepatic cholesterol synthesis.¹ Reduces serum concentrations of total cholesterol, LDL-cholesterol, apo B, and triglycerides.¹

  
  


• 
  

  Statins may slow progression of and/or induce regression of atherosclerosis in coronary and/or carotid arteries, modulate BP in hypercholesterolemic patients with hypertension, and possess anti-inflammatory activity.

  
  

Advice to Patients

Pending revision, the material in this section should be considered in light of more recently available information in the MedWatch notification at the beginning of this monograph.

• 
  

  Importance of informing patients about risks, especially rhabdomyolysis, associated with statins alone or combined with other drugs.¹ Importance of patients promptly reporting muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever.¹

  
  


• 
  

  Importance of adhering to nondrug therapies and measures (i.e., therapeutic lifestyle changes), including dietary management, weight control, physical activity, and management of potentially contributory disease [e.g., diabetes mellitus]).

  
  


• 
  

  Importance of women informing their clinician if they are or plan to become pregnant or plan to breast-feed.¹ Necessity for clinicians to advise women to avoid pregnancy during therapy and to advise pregnant women of risk to fetus.¹

  
  


• 
  

  Importance of informing clinician of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.¹

  
  


• 
  

  Importance of informing patients of other important precautionary information.¹ (See Cautions.)

  
  

Preparations

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

Fluvastatin Sodium

Routes	Dosage Forms	Strengths	Brand Names	Manufacturer
Oral	Capsules	20 mg (of fluvastatin)	Lescol (with benzyl alcohol and parabens)	Reliant, (also promoted by Novartis)
		40 mg (of fluvastatin)	Lescol (with benzyl alcohol and parabens)	Reliant, (also promoted by Novartis)
	Tablets, extended-release	80 mg (of fluvastatin)	Lescol XL	Reliant, (also promoted by Novartis)

Comparative Pricing

This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 04/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.

Lescol 20MG Capsules (NOVARTIS): 30/$111.99 or 90/$301.97

Lescol 40MG Capsules (NOVARTIS): 30/$103.99 or 90/$279.96

Lescol XL 80MG 24-hr Tablets (NOVARTIS): 30/$137.99 or 90/$383.98

Disclaimer

This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.

The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.

AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions October 01, 2008. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

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

References

1. Novartis. Lescol (fluvastatin sodium) capsules and Lescol XL (fluvastatin) extended-release tablets prescribing information. East Hanover, NJ: 2006 Apr.

2. The Expert Panel. Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Arch Intern Med. 1988; 148:36-69. [IDIS 236890] [PubMed 3422148]

3. Grundy SM, Bilheimer D, Chait A et al. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993; 269:3015-23. [IDIS 315201] [PubMed 8501844]

4. Anon. Fluvastatin for lowering cholesterol. Med Lett Drugs Ther. 1994; 36:45-6. [PubMed 8177137]

5. Jokubatis LA. Updated clinical safety experience with fluvastatin. Am J Cardiol. 1994; 73(suppl D):18D-24D. [IDIS 331720] [PubMed 8198019]

6. Baggio G, De Candia O, Forte PL et al. Efficacy and safety of fluvastatin in elderly hypercholesterolemic patients: a pilot study. Curr Ther Res. 1994; 55:401-7.

7. Davidson MH on behalf of the FLUENT Investigators Group. Fluvastatin long-term extension trial (FLUENT): summary of efficacy and safety. Am J Med. 1994; 96(suppl 6A):41S-4S.

8. Peters TK, Muratti EN, Mehra M. Fluvastatin in primary hypercholesterolemia: efficacy and safety in patients at high risk. An analysis of a clinical trial database. Am J Med. 1994; 96(suppl 6A):79S-83S. [IDIS 332445] [PubMed 8017471]

9. Banga JD, Jacotot B, Pfister P et al. Long-term treatment of hypercholesterolemia with fluvastatin: a 52-week multicenter safety and efficacy study. Am J Med. 1994; 96(suppl 6A):87S-93S. [IDIS 332447] [PubMed 8017473]

10. Peters TK. Safety profile of fluvastatin. Br J Clin Pract. 1996; 77(suppl A):20-3.

11. Suzumura K, Yasuhara M, Tanaka K et al. Protective effect of fluvastatin sodium (XU-62-320), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on oxidative modification of human low-density lipoprotein in vitro. Biochem Pharmacol. 1999; 57:697-703. [PubMed 10037456]

