1. SLCO1B1 521T > C polymorphism associated with rosuvastatin-induced myotoxicity in Chinese coronary artery disease patients: a nested case-control study.
- Author
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Liu, Ju-E, Liu, Xiao-Ying, Chen, Sheng, Zhang, Yan, Cai, Li-Yun, Yang, Min, Lai, Wei-Hua, Ren, Bin, and Zhong, Shi-Long
- Subjects
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ALLELES , *CLINICAL trials , *CONFIDENCE intervals , *CORONARY disease , *GENETIC polymorphisms , *CARDIAC patients , *MUSCLE diseases , *STATINS (Cardiovascular agents) , *CASE-control method , *ATORVASTATIN , *DESCRIPTIVE statistics , *SIMVASTATIN , *ROSUVASTATIN , *ODDS ratio , *GENOTYPES , *DISEASE risk factors - Abstract
Purpose: This nested case-control study aimed to evaluate the association of candidate genetic variants with statin-induced myotoxicity in Chinese patients with coronary artery disease (CAD). Methods: One hundred forty-eight Chinese patients experiencing statin-induced myotoxicity were included in our study, and 255 patients without muscular side effects served as controls. Five SNPs in CYP3A5, SLCO1B1, and APOE were genotyped. The effect of genetic variants on statin-induced myotoxicity was assessed. Results: Patients who carried at least one SLCO1B1 521C allele had a higher risk for myotoxicity (OR = 1.69, 95%CI = 1.07-2.67, P = 0.024). Significant association was found between SLCO1B1 521C mutant allele mutation and risk of myotoxicity in individuals that received rosuvastatin (OR = 3.67, 95%CI = 1.42-9.47, P = 0.007). However, non-significant association was observed between 521C mutant allele and risk of myotoxicity ( P > 0.5) in patients that received atorvastatin and simvastatin. The other four single nucleotide polymorphisms (SNPs), namely rs776746, rs2306283, rs7412, and rs429358, showed no significant association with any statin induced myotoxicity ( P > 0.5). Conclusions: SLCO1B1 (rs4149056, 521T > C) is associated with statin-induced myotoxicity in Chinese patients with coronary artery disease. In addition, SLCO1B1 521C mutant allele increased the risk of rosuvastatin-associated myotoxicity. [ABSTRACT FROM AUTHOR]
- Published
- 2017
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