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Fluvastatin

Also indexed as: Lescol®

Illustration

Fluvastatin is a member of the HMG-CoA reductase inhibitor family of drugs that blocks the body’s production of cholesterol. Fluvastatin is used to lower elevated cholesterol and to slow or prevent hardening of the arteries.

Summary of Interactions with Vitamins, Herbs, and Foods
In some cases, a herb or supplement may appear in more than one category, which may seem contradictory. For clarification, read the full article for details about the summarized interactions.

Beneficial May be Beneficial: Depletion or interference—The medication may deplete or interfere with the absorption or function of the nutrient. Taking these nutrients may help replenish them.

Coenzyme Q10

Beneficial May be Beneficial: Supportive interaction—Taking these supplements may support or otherwise help your medication work better.

Sitostanol

Avoid Avoid: Adverse interaction—Avoid these supplements when taking this medication because taking them together may cause undesirable or dangerous results.

Red yeast rice

Vitamin A*

Check Check: Other—Before taking any of these supplements or eating any of these foods with your medication, read this article in full for details.

Niacin

Side effect reduction/prevention

None known

Reduced drug absorption/bioavailability

None known

An asterisk (*) next to an item in the summary indicates that the interaction is supported only by weak, fragmentary, and/or contradictory scientific evidence.

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Interactions with Dietary Supplements

Coenzyme Q10
In a randomised, double-blind trial, blood levels of coenzyme Q10 (CoQ10) were measured in 45 people with high cholesterol treated with lovastatin or pravastatin (drugs related to fluvastatin) for 18 weeks.1 A significant decline in blood levels of CoQ10 occurred with either drug. One study found that supplementation with 100 mg of CoQ10 prevented declines in CoQ10 when taken with simvastatin (another HMG-CoA reductase inhibitor drug).2 Many doctors recommend that people taking HMG-CoA reductase inhibitor drugs such as fluvastatin also supplement with approximately 100 mg CoQ10 per day, although lower amounts, such as 10–30 mg per day, might conceivably be effective in preventing the decline in CoQ10 levels.

Niacin
Niacin is the form of vitamin B3 used to lower cholesterol. Fluvastatin and niacin used together have been shown to be more effective than either substance alone.3 Ingestion of large amounts of niacin along with HMG-CoA reductase inhibitors such as fluvastatin may cause muscle disorders (myopathy) that can become serious (rhabdomyolysis).4 5 Such problems appear to be uncommon.6 7 Nonetheless, individuals taking fluvastatin should consult with their doctor before taking niacin.

Sitostanol
A synthetic molecule related to beta-sitosterol, sitostanol, is available in a special margarine and has been shown to lower cholesterol levels. In one study, supplementing with 1.8 grams of sitostanol per day for six weeks enhanced the cholesterol-lowering effect of various statin drugs.8

Vitamin A
A study of 37 people with high cholesterol treated with diet and HMG-CoA reductase inhibitors found blood vitamin A levels increased during two years of therapy.9 Until more is known, people taking HMG-CoA reductase inhibitors, including fluvastatin, should have blood levels of vitamin A monitored if they intend to supplement vitamin A.

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Interactions with Herbs

Red yeast rice(Monascus purpureas)
A supplement containing red yeast rice (Cholestin) has been shown to effectively lower cholesterol and triglycerides in people with moderately elevated levels of these blood lipids.10 This extract contains small amounts of naturally occurring HMG-CoA reductase inhibitors such as lovastatin and should not be used if you are currently taking a statin medication.

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Interactions with Foods and Other Compounds

Food
Fluvastatin is equally effective taken with or without food in the evening.11

Alcohol
In a study of 31 people with primary hypercholesterolaemia treated with fluvastatin, six weeks of daily, moderate alcohol consumption slowed the absorption and metabolism of fluvastatin but did not interfere with its effectiveness.12

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References
(To view, roll mouse over heading; to hide, click on heading)

1. Mortensen SA, Leth A, Agner E, Rohde M. Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors. Mol Aspects Med 1997;18(suppl):S137–44.

2. Bargossi AM, Grossi G, Fiorella PL, et al. Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors. Molec Aspects Med 1994;15(suppl):s187–93.

3. Jacobson TA, Chin MM, Fromell GJ, et al. Fluvastatin with and without niacin for hypercholesterolemia. Am J Cardiol 1994;74:149–54.

4. Garnett WR. Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors. Am J Health Syst Pharm 1995;52:1639–45.

5. Yee HS, Fong NT. Atorvastatin in the treatment of primary hypercholesterolemia and mixed dyslipidemias. Ann Pharmacother 1998;32:1030–43.

6. Jacobson TA, Amorosa LF. Combination therapy with fluvastatin and niacin in hypercholesterolemia: a preliminary report on safety. Am J Cardiol 1994;73:25D–9D.

7. Jokubaitis LA. Fluvastatin in combination with other lipid-lowering agents. Br J Pract Suppl 1996;77A:28–32.

8. Goldberg AC, Ostlund RE Jr, Bateman JH, et al. Effect of plant stanol tablets on low-density lipoprotein cholesterol lowering in patients on statin drugs. Am J Cardiol 2006;97:376–9.

9. Muggeo M, Zenti MG, Travia D, et al. Serum retinol levels throughout 2 years of cholesterol-lowering therapy. Metabolism 1995;44:398–403.

10. Heber D, Yip I, Ashley JM, et al. Cholesterol-lowering effects of a proprietary Chinese red-yeast-rice dietary supplement. Am J Clin Nutr 1999;69:231–6.

11. 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;96:37S–40S.

12. Smit JW, Wijnne HJ, Schobben F, et al. Effects of alcohol and fluvastatin on lipid metabolism and hepatic function. Ann Intern Med 1995;122:678–80.

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