12. Pauciullo P, Borgnino C, Paoletti R et al. Efficacy and safety of a combination of fluvastatin and bezafibrate in patients with mixed hyperlipidaemia (FACT) study. Atherosclerosis. 2000; 150:429-36. [PubMed 10856536]

13. Pedersen TR, Tobert JA. Benefits and risks of HMG-CoA reductase inhiitors in the prevention of coronary heart disease: a reappraisal. Drug Safety. 1996; 14:11-24. [PubMed 8713485]

14. Food and Drug Administration. Specific requirements on content and format of labeling for human prescription drugs; proposed addition of “geriatric use“ subsection in the labeling. 21 CFR Part 201. Proposed rule. [Docket No. 89N-0474] Fed Regist. 1990; 55:46134-7.

15. Woodhouse K, Wynne HA. Age-related changes in hepatic function: implications for drug therapy. Drugs Aging. 1992; 2:243-55. [PubMed 1606355]

16. Montamat SC, Cusack BJ, Vestal RE. Management of drug therapy in the elderly. N Engl J Med. 1989; 321:303-9. [IDIS 257650] [PubMed 2664519]

17. Durnas C, Loi CM, Cusack BJ. Hepatic drug metabolism and aging. Clin Pharmacokinet. 1990; 19:359-89. [PubMed 2268986]

18. Pomara N, Stanley B, Block R et al. Caution in the use of drugs in the elderly. N Engl J Med. 1983; 308:1600-1.

19. Lipsitz L. Orthostatic hypotension in the elderly. N Engl J Med. 1989; 321:952-7. [IDIS 259578] [PubMed 2674714]

20. Schrama YC, Hene RJ, de Jonge N et al. Efficacy and muscle safety of fluvastatin in cyclosporine-treated cardiac and renal transplant recipients. Transplantation. 1998; 66:1175-81. [IDIS 417742] [PubMed 9825814]

21. Austen JL, Shifrin FA, Bartucci MR et al. Effects of fluvastatin on hyperlipidemia after renal transplantation: influence of steroid therapy. Ann Pharmacother. 1996; 30:1386-9. [IDIS 376975] [PubMed 8968448]

22. Goldberg R, Roth D. Evaluation of fluvastatin in the treatment of hypercholesterolemia in renal transplant recipients taking cyclosporine. Transplantation. 1996; 62:1559-64. [IDIS 378880] [PubMed 8970607]

23. Li PKT, Mak TWL, Wang AYM et al. The interaction of fluvastatin and cyclospori A in renal transplant patients. Int J Clin Pharmacol Ther. 1995:33:246-8.

24. Matzkies FK, Bahner U, Teschner M et al. Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients. Am J Nephrol. 1999; 19:492-4. [PubMed 10460940]

25. Eliav O, Schurr D, Pfister P et al. High-dose fluvastatin and bezafibrate combination treatment for heterozygous familial hypercholesterolemia. Am J Cardiol. 1995; 76:76-9A. [PubMed 7793410]

26. Smit JWA, Jansen GH, de Bruin TWA et al. Treatment of combined hyperlipidemia with fluvastatin and gemfibrozil, alone or combination, does not induce muscle damage. Am J Cardiol. 1995; 76:126-8A.

27. Goldberg RB, Roth D. A preliminary report of the safety and efficacy of fluvastatin for hypercholesterolemia in renal transplant patients receiving cyclosporine. Am J Cardiol. 1995; 76:107-9A. [IDIS 351132] [PubMed 7611141]

28. Teramoto T, Goto Y, Kurokawa K et al. Clinical efficacy of fluvastatin for hyperlipidemia in Japanese patients. Am J Cardiol. 1995; 76:33-6A.

29. American Heart Association Committee to Design a Dietary Treatment of Hyperlipoproteinemia. Recommendations for treatment of hyperlipidemia in adults: a joint statement of the Nutrition Committee and the Council on Arteriosclerosis. Circulation. 1984; 69:1065-90A. [PubMed 6713610]

30. Reviewers’ comments (personal observations) on Lovastatin 24:06.08.

31. Zavoral JH, Haggerty BJ, Winick AG et al. Efficacy of fluvastatin, a totally synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Am J Cardiol. 1995; 76:37-40A.

32. Broyles FE, Walden CE, Hunninghake DB et al. Effect of fluvastatin on intermediate density lipoprotein (remnants) and other lipoprotein levels in hypercholesterolemia. Am J Cardiol. 1995; 76:129-35A.

