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At a genome\u2010wide significance level, single nucleotide polymorphisms (<jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s) in <jats:italic><jats:styled-content style=\"fixed-case\">PCSK<\/jats:styled-content>9<\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">HMGCR<\/jats:styled-content><\/jats:italic> have been implicated in this differential response. However, the influence of these variants is uncertain in the Chilean population. Hence, we aimed to evaluate the contribution of <jats:italic><jats:styled-content style=\"fixed-case\">PCSK<\/jats:styled-content>9<\/jats:italic> rs7552841 and <jats:italic><jats:styled-content style=\"fixed-case\">HMGCR<\/jats:styled-content><\/jats:italic> rs17671591 <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s as genetic determinants of atorvastatin response in Chilean hypercholesterolaemic individuals. One hundred and one hypercholesterolaemic patients received atorvastatin 10 mg\/day for 4 weeks. Plasma lipid profile (<jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> HDL<\/jats:styled-content>\u2010C, <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\u2010C and <jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content>) was determined before and after statin treatment, and <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content>s were identified by allelic discrimination using TaqMan<jats:sup>\u00ae<\/jats:sup> <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> Genotyping Assays. Adjusted univariate and multivariate analyses' models were used for statistical analyses, and a <jats:italic>p<\/jats:italic>\u2010value &lt;0.05 was considered significant. From baseline (week 0) to the study end\u2010point (week 4), significant reductions were observed in plasma <jats:styled-content style=\"fixed-case\">TC<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> LDL<\/jats:styled-content>\u2010C and <jats:styled-content style=\"fixed-case\">TG<\/jats:styled-content> (<jats:italic>p<\/jats:italic> &lt; 0.001), while <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C levels were increased (<jats:italic>p<\/jats:italic> &lt; 0.001). Multivariate analysis showed no association between lipid levels and atorvastatin therapy for the <jats:italic><jats:styled-content style=\"fixed-case\">PCSK<\/jats:styled-content>9<\/jats:italic> variant. However, the <jats:italic><jats:styled-content style=\"fixed-case\">HMGCR<\/jats:styled-content><\/jats:italic> rs17671591 T allele contributed to basal <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C concentration variability along with a higher increase in this lipid fraction after statin medication. In addition, this allele determined greater plasma <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\u2010C reductions after therapy with atorvastatin. Our data suggest that the <jats:italic><jats:styled-content style=\"fixed-case\">HMGCR<\/jats:styled-content><\/jats:italic> rs17671591 polymorphism can constitute a genetic marker of lower plasma <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content>\u2010C and enhanced <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010C concentration after atorvastatin therapy in the Chilean population.<\/jats:p>","DOI":"10.1111\/bcpt.12493","type":"journal-article","created":{"date-parts":[[2015,9,26]],"date-time":"2015-09-26T08:05:58Z","timestamp":1443254758000},"page":"292-297","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["<scp>HMGCR<\/scp> rs17671591 <scp>SNP<\/scp> Determines Lower Plasma <scp>LDL<\/scp>\u2010C after Atorvastatin Therapy in Chilean Individuals"],"prefix":"10.1111","volume":"118","author":[{"given":"Alejandro","family":"Cuevas","sequence":"first","affiliation":[{"name":"Center of Molecular Biology &amp; Pharmacogenetics Department of Basic Sciences Scientific and Technological Bioresources Nucleus University of La Frontera (BIOREN\u2010UFRO) Temuco Chile"},{"name":"Preclinical Sciences Department Faculty of Medicine University of La Frontera Temuco Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C\u00e9sar","family":"Fern\u00e1ndez","sequence":"additional","affiliation":[{"name":"Preclinical Sciences Department Faculty of Medicine University of La Frontera Temuco Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luis","family":"Ferrada","sequence":"additional","affiliation":[{"name":"Preclinical Sciences Department Faculty of Medicine University of La Frontera Temuco Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tom\u00e1s","family":"Zambrano","sequence":"additional","affiliation":[{"name":"Center of Molecular Biology &amp; Pharmacogenetics Department of Basic Sciences Scientific and Technological Bioresources Nucleus University of La Frontera (BIOREN\u2010UFRO) Temuco Chile"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alexy","family":"Rosales","sequence":"additional","affiliation":[{"name":"Center of Molecular Biology &amp; 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