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探讨低密度脂蛋白受体（ＬＤＬＲ）基因ＨｉｎｃⅡ酶切位点多态性对血脂康调脂疗效的影响。高脂血症患者血清总胆固醇（ＴＣ）≥５．２０ｍｍｏｌ／Ｌ和（或）三酰甘油在２．００～５．６５ｍｍｏｌ／Ｌ之间者，共６６例，随机分为血脂康组和安慰剂组，每组３３例。根据ＬＤＬＲ基因ＨｉｎｄⅡ酶切多态性分层比较血脂康和安慰剂的调脂疗效，发现血脂康组Ｈ１Ｈ１和Ｈ１Ｈ２基因型患者的总胆固醇或低密度脂蛋白胆固醇（ＬＤＬＣ）下降的有效率（ＴＣ和ＬＤＬＣ分别下降≥１０％），均明显低于Ｈ２Ｈ２基因型者（Ｐ均＜０．０５）；Ｈ１Ｈ１和Ｈ１Ｈ２基因型的ＴＣ或ＬＤＬＣ下降幅度亦均明显低于Ｈ２Ｈ２基因型者（ＴＣ依次平均下降１７．１％、２０．６％和２９．０％，ＬＤＬＣ依次平均下降１９．５％、２５．０％和３３．９％，Ｐ均＜０．０５）。说明具有ｈ１等位基因的高脂血症患者对降低胆固醇治疗药物血脂康的反应较差，而ｈ２等位基因反应较为敏感。安慰剂组未发现上述现象。提示ＬＤＬＲＨｉｎｃⅡ酶切位点间接参与了人体内胆固醇代谢和（或）血脂康控制血清胆固醇的重要环节。
To investigate the effect of Hinc Ⅱ polymorphism of low density lipoprotein receptor (LDLR) gene on the lipid-lowering efficacy of Xuezhikang. Patients with hyperlipidemia serum total cholesterol (TC) ≥5.20mmol / L and (or) triglyceride between 2.00 ~ 5.65mmol / L, a total of 66 cases were randomly divided into Xuezhikang and comfort Agent group, 33 cases in each group. According to LDLR Hind Ⅱ polymorphism stratified stratification compared Xuezhikang and placebo lipid-lowering efficacy found Xuezhikang H1H1 and H1H2 genotype patients with total cholesterol or low density lipoprotein cholesterol (LDLC) decreased the efficiency (TC (P <0.05). The decrease of TC or LDLC in H1H1 and H1H2 genotypes was also significantly lower than that of H2H2 genotype Decreased by 17.1%, 20.6% and 29.0% respectively, and the average LDLC decreased by 19.5%, 25.0% and 33.9% respectively (all P <0.05). This suggests that patients with hyperlipidemia who have the h1 allele have poor response to Cholesterol lowering therapy, a cholesterol lowering drug, and the h2 allele response is more sensitive. The placebo group did not find the above phenomenon. Tip LDLRHinc Ⅱ restriction sites indirectly involved in the body’s cholesterol metabolism and (or) Xuezhikang important part of the control of serum cholesterol.