This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Purchase Article View Shopping Cart Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wägner, A. M. Articles by Pérez, A. Search for Related Content PubMed PubMed Citation Articles by Wägner, A. M. Articles by Pérez, A.

Efficacy of Atorvastatin and Gemfibrozil, Alone and in Low Dose Combination, in the Treatment of Diabetic Dyslipidemia

Departments of Endocrinology and Biochemistry (O.J., R.B., J.O.-L.), Hospital Sant Pau, and Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona (J.O.-L.), 08025 Barcelona, Spain

Address all correspondence and requests for reprints to: Dr. Antonio Pérez, Department of Endocrinology, Hospital Sant Pau, S. Antoni M. Claret 167, 08025 Barcelona, Spain. E-mail: aperez{at}hsp.santpau.es.

To compare the effects of atorvastatin, gemfibrozil, and their combination on the components of diabetic dyslipidemia, 44 type 2 diabetic patients with low density lipoprotein cholesterol (LDLc) levels greater than 100 mg/dl and triglyceride levels less than 400 mg/dl were included. Twelve-week treatments with atorvastatin (10–20 mg/d) and gemfibrozil (900–1200 mg/d) were given in random order in an open, cross-over study and then combined (10 mg atorvastatin and 900 mg gemfibrozil) for 12 additional wk. Triglyceride, LDLc, high density lipoprotein cholesterol (HDLc), non-HDLc, apolipoprotein B (apoB), and LDL size were measured at baseline and after each treatment. Atorvastatin was more effective (P < 0.001) in lowering LDLc, non-HDLc, and apoB and in achieving treatment goals, whereas gemfibrozil lowered triglyceride levels more effectively (P < 0.001) and increased LDL size (from 25.59 ± 0.06 to 25.69 ± 0.06 nm; P < 0.05). Combined treatment with both drugs reduced LDLc, triglyceride, non-HDLc, and apoB by 26.5%, 24.1%, 30.4%, and 21.8%, respectively; increased HDLc by 4.8% and LDL size by 0.1 nm; and was the most effective treatment in reaching the therapeutic targets, especially in patients with triglyceride levels higher than 150 mg/dl. In conclusion, statins are first choice drugs in diabetic patients with low to moderate risk LDLc, although their combination with fibrates might be the most appropriate treatment, especially when triglyceride levels are above the therapeutic goal.

This work was supported by a grant from the Catalonian Research Board (1999 FI-712; to A.M.W.) during the performance of the study. The study drugs and funding for some of the laboratory measurements were provided by Pfizer (Barcelona, Spain). Pfizer was not involved in the collection or interpretation of data, the correction of the manuscript, or the decision of whether or how to publish it.

Present address for O.J., R.B., and J.O.-L.: Department of Endocrinology, Hospital Sant Pau, S. Antoni M. Claret 167, Barcelona 08025, Spain.

Present address for A.M.W.: Department of Biochemistry, Hospital Sant Pau, S. Antoni M. Claret 167, Barcelona 08025, Spain.

Abbreviations: apoB, Apolipoprotein B; HDLc, high density lipoprotein cholesterol; LDLc, low density lipoprotein cholesterol.

This article has been cited by other articles:

				M. Rizzo and K. Berneis Low-density lipoprotein size and cardiovascular risk assessment QJM, January 1, 2006; 99(1): 1 - 14. [Abstract] [Full Text] [PDF]

				J.-F. Landrier, C. Thomas, J. Grober, H. Duez, F. Percevault, M. Souidi, C. Linard, B. Staels, and P. Besnard Statin Induction of Liver Fatty Acid-Binding Protein (L-FABP) Gene Expression Is Peroxisome Proliferator-activated Receptor-{alpha}-dependent J. Biol. Chem., October 29, 2004; 279(44): 45512 - 45518. [Abstract] [Full Text] [PDF]

				J. M. Huss and D. P. Kelly Nuclear Receptor Signaling and Cardiac Energetics Circ. Res., September 17, 2004; 95(6): 568 - 578. [Abstract] [Full Text] [PDF]