{"doi":"10.2217/pgs-2017-0146","title":"Genetic Variation in Statin Intolerance and a Possible Protective Role for\n            <i>UGT1A1</i>","abstract":null,"journal":"Pharmacogenomics","year":2018,"id":637696,"datarank":0.3958585994422889,"base_score":2.639057329615259,"endowment":2.639057329615259,"self_citation_contribution":0.3958585994422889,"citation_network_contribution":0.0,"self_endowment_contribution":0.3958585994422889,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":13,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1655914,"name":"Erin J Kaleta","orcid":null,"position":1,"is_corresponding":false},{"id":1655915,"name":"Sandra C Bryant","orcid":null,"position":2,"is_corresponding":false},{"id":1655916,"name":"Grant M Spears","orcid":null,"position":3,"is_corresponding":false},{"id":1641627,"name":"Laura J Train","orcid":null,"position":4,"is_corresponding":false},{"id":1655917,"name":"Sandra E Peterson","orcid":null,"position":5,"is_corresponding":false},{"id":1655918,"name":"Vanda A Lennon","orcid":null,"position":6,"is_corresponding":false},{"id":1655920,"name":"Stephen L Kopecky","orcid":null,"position":7,"is_corresponding":false},{"id":1641629,"name":"Linnea M Baudhuin","orcid":null,"position":8,"is_corresponding":false},{"id":1655913,"name":"Maria Alice V Willrich","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Genetic Variation in Statin Intolerance and a Possible Protective Role for\n            <i>UGT1A1</i>","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.","is_dataset_classified":null,"base_score":2.639057329615259,"endowment":2.639057329615259,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"29210320","pmcid":null,"openalex_id":"https://openalex.org/W2772408441","authors":[],"funders":[{"funder_name":"Department of Laboratory Medicine and Pathology at Mayo Clinic","grant_id":"UL1 TR000135","title":null},{"funder_name":"National Center for Advancing Translational Sciences","grant_id":"","title":null}],"total_grants":2,"fwci":0.709,"citation_percentile":0.73140107,"influential_citations":0,"citation_trend":[{"year":2018,"count":1},{"year":2020,"count":2},{"year":2021,"count":3},{"year":2022,"count":2},{"year":2024,"count":2},{"year":2025,"count":3}],"oa_status":"closed","license":null,"oa_locations":[{"url":"https://www.tandfonline.com/doi/pdf/10.2217/pgs-2017-0146","host_type":"publisher"},{"url":"https://doi.org/10.2217/pgs-2017-0146","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/29210320","host_type":"repository"}],"fields_of_study":["Lipoproteins and Cardiovascular Health","Cancer, Lipids, and Metabolism","Diabetes, Cardiovascular Risks, and Lipoproteins","Aged","Case-Control Studies","Creatine Kinase","Female","Gene Frequency","Genetic Variation","Glucuronosyltransferase","Humans","Hydroxymethylglutaryl-CoA Reductase Inhibitors","Hyperlipidemias","Lipids","Male","UGT1A1 Enzyme"],"mesh_terms":["UGT1A1 Enzyme","Aged","Creatine Kinase","Female","Gene Frequency","Humans","Hyperlipidemias","Lipids","Male","Glucuronosyltransferase","Genetic Variation","Case-Control Studies","Hydroxymethylglutaryl-CoA Reductase Inhibitors"],"keywords":["Statin","SLCO1B1","Pharmacogenetics","Medicine","Internal medicine","Atorvastatin","Genetic variation","CYP3A4","Etiology","Cohort","Minor allele frequency","Genetic variability","Allele","Pharmacology","Endocrinology","Allele frequency","Biology","Genetics","Cytochrome P450","Gene","Metabolism","Genotype","Population","Myotoxicity","Genetic Variants","Abc Transporters","statins","CYP3A","Ugt","Statin Intolerance","Precision Medicine","Slc Transporters","Gatm"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-06T19:21:53.904764Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}