Abstract:
:The etiology of statin intolerance is hypothesized to be due to genetic variants that impact statin disposition and clearance. We sought to determine whether genetic variants were associated to statin intolerance. The studied cohort consisted of hyperlipidemic participants (n = 90) clinically diagnosed with statin intolerance by a cardiologist and matched controls without statin intolerance. Creatine kinase activity, lipid profiles and genetic analyses were performed on genes involved in statin metabolism and included UGT1A1 and UGT1A3 sequencing and targeted analyses of CYP3A4*22, CYP3A5*3, SLCO1B1*5 and *1b, ABCB1 c.3435C>T, ABCG2 c.421C>A and GATM rs9806699. Although lipids were higher in cases, genetic variant minor allele frequencies were similar between cases and controls, except for UGT1A1*28, which was less prevalent in cases than controls.
journal_name
Pharmacogenomicsjournal_title
Pharmacogenomicsauthors
V Willrich MA,Kaleta EJ,Bryant SC,Spears GM,Train LJ,Peterson SE,Lennon VA,Kopecky SL,Baudhuin LMdoi
10.2217/pgs-2017-0146subject
Has Abstractpub_date
2018-01-01 00:00:00pages
83-94issue
2eissn
1462-2416issn
1744-8042journal_volume
19pub_type
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