Journal of Lipid Research, Vol 32, 935-940, Copyright © 1991 by Lipid Research, Inc.

ARTICLES

Effects of pravastatin and cholestyramine on products of the mevalonate pathway in familial hypercholesterolemia

PG Elmberger, A Kalen, E Lund, E Reihner, M Eriksson, L Berglund, B Angelin and G Dallner
Department of Clinical Pathology, Huddinge University Hospital, Karolinska Institutet, Sweden.

Patients with heterozygous familial hypercholesterolemia (n = 12) were treated either with pravastatin, a specific inhibitor of HMG-CoA reductase, or cholestyramine, followed by a period of combined treatment with both drugs. Initially, these patients had increased serum levels of low density lipoprotein (LDL) cholesterol (8.77 +/- 0.48 mmol/l; SEM), lathosterol (5.32 +/- 0.60 mg/l), and ubiquinone (0.76 +/- 0.09 mg/l), while the serum dolichol concentration was in the normal range. Cholestyramine treatment (n = 6) decreased the levels of LDL cholesterol (-32%) and increased lathosterol (+125%), but did not change dolichol or ubiquinone levels in a significant manner. Pravastatin treatment (n = 6) decreased LDL cholesterol (-27%), lathosterol (-46%), and ubiquinone (-29%). In this case, the amount of dolichol in serum also showed a small but statistically insignificant decrease (-16%) after 12 weeks of treatment. Combined treatment with cholestyramine and pravastatin (n = 6) resulted in changes that were similar to, but less pronounced than, those observed during pravastatin treatment alone. In no case was the ratio between ubiquinone and LDL cholesterol reduced. Possible effects on hepatic cholesterol, ubiquinone, and dolichol concentrations were studied in untreated (n = 2), cholestyramine-treated (n = 2), and pravastatin-treated (n = 4) gallstone patients and no consistent changes could be observed. The results indicate that treatment with pravastatin in familial hypercholesterolemia decreases serum ubiquinone levels in proportion to the reduction in LDL cholesterol.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				L. Marcoff and P. D. Thompson The Role of Coenzyme Q10 in Statin-Associated Myopathy: A Systematic Review J. Am. Coll. Cardiol., June 12, 2007; 49(23): 2231 - 2237. [Abstract] [Full Text] [PDF]

				H. B. Levy and H. K Kohlhaas Considerations for Supplementing with Coenzyme Q10 During Statin Therapy Ann. Pharmacother., February 1, 2006; 40(2): 290 - 294. [Abstract] [Full Text] [PDF]

				J. W. Fenton, G. X. Shen, F. L. Minnear, D. V. Brezniak, J. M. Walenga, J. J. Bognacki, and F. A. Ofosu State-of-the-Art-Review : Statins Induce Hypothrombotic States? Clinical and Applied Thrombosis/Hemostasis, January 1, 2000; 6(1): 18 - 21. [Abstract] [PDF]

				G. M. B. Berger, R. J. Pegoraro, S. B. Patel, P. Naidu, L. Rom, H. Hidaka, A. D. Marais, A. Jadhav, R. P. Naoumova, and G. R. Thompson HMG-CoA reductase is not the site of the primary defect in phytosterolemia J. Lipid Res., May 1, 1998; 39(5): 1046 - 1054. [Abstract] [Full Text]