title: Gene Polymorphisms Affect the Effectiveness of Atorvastatin in Treating Ischemic Stroke Patients.
abstract: OBJECTIVE
  The aim of the present study is to investigate whether the single nucleotide polymorphism (SNP) in lipid metabolism related genes would affect the effectiveness of atorvastatin in both Han and Uighur populations.
  
  
  METHODS
  200 ischemic stroke patients were treated with atorvastatin. The differences of blood lipid level and their ratios were measured. Six lipid related genes, HMGCR, APOA5, LPL, CETP, LDLR and PCSK9 were selected as candidate genes. And nine SNP loci in these six genes were genotyped by SNaPshot technique.
  
  
  RESULTS
  In all patients treated with atorvastatin, the SNP rs662799 significantly affected the ratio of x0394;LDL and x0394;LDL/LDL (p < 0.05); the SNP rs320 significantly affected the ratio of x0394;LDL/LDL and x0394;(LDL/HDL)/(LDL/HDL) (p < 0.01) and the SNP rs708272 significantly affected the ratio of x0394;LDL (p < 0.05). In Han population treated with atorvastatin, the SNP rs662799 significantly affected the ratio of x0394;TG (p < 0.05); the SNP rs320 significantly affected the ratio of x0394;LDL/LDL and x0394;(LDL/HDL)/(LDL/HDL) (p < 0.01). In Uighur population treated with atorvastatin, the SNP rs2266788 significantly affected the ratio of x0394;HDL (p < 0.05); the SNP rs662799 significantly affected the ratio of x0394;LDL/LDL (p < 0.05) and the SNP rs708272 significantly affected the ratio of x0394;LDL (p < 0.05).
  
  
  CONCLUSIONS
  Polymorphisms of rs662799 and rs2266788 in APOA5 gene, rs320 in LPL gene and rs708272 in CETP gene had significant association with the effect of the lipid-lowering therapy via atorvastatin calcium on ischemic stroke patients.
authors.affiliation: Department of Neurology, Yangpu Hospital Tongji University School of Medicine, Shanghai, China.
authors.forename: Yun-Hua
authors.initials: YH
authors.lastname: Yue
authors.forename: Xu-Dong
authors.initials: XD
authors.lastname: Bai
authors.forename: Hui-Jun
authors.initials: HJ
authors.lastname: Zhang
authors.forename: You-Mei
authors.initials: YM
authors.lastname: Li
authors.forename: Liang
authors.initials: L
authors.lastname: Hu
authors.forename: Ling-Yun
authors.initials: LY
authors.lastname: Liu
authors.forename: Jie-Ping
authors.initials: JP
authors.lastname: Mao
authors.forename: Xiao-Ying
authors.initials: XY
authors.lastname: Yang
authors.forename: Na-Mu
authors.initials: NM
authors.lastname: Dila
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D000072040:Apolipoprotein A-V / Q000235:genetics / Q000378:metabolism; D000069059:Atorvastatin / Q000627:therapeutic use*; D002545:Brain Ischemia / Q000150:complications; D053480:Cholesterol Ester Transfer Proteins / Q000235:genetics / Q000378:metabolism; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000235:genetics / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000235:genetics / Q000378:metabolism; D008075:Lipoproteins, HDL / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D000071449:Proprotein Convertase 9 / Q000235:genetics / Q000378:metabolism; D020521:Stroke / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics
chemical_list: D000924:Anticholesteremic Agents; D000072040:Apolipoprotein A-V; C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D000069059:Atorvastatin; C553220:HMGCR protein, human; D006903:Hydroxymethylglutaryl CoA Reductases; C548261:LPL protein, human; D008071:Lipoprotein Lipase; C472125:PCSK9 protein, human; D000071449:Proprotein Convertase 9