Short CommunicationAssociation of SLCO1B1 c.521T>C (rs4149056) with discontinuation of atorvastatin due to statin-associated muscle symptomsLinskey, Derek W.a; English, Joseph D.a; Perry, Daniel A.b; Ochs-Balcom, Heather M.c; Ma, Changxingd; Isackson, Paul J.e,,f; Vladutiu, Georgirene D.e,,g,,h; Luzum, Jasmine A.aAuthor Information aDepartment of Clinical Pharmacy, University of Michigan College of Pharmacy bDivision of Cardiovascular Medicine, Frankel Cardiovascular Center, University of Michigan, Ann Arbor, Michigan cDepartment of Epidemiology and Environmental Health, School of Public Health and Health Professions dDepartment of Biostatistics, School of Public Health and Health Professions eDepartment of Pediatrics fKaleida Health Laboratories gDepartment of Neurology hDepartment of Pathology and Anatomical Sciences, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA Received 14 January 2020 Accepted 27 April 2020 Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's website, www.pharmacogeneticsandgenomics.com. Correspondence to Jasmine A. Luzum, PharmD, PhD, University of Michigan College of Pharmacy, 1100 North University Avenue, Ann Arbor, Michigan, USA, E-mail: [email protected] Pharmacogenetics and Genomics: December 2020 - Volume 30 - Issue 9 - p 208-211 doi: 10.1097/FPC.0000000000000412 Buy SDC Metrics Abstract The most common adverse drug reaction from statins are statin-associated muscle symptoms (SAMS), characterized by myopathy (weakness), myalgia (muscle pain), and commonly elevation in serum creatine kinase. All statins are substrates of the organic anion transporter 1B1 (OATP1B1; gene: SLCO1B1), albeit to different degrees. A genetic polymorphism in SLCO1B1, c.521T>C (rs4149056), markedly decreases OATP1B1 function. The literature is currently unclear as to whether SLCO1B1 c.521T>C is significantly associated with discontinuation of atorvastatin specifically due to SAMS. Our hypothesis was that individuals carrying the SLCO1B1 decreased function 521C allele are more likely to discontinue atorvastatin due to SAMS. This was a retrospective analysis of survey data from 379 Caucasians genotyped for rs4149056 and treated with atorvastatin for at least 12 months. Crude and multivariable logistic regression, adjusted for established risk factors for SAMS, determined the association of SLCO1B1 c.521T>C with discontinuation of atorvastatin due to SAMS (SLCO1B1 521T-homozygotes vs. 521C-carriers). The sample was 51% male, with a mean age of 57 years (SD = 11). Sixty-one percent of participants reported discontinuing atorvastatin due to SAMS, and 32% overall carried the 521C allele. SLCO1B1 521C-carrier status was not a significant predictor of atorvastatin discontinuation in any model: crude OR = 1.07; 95% CI, 0.68–1.66; P = 0.78 and adjusted OR = 1.07; 95% CI, 0.68–1.69; P = 0.76. The results were similar in a sub-group of participants treated with higher doses of atorvastatin (>20 mg). In summary, SLCO1B1 c.521T>C was not significantly associated with discontinuation of atorvastatin therapy due to SAMS. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.