33. 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. [IDIS 391970] [PubMed 9264419]

34. Ballantyne CM. Clinical trial endpoints: angiograms, events, and plaque instability. Am J Cardiol. 1998; 82:5M-11M. [IDIS 412364] [PubMed 9766342]

35. Tomlinson B, Mak TWL, Tsui JYY et al. Effects of fluvastatin on lipid profile and apolipoproteins in Chinese patients with hypercholesterolemia. Am J Cardiol. 1995; 76:136-9A.

36. Buzzi AP, Pastore MA, on behalf of the argentine and multicenter evaluation investigators. Argentine multicenter evaluation of fluvastatin in the treatment of patients with hypercholesterolemia. Curr Ther. 1997; 58:1013-28.

37. Rindone JP, Hiller D, Arriola G. A comparison of fluvastatin 40 mg every other day versus 20 mg every day in patients with hypercholesterolemia. Pharmacotherapy. 1998; 18:836-9. [IDIS 415609] [PubMed 9692657]

38. Insull W, Black D, Dujovne C et al. Efficacy and safety of once-daily vs twice-daily dosing with fluvastatin, a synthetic reductase inhibitor, in primary hypercholesterolemia. Arch Intern Med. 1994; 154:2449-55. [IDIS 338785] [PubMed 7979841]

39. Dujovne CA, Davidson MH. Fluvastatin administration at bedtime versus with the evening meal: a multicenter comparison of bioavailability, safety, and efficacy. Am J Med. 1994; 96(suppl 6A):37-40S.

40. Jones P, Kafonek S, Laurora I et al. Comparative dose efficacy study of atorvastatin versus fluvastatin, pravastatin, lovastatin, and fluvastatin in patients with hypercholesterolemia (the CURVES study). Am J Cardiol. 1998; 81:582-7. [IDIS 402927] [PubMed 9514454]

41. Nash DT. Meeting national cholesterol education goals in clinical practice-a comparison of lovastatin and fluvastatin in primary prevention. Am J Cardiol. 1996(suppl 6A):26-31.

42. Ose L, Scott RS, and the fluvastatin-Fluvastatin Study Group. Double-blind comparison of the efficacy and tolerability of fluvastatin and fluvastatin in patients with primary hypercholesterolaemia. Clin Drug Invest. 1995; 10:127-38.

43. Deslypere JP. fluvastatin-fluvastatin comparative study. Clin Drug Invest. 1995; 11:362-4.

44. Schulte KL, Beil S. Efficacy and tolerability of fluvastatin and fluvastatin in hypercholesterolaemic patients. Clin Drug Invest. 1996; 12:119-26.

45. Sprecher DL, Abrams J, Allen JW et al. Low-dose combined therapy with fluvastatin and cholestyramine in hyperlipidemic patients. Ann Intern Med. 1994; 120:537-43. [IDIS 327549] [PubMed 8093139]

46. Jacotot B, Banga JD, Waite R et al. Long-term efficacy with fluvastatin as monotherapy and combined with cholestyramine (a 156-week multicenter study). Am J Cardiol. 1995; 76:41-6A.

47. Fanghanel G, Espinosa J, Olivares D et al. Open-label study to assess the efficacy, safety, and tolerability of fluvastatin versus bezafibrate for hypercholesterolemia. Am J Cardiol. 1995; 76:57-61A.

48. Jacobson TA, Chin MM, Fromell GJ et al. Fluvastatin with and without niacin for hypercholesterolemia. Am J Cardiol. 1994; 74:149-54. [IDIS 332209] [PubMed 8023779]

49. Leitersdorf E, Muratti EN, Eliav O et al. Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination. Am J Med. 1994; 96:401-7. [IDIS 330972] [PubMed 8192170]

50. Leitersdorf E, Muratti EN, Eliav O et al. Efficacy and safety of triple therapy (fluvastatin-bezafibrate-cholestyramine) for severe familial hypercholesterolemia. Am J Cardiol. 1995; 76:84-8A.

51. Sigurdsson G, Haraldsdottir SO, Melberg TH et al. fluvastatin compared to fluvastatin in the reduction of serum lipids and apolipoproteins in patients with ischaemic heart disease and moderate hypercholesterolaemia. Acta Cardiol. 1998; 1:7-14.

