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Comparison of Efficacy and Safety of Rosuvastatin, Atorvastatin and Pravastatin among Dyslipidemic Diabetic Patients

DOI: 10.1155/2013/146579

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Abstract:

Objectives. To investigate the efficacy and the safety of the three most commonly prescribed statins (rosuvastatin, atorvastatin, and pravastatin) for managing dyslipidemia among diabetic patients in Qatar. Subjects and Methods. This retrospective observational population-based study included 350 consecutive diabetes patients who were diagnosed with dyslipidemia and prescribed any of the indicated statins between September 2005 and September 2009. Data was collected by review of the Pharmacy Database, the Electronic Medical Records Database (EMR viewer), and the Patient's Medical Records. Comparisons of lipid profile measurements at baseline and at first- and second-year intervals were taken. Results. Rosuvastatin (10?mg) was the most effective at reducing LDL-C (29.03%). Atorvastatin reduced LDL-C the most at a dose of 40?mg (22.8%), and pravastatin reduced LDL-C the most at a dose of 20?mg (20.3%). All three statins were safe in relation to muscular and hepatic functions. In relation to renal function, atorvastatin was the safest statin as it resulted in the least number of patients at the end of 2 years of treatment with the new onset of microalbuminuria (10.9%) followed by rosuvastatin (14.3%) and then pravastatin (26.6%). Conclusion. In the Qatari context, the most effective statin at reducing LDL-C was rosuvastatin 10?mg. Atorvastatin was the safest statin in relation to renal function. Future large-scale prospective studies are needed to confirm these results. 1. Introduction Diabetes is now commonly recognized as a “coronary heart disease risk equivalent” [1–4]. This is mainly attributed to the high rates of dyslipidemia among diabetic patients which is believed to be one of the major factors accounting for the high percentage of deaths among diabetics due to cardiovascular disease (CVD) [5]. The differences in the lipid profile between diabetics (especially type 2 diabetics) and nondiabetics account for the increased CVD risk [6]. Essentially, T2DM lipid profiles consist of elevations in triglyceride (TG) levels (>2?mmol/L) and reductions in high-density lipoprotein cholesterol (HDL-C). While low-density lipoproteins cholesterol (LDL-C) concentration levels are normal, the particles are denser and smaller in size, which is believed to enhance their atherogenic potential [7]. Numerous epidemiological studies and randomized controlled trials have documented the association between elevated LDL-C levels with increased CVD risk in both diabetic and nondiabetic populations [8, 9]. Thus reducing LDL-C levels is the primary goal of therapy for

