Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients

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Clinical Transplantation

Volume 22 Issue 1 Page 113-119, January/February 2008

To cite this article: Jill E. , M. Cavanaugh, Trumbull, etta Bass, Fredrick Weber Jr, Aranda-Michel, Hanaway, Rudich (2008) Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients Clinical Transplantation 22 (1), 113–119. doi:10.1111/j.1399-0012.2007.00780.x

Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients

Jill E. aaCollege of Pharmacy, M. CavanaughaaCollege of Pharmacy, TrumbullbbTransplant and Hepatobiliary Division, University of Cincinnati, Cincinnati, OH, etta BassbbTransplant and Hepatobiliary Division, University of Cincinnati, Cincinnati, OH, Fredrick Weber JrbbTransplant and Hepatobiliary Division, University of Cincinnati, Cincinnati, OH, Aranda-MichelccMayo Clinic, Gastroenterology, ville, FL, HanawayddUAB Hospital, Transplant Surgery, Birmingham, AL, USA and RudichbbTransplant and Hepatobiliary Division, University of Cincinnati, Cincinnati, OH

aCollege of Pharmacy, bTransplant and Hepatobiliary Division, University of Cincinnati, Cincinnati, OH, cMayo Clinic, Gastroenterology, ville, FL and dUAB Hospital, Transplant Surgery, Birmingham, AL, USA

Corresponding author: Jill E. , PharmD, FASHP, College of Pharmacy, 301-I Wherry Hall, 3225 Eden Ave, University of Cincinnati Medical Center, PO Box 670004, Cincinnati, OH 45267, USA.Tel.: ; fax: ;e-mail: teresa.cavanaugh@...

JE, Cavanaugh TM, Trumbull L, Bass M, Weber F Jr, Aranda-Michel J, Hanaway M, Rudich S. Incidence of adverse events with HMG-CoA reductase inhibitors in liver transplant patients.Clin Transplant 2007 DOI: 10.1111/j.1399-0012.2007.00780.x© Blackwell Munksgaard, 2007

Abstract

Abstract: Transplant patients are at increased risk of developing dyslipidemia, which contributes to coronary artery disease and cardiovascular events. The purpose of this study was to explore documented adverse effects of liver transplant recipients receiving lipid-lowering therapies.

Methods: A retrospective chart review of 69 liver transplant patients was conducted to evaluate the incidence of adverse effects, especially rhabdomyolysis and liver function abnormalities, in liver transplant patients treated with a lipid lowering agent (LLA). Data were collected from the time of initiation of LLA to 12 months later, looking at the type, dose, and duration of LLA, concurrent cytochrome P450 inhibitors, immunosuppression used, and laboratory parameters.

Results: For HMG-CoA reductase inhibitor therapy, simvistatin was used in five (7.8%) patients, pravastatin in 40 (62.5%), fluvastatin in one (1.6%), atorvastatin in five (7.8%), and lovastatin in three (4.7%). Gemfibrozil, a fibric acid derivative, was employed as monotherapy in 10 (15.6%) of patients. There were five patients who received combination therapy with a fibric acid derivative, four (80%) with gemfibrozil + pravastatin, and one (20%) with gemfibrozil + simvastatin. Six patients studied had adverse effects, five (7.2%) with myalgia and one (1.4%) with myopathy. LLA monotherapy with either pravastatin or atorvastatin was used in these patients. The five patients with myalgia were on concurrent therapy with cyclosporin, and the patient with myopathy was on concurrent cyclosporin + diltiazem therapy, both of which are P450 inhibitors. One out of 23 patients on a non-immunosuppressant P450 inhibitor developed adverse effects. No significant elevation of alanine aminotransferase, aspartate aminotransferase, or alkaline phosphatase was noted in any patient.

Conclusions: Overall, there was a general tolerability with a low incidence of adverse events, no incidence of severe complications, and no alterations in liver function tests in the study population with the use of LLA.