Impacts of SLCO1B1 c.388A > G polymorphisms on lipid-lowering and anti-atherosclerosis effects of atorvastatin in Chinese patients with ischemic stroke / 国际脑血管病杂志
International Journal of Cerebrovascular Diseases
;
(12): 33-38, 2017.
Article
in Chinese
| WPRIM
| ID: wpr-513296
ABSTRACT
Objective To investigate the impacts of c.388A > G polymorphism of the solute carrier organic anion transporter 1B1 (SLCO1B1) gene on lipid-lowering and anti-atherosclerosis effects of atorvastatin in Chinese patients with ischemic stroke.Methods The patients with ischemic stroke whose baseline low-density lipoprotein cholesterol (LDL-C) > 1.8 mmol/L were enrolled prospectively.They received atorvastatin (20 mg/d) for 12 months.The lipid and bilateral carotid intima-media thickness (CIMT) were measured respectively before and after treatment.The CIMT differences between SLCO1B1 c.388A>G genotype groups were compared.Results A total of 71 patients with ischemic stroke were enrolled,including 5 AA genotype,31 AG genotype,and 35 GG genotype.The A allele frequency was 28.9% and the G allele frequency was 71.1%.After treatment,the total cholesterol (TC),triglyceride (TG),and LDL-C in all patients were significantly lower than those before treatment,and high-density lipoprotein cholesterol (HDL-C) was significantly increase (all P<0.001),but CIMT did not have significant change (P=0.475).The proportion of patients whose LDL-C < 1.8 mmol/L or LDL-C decreased ≥50% in the GG genotype group was significantly higher than the AG + AA genotypes group (74.29% vs.44.44%;x2 =6.540,P =0.011).Conclusions SLCO1B1 gene c.388A > G polymorphism could influence the lipidlowering effect of atorvastatin,lipid-lowering effect in the GG genotype group was better than that in the AG+ AA genotype group.SLCO1B1 gene c.388A > G polymorphism did not have effect on the antiatherosclerosis effect of atorvastatin,but it might be associated with too short follow-up time.
Full text:
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Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
International Journal of Cerebrovascular Diseases
Year:
2017
Type:
Article
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