References

[1]  National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), “Third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III) final report,” Circulation, vol. 106, no. 25, article 3143, 2002.
[2]  A. Bener, M. Zirie, I. M. Janahi, A. O. A. A. Al-Hamaq, M. Musallam, and N. J. Wareham, “Prevalence of diagnosed and undiagnosed diabetes mellitus and its risk factors in a population-based study of Qatar,” Diabetes Research and Clinical Practice, vol. 84, no. 1, pp. 99–106, 2009.
[3]  A. Bener, M. Zirie, M. Musallam, Y. S. Khader, and A. O. A. A. Al-Hamaq, “Prevalence of metabolic syndrome according to adult treatment panel III and international diabetes federation criteria: a population-based study,” Metabolic Syndrome and Related Disorders, vol. 7, no. 3, pp. 221–230, 2009.
[4]  A. Bener, E. Dafeeah, S. Ghuloum, and A. O. A. A. Al-Hamaq, “Association between psychological distress and gastrointestinal symptoms in type 2 diabetes mellitus,” World Journal of Diabetes, vol. 3, no. 6, pp. 123–129, 2012.
[5]  J. D. Brunzell, M. Davidson, C. D. Furberg et al., “Lipoprotein management in patients with cardiometabolic risk: consensus statement from the American diabetes association and the american college of cardiology foundation,” Diabetes Care, vol. 31, no. 4, pp. 811–822, 2008.
[6]  T. O'Brien, T. T. Nguyen, and B. R. Zimmerman, “Hyperlipidemia and diabetes mellitus,” Mayo Clinic Proceedings, vol. 73, no. 10, pp. 969–976, 1998.
[7]  R. M. Krauss, “Lipids and lipoproteins in patients with type 2 diabetes,” Diabetes Care, vol. 27, no. 6, pp. 1496–1504, 2004.
[8]  H. M. Colhoun, D. J. Betteridge, P. N. Durrington et al., “Primary prevention of cardiovascular disease with atorvastatin in type 2 diabetes in the collaborative atorvastatin diabetes study (CARDS): multicentre randomised placebo-controlled trial,” The Lancet, vol. 364, no. 9435, pp. 685–696, 2004.
[9]  J. Shepherd, P. Barter, R. Carmena et al., “Effect of lowering LDL cholesterol substantially below currently recommended levels in patients with coronary heart disease and diabetes: the treating To new targets (TNT) study,” Diabetes Care, vol. 29, no. 6, pp. 1220–1226, 2006.
[10]  American Diabetes Association, “Standards of medical care in diabetes,” Diabetes Care, vol. 32, supplement 1, pp. S13–S61, 2009.
[11]  S. J. Nicholls, E. M. Tuzcu, I. Sipahi et al., “Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis,” The Journal of the American Medical Association, vol. 297, no. 5, pp. 499–508, 2007.
[12]  R. R. Henry, “Preventing cardiovascular complications of type 2 diabetes: focus on lipid management,” Clinical Diabetes, vol. 19, no. 3, pp. 113–120, 2001.
[13]  D. J. Maron, S. Fazio, and M. F. Linton, “Current perspectives on statins,” Circulation, vol. 101, no. 2, pp. 207–213, 2000.
[14]  R. S. Rosenson, “Rosuvastatin: a new inhibitor of HMG-coA reductase for the treatment of dyslipidemia,” Expert Review of Cardiovascular Therapy, vol. 1, no. 4, pp. 495–505, 2003.
[15]  P. H. Jones, M. H. Davidson, E. A. Stein et al., “Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* trial),” American Journal of Cardiology, vol. 92, no. 2, pp. 152–160, 2003.
[16]  A. S. Brown, R. G. Bakker-Arkema, L. Yellen et al., “Treating patients with documented atherosclerosis to national cholesterol education program-recommended low-density-lipoprotein cholesterol goals with atorvastatin, fluvastatin, lovastatin and simvastatin,” Journal of the American College of Cardiology, vol. 32, no. 3, pp. 665–672, 1998.
[17]  B. A. Hamelin and J. Turgeon, “Hydrophilicity/Lipophilicity: relevance for the pharmacology and clinical effects of HMG-CoA reductase inhibitors,” Trends in Pharmacological Sciences, vol. 19, no. 1, pp. 26–37, 1998.
[18]  A. R. Vasudevan, Y. S. Hamirani, and P. H. Jones, “Safety of statins: effects on muscle and the liver,” Cleveland Clinic Journal of Medicine, vol. 72, no. 11, pp. 990–1001, 2005.
[19]  A. A. Alsheikh-Ali and R. H. Karas, “The relationship of statins to rhabdomyolysis, malignancy, and hepatic toxicity: evidence from clinical trials,” Current Atherosclerosis Reports, vol. 11, no. 2, pp. 100–104, 2009.
[20]  A. Kashani, C. O. Phillips, J. M. Foody et al., “Risks associated with statin therapy: a systematic overview of randomized clinical trials,” Circulation, vol. 114, no. 25, pp. 2788–2797, 2006.
[21]  J. Armitage, “The safety of statins in clinical practice,” The Lancet, vol. 370, no. 9601, pp. 1781–1790, 2007.
[22]  M. Evans and A. Rees, “Effects of HMG-CoA reductase inhibitors on skeletal muscle: are all statins the same?” Drug Safety, vol. 25, no. 9, pp. 649–663, 2002.
[23]  Annual Health Report, Vital Health Statistics, Hamad Medical Corporation, Doha, Qatar, 2010.
[24]  World Health Organization, “Definition, diagnosis and classification of diabetes mellitus and its complications,” Report of a WHO Consultation WHOINCDINCS/99. 2, World Health Organization, Geneva, Switzerland, 1999.
[25]  J. M. Mckenney, “Efficacy and safety of rosuvastatin in treatment of dyslipidemia,” American Journal of Health-System Pharmacy, vol. 62, no. 10, pp. 1033–1047, 2005.
[26]  M. B. Clearfield, J. Amerena, J. P. Bassand et al., “Comparison of the efficacy and safety of rosuvastatin 10 mg and atorvastatin 20 mg in high-risk patients with hypercholesterolemia—prospective study to evaluate the Use of Low doses of the Statins Atorvastatin and Rosuvastatin (PULSAR),” Trials, vol. 7, article 35, 2006.
[27]  B. G. Brown, X. Q. Zhao, and M. C. Cheung, “Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence,” Journal of Clinical Lipidology, vol. 1, no. 1, pp. 88–94, 2007.
[28]  A. Tiwari, V. Bansal, A. Chugh, and K. Mookhtiar, “Statins and myotoxicity: a therapeutic limitation,” Expert Opinion on Drug Safety, vol. 5, no. 5, pp. 651–666, 2006.
[29]  E. Bj?rnsson, E. I. Jacobsen, and E. Kalaitzakis, “Hepatotoxicity associated with statins: reports of idiosyncratic liver injury post-marketing,” Journal of Hepatology, vol. 56, no. 2, pp. 374–380, 2012.
[30]  K. Douglas, P. G. O'Malley, and J. L. Jackson, “Meta-analysis: the effect of statins on albuminuria,” Annals of Internal Medicine, vol. 145, no. 2, pp. 117–124, 2006.
[31]  J. Atthobari, A. H. Brantsma, R. T. Gansevoort et al., “The effect of statins on urinary albumin excretion and glomerular filtration rate: results from both a randomized clinical trial and an observational cohort study,” Nephrology Dialysis Transplantation, vol. 21, no. 11, pp. 3106–3114, 2006.
[32]  J. M. McKenney, “Defining the pharmacological profile of rosuvastatin: a look at statin therapy for dyslipidemia,” France foundation web site poster: advances in managing hyperlipidemia online continuing medical education activity, 2005, http://www.francefoundation.com/cme/posttest/pages/amh_posters.pdf.

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