• Gemfibrozil
  

In one study, gemfibrozil treatment in men with combined hyperlipidemia reduced serum coenzyme Q10 levels (Aberg et al. 1998). The clinical significance of these results is not known; more research is needed to determine whether chronic gemfibrozil therapy depletes CoQ10.

Although CoQ10 is manufactured by the body, deficiencies occur in some physiological and pathological conditions (Artuch et al. 1999). CoQ10 deficiency may be related to certain conditions such as gingivitis (Nakamura et al. 1974); breast cancer (Jolliet et al. 1998); congestive heart failure (Munkholm et al. 1999); angina pectoris (Kamikawa et al. 1985); acute myocardial infarction (Singh et al. 1998); mitochondrial encephalomyopathies (Chan et al. 1998); hypertension, and cardiac function (Singh et al. 1999). In addition, CoQ10 depletion may contribute to aging and photoaging (Hoppe et al. 1999). Low levels of CoQ10 may also compromise immune function (Folkers et al. 1993) and play a role in male infertility (Overvad et al. 1999).

Daily doses of coenzyme Q10 as high as 200 mg for periods of 6 to 12 months or 100 mg for up to 6 years have not been associated with reports of serious adverse effects in clinical studies (Overvad et al. 1999). There are no known studies showing clinical benefits of CoQ10 replacement in the presence of gemfibrozil specifically.

There are conflicting reports regarding the effect of gemfibrozil on vitamin E status in hyperlipidemic patients. In one study, gemfibrozil treatment in men with combined hyperlipidemia reduced serum gamma- and alpha-tocopherol levels (Aberg et al. 1998). In another study, gemfibrozil had no effect on vitamin E status and increased the LDL vitamin E/lipid peroxide ratio concentrations (Yoshida et al. 1998). The clinical significance of these results is not known; more research is needed to establish whether chronic gemfibrozil therapy depletes vitamin E.

While clinical deficiency of this nutrient is uncommon, vitamin E deficiency negatively affects muscle tissue, erthrocytes, nervous and reproductive systems (Covington 1999). Depleted levels of this nutrient may be associated with cancer, heart disease, and immune dysfunction (Ames 2000).

Supplementation with doses of vitamin E ranging from 50 IU/day to 560 IU/day have been associated with positive effects, including significantly reduced risk of coronary heart disease as well as colon and prostate cancer (Ames 2000). Additionally, adequate levels of vitamin E lower lipid peroxidation and enhance immunity. However, high doses (1050 IU) of vitamin E may increase lipid peroxidation. Optimal and toxic levels of this nutrient have not yet been established.

This information is intended to serve as a concise reference for healthcare professionals to identify substances that may be depleted by many commonly prescribed medications. Depletion of these substances depends upon a number of factors including medical history, lifestyle, dietary habits, and duration of treatment with a particular medication. The signs and symptoms associated with deficiency may be nonspecific and could be indicative of clinical conditions other than deficiency. The material presented in these monographs should not in any event be construed as specific instructions for individual patients.

Aberg F, Appelkvist EL, Broijersen A, et al. Gemfibrozil-induced decrease in serum ubiquinone and alpha- and gamma-tocopherol levels in men with combined hyperlipidaemia. Eur J Clin Invest. 1998;28(3):235-242.

Ames BN. Micronutrient deficiencies: A major cause of DNA damage. Ann NY Acad Sci. 2000;889:87-106.

Artuch R, Colome C, Vilaseca MA, et al. [Ubiquinone: metabolism and functions. Ubiquinone deficiency and its implications in mitochondrial encephalopathies. Treatment with ubiquinone]. Rev Neurol. 1999;29(1):59-63.

Chan A, Reichmann H, Kogel A, Beck A, Gold R. Metabolic changes in patients with mitochondrial myopathies and effects of coenzyme Q10 therapy. J Neurol. 1998;245(10):681-685.

Covington T, ed. Nonprescription Drug Therapy Guiding Patient Self-Care. St Louis, MO: Facts and Comparisons; 1999:467-545.

Folkers K, Morita M, McRee J Jr. The actvities of coenzyme Q10 and vitamin B6 for immune responses. Biochem Biophys Res Commun. 1993;19391):88-92.

Hoppe U, Bergemann J, Diembeck W, et al. Coenzyme Q10, a cutaneous antioxidant and energizer. Biofactors. 1999;9(2-4):371-378.

Jolliet P, Simon N, Barre J, et al. Plasma coenzyme Q10 concentrations in breast cancer: prognosis and therapeutic consequences. Int J Clin Pharmacol Ther. 1998;36(9):506-509.

Kamikawa T, Kobayashi A, Yamashita T, et al. Effects of coenzyme Q10 on exercise tolerance in chronic stable angina pectoris. Am J Cardiol. 1985;56(4):247-251.

Munkholm H, Hansen HH, Rasmussen K. Coenzyme Q10 treatment in serious heart failure. Biofactors. 1999;9(2-4):285-289.

Nakamura R, Littarru GP, Folkers K, Wilkinson EG. Study of CoQ10-enzymes in gingiva from patients with periodontal disease and evidence for a deficiency of coenzyme Q10. Proc Natl Acad Sci USA. 1974;71(4):1456-1460.

Overvad K, Diamant B, Holm L, Holmer G, Mortensen SA, Stender S. Coenzyme Q10 in health and disease. Eur J Clin Nutr. 1999;53:764-770.

Singh RB, Niaz MA, Rastogi SS, et al. Effect of hydrosoluble coenzyme Q10 on blood pressure and insulin resistance in hypertensive patients with coronary heart disease. J Hum Hypertens. 1999;13(3):203-208.

Singh RB, Wander GS, Rastogi A, et al. Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther. 1998;12(4):347-353.

Yoshida H, Ishikawa T, Ayaori M, et al. Beneficial effect of gemfibrozil on the chemical composition and oxidative susceptibility of low density lipoprotein: a randomized, double-blind, placebo-controlled study. Atherscl. 1998;139(1):179-187.