SLC01B1c．388A〉G多态性对于中国缺血性卒中患者阿托伐他汀降脂和抗动脉粥样硬化作用的影响

Impacts of SLCO1B1 c.388A 〉 G polymorphisms on lipid-lowering and anti-atherosclerosis effects of atorvastatin in Chinese patients with ischemic stroke

目的探讨溶质载体有机阴离子转运体家族1B1（solute carrier organic anion transporter family member 1B1, SLCO1B1）基因c.388A〉G多态性对中国缺血性卒中患者阿托伐他汀降脂和抗动脉粥样硬化作用的影响。 方法前瞻性纳入基线低密度脂蛋白胆固醇（low-density lipoprotein cholesterol, LDL-C）〉1.8 mmol/L的缺血性卒中患者，口服阿托伐他汀（20 mg/d）治疗12个月，分别在治疗前后检测血脂和双侧颈动脉内膜－中膜厚度（carotid intima-media thickness, CIMT）。比较SLCO1B1基因c.388A〉G基因型组之间CIMT的差异。 结果共纳入71例缺血性卒中患者，其中AA基因型5例，AG基因型31例，GG基因型35例；A等位基因频率为28.9%，G等位基因频率为71.1%。所有患者治疗后总胆固醇、三酰甘油和LDL-C均较治疗前显著降低，而高密度脂蛋白胆固醇显著升高（P均〈0.001），但CIMT无显著改变（P＝0.475）。GG基因型组LDL-C〈1.8 mmol/L或LDL-C下降≥50%的患者比例显著高于AG＋AA基因型组（74.29%对44.44%；χ2＝6.540，P＝0.011）。 结论SLCO1B1基因c.388A 〉 G多态性会影响阿托伐他汀的降脂效果，GG基因型组的降脂效果优于AG＋AA基因型组；SLCO1B1基因c.388A 〉 G多态性对阿托伐他汀抗动脉粥样硬化疗效无影响，但可能与随访时间过短有关。

ObjectiveTo 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. MethodsThe 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. ResultsA 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%; χ2=6.540, P=0.011）. ConclusionsSLCO1B1 gene c. 388A 〉G polymorphism could influence the lipid-lowering 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 anti-atherosclerosis effect of atorvastatin, but it might be associated with too short follow-up time.