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Clinical Reports |
SCOTT W. LEONARD, M.S., is Faculty Research Assistant, Linus Pauling Institute, Oregon State University (OSU), Corvallis. JACQUELINE D. JOSS, PHARM.D., is Clinical Pharmacy Specialist, Good Samaritan. Regional Medical Center, Samaritan Health Services (SHS), Corvallis. DEBBIE J. MUSTACICH, PH.D., is Faculty Research Associate, Linus Pauling Institute, OSU. DAVID H. BLATT, M.D., is Physician; and YOUNG SOOK LEE, PHARM.D., is Pharmacy Practice Resident, SHS. MARET G. TRABER, PHD., is Professor, Linus Pauling Institute, OSU.
Address correspondence to Dr. Traber at the Linus Pauling Institute, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331 (maret.traber{at}oregonstate.edu).
Methods. In this prospective, single-blind, placebo-controlled, randomized trial, patients who were currently taking either lovastatin or simvastatin for a primary diagnosis of hypercholesterolemia were given placebo for two weeks and then randomized to receive a supplement of either 400 IU of vitamin E or matching placebo after dinner for eight weeks, followed by a two-week washout period.
Results. Vitamin E supplementation increased plasma
Conclusion. Vitamin E supplementation did not affect total or low-density-lipoprotein cholesterol levels in hypercholesterolemic patients receiving lovastatin or simvastatin. A small but significant decrease in HDL cholesterol levels was observed in the group that received vitamin E supplementation during the supplementation period, but this decrease was no longer significantly different from the placebo groups levels two weeks postsupplementation. The decrease in HDL cholesterol levels did not appear to be related to either CYP3A or CETP.
Index terms: Antilipemic agents; Blood levels; Drug interactions; Excretion; Hypercholesterolemia; Lovastatin; Metabolism; Pharmacokinetics; Simvastatin; Vitamin E; Vitamins
Purpose. The effects of vitamin E supplementation on the cholesterol levels of hypercholesterolemic patients receiving statin therapy were studied.
-tocopherol concentrations approximately 1.6-fold and increased excretion of its urinary metabolite 4-fold significantly from week 2 to week 6 (p < 0.001 for both comparisons). During the eight-week supplementation period, no statistically significant differences in any lipoprotein cholesterol fraction were detected between groups; however, a 6% decrease in high-density-lipoprotein (HDL) cholesterol was detected within the vitamin E group from week 2 to week 6 (p < 0.05), but the decrease was not sufficient to change the cardiac risk ratio. Neither cytochrome P-450 isoenzyme (CYP) 3A (as measured by hydroxylation of urinary cortisol) nor cholesteryl ester transfer protein (CETP) activity was significantly altered during the study.
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