52. Ballantyne CM, Herd JA, Ferlic LL et al. Influence of low HDL on progression of coronary artery disease and response to fluvastatin therapy. Circulation. 1999; 99:736-43. [IDIS 423955] [PubMed 9989957]

53. Serruys PW, Foley DP, Jackson G et al. A randomized placebo-controlled trial of fluvastatin for prevention of restenosis after successful coronary balloon angioplasty. Eur Heart J. 1999; 20:58-69. [PubMed 10075142]

54. Knopp RH, Frolich JJ. Efficacy and safety of fluvastatin in patients with non-insulin-dependent diabetes mellitus and hyperlipidemia: preliminary report. Am J Cardiol. 1994; 73:39-41D.

55. Locsey L, Asztalos L, Kincses Z et al. Fluvastatin (Lescol) treatment of hyperlipidaemia in patients with renal transplants. Int Urol and Nephrol. 1997; 29:95-106.

56. Christians U, Jacobsen W, Floren LC. Metabolism and drug interactions of 3-hydroxy-3-methylglutaryl Coenzyme A reductase inhibitors in transplant patients: are the statins mechanistically similar? Pharmacol Ther. 1998; 80:1-34.

57. Podder H, Gero L, Foldes K et al. Treatment of metabolic disorders with fluvastatin after renal transplantation. Transplantation Proc. 1997; 29:216-9.

58. Novartis. Lescol formulary information. East Hanover, NJ. 1998 Nov.

59. Buemi M, Allegra A, Corica F et al. Effect of fluvastatin on proteinuria in patients with immunoglobulin A nephropathy. Clin Pharmacol Ther. 2000; 67:427-31. [IDIS 446578] [PubMed 10801253]

60. Langtry HD, Markham A. Fluvastatin. A review of its use in lipid disorders. Drugs. 1999; 57:583-606. [PubMed 10235694]

61. Plosker GL, Wagstaff AJ. Fluvastatin. A review of its pharmacology and use in the management of hypercholesterolemia. Drugs. 1996; 51:433-59. [PubMed 8882381]

62. Lennernas H, Fager G. Pharmacodynamics and pharmacokinetics of the HMG-CoA reductase inhibitors. Clin Pharmacokinet. 1997; 32:403-25. [PubMed 9160173]

63. Lintott CJ, Scott RS, Bremer JM et al. Fluvastatin for dyslipoproteinemia, with or without concomitant chronic renal insufficiency. Am J Cardiol. 1995; 76:97-101A. [PubMed 7793418]

64. Holdaas H, Hartmann A, Stenstrom J et al. Effect of fluvastatin for safely lowering atherogenic lipids in renal transplant patients receiving cyclosporine. Am J Cardiol. 1995; 76:102-6A.

65. Matzkies FK, Bahner U, Teschner M et al. Efficiency of 1-year treatment with fluvastatin in hyperlipidemic patients with nephrotic syndrome. Am J Nephrol. 1999; 19:492-4. [PubMed 10460940]

66. Hagen E, Istad H, Ose L et al. Fluvastatin efficacy and tolerability in comparison and in combination with cholestyramine. Eur J Clin Pharmacol. 1994; 46:445-9. [IDIS 333319] [PubMed 7957541]

67. National Institutes of Health, National Heart, Lung, and Blood Institute, National Cholesterol Education Program. Cholesterol lowering in the patient with coronary heart disease. Physician monograph. NIH Publication. 1997; 97-3794.

68. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA. 1993;269:3015-23.

69. Expert Panel on Detection, Evaluation, and Treatment of high Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of high Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001; 285:2486-97. [IDIS 464555] [PubMed 11368702]

70. National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: Adult Treatment Panel III Report. From AHA web site.

71. Serruys PWJC, de Feyter P, Macaya C et al for the Lescol Intervention Prevention Study (LIPS) investigators. Fluvastatin for prevention of cardiac events following successful first percutaneous coronary intervention: a randomized controlled trial. JAMA. 2002; 287:3215-22. [IDIS 482358] [PubMed 12076217]

More Fluvastatin Sodium resources

• Fluvastatin Sodium Side Effects (in more detail)
• Fluvastatin Sodium Use in Pregnancy & Breastfeeding
• Fluvastatin Sodium Drug Interactions
• Fluvastatin Sodium Support Group
• 2 Reviews for Fluvastatin Sodium - Add your own review/rating

Compare Fluvastatin Sodium with other medications

• High Cholesterol
• High Cholesterol, Familial Heterozygous
• Hyperlipoproteinemia
• Hyperlipoproteinemia Type IIa, Elevated LDL
• Hyperlipoproteinemia Type IIb, Elevated LDL VLDL