Bhavani A B, Sastry K B, Reddy N Krishna, Padma T
Departments of Genetics and Cardiology, Osmania University and CARE Hospital, Hyderabad.
Indian Heart J. 2005 Mar-Apr;57(2):151-7.
Studies in several populations have indicated that genetic variation at the apolipoprotein E structural locus influences atherosclerosis leading to cardiovascular diseases. The possible role of apolipoprotein E polymorphism in the development of essential hypertension has not been sufficiently investigated. In this case-control study, we aimed to determine the significance of association between essential hypertension and apolipoprotein E genotypes. In addition, apolipoprotein E genotypes were correlated with serum lipid levels in order to understand the possible interaction between the specific genotype and the lipid profiles that can contribute to hypertension.
The apolipoprotein E genotypes were assayed in 185 patients and 200 controls by polymerase chain reaction followed by enzymatic digestion with Hha I. Using logistic regression analysis, the multivariate-adjusted odds of hypertension were calculated. The incidence of epsilon4 allele was found to be significantly higher in patients (12.16%) than in controls (5.75%, chi2=10.87; p<0.05) and also in patients with positive family history (16.7%) as compared to negative family history (8.87%, chi2 = 8.45; p<0.1). Further, it was observed that carriers of epsilon4 allele have twice as much risk (p<0.05) for developing hypertension as compared to carriers of other alleles. Patients with epsilon4 allele had significantly higher levels of total cholesterol and low-density lipoprotein- cholesterol as compared to epsilon4 allele non-carriers (p<0.05). The adjusted odds ratios for epsilon4 and epsilon2 alleles versus epsilon3 allele were 2.2 (95% confidence interval 1.2 to 3.8, p<0.05) and 1.2 (95% CI, 0.75 to 1.77, p<0.514), respectively.
Our study revealed a strong association of apolipoprotein E locus with hypertension and lipid profile. However, large population-based studies are needed to understand the exact role played by the locus in causing the condition.
在多个人群中进行的研究表明,载脂蛋白E结构位点的基因变异会影响动脉粥样硬化,进而导致心血管疾病。载脂蛋白E基因多态性在原发性高血压发病中的可能作用尚未得到充分研究。在这项病例对照研究中,我们旨在确定原发性高血压与载脂蛋白E基因型之间关联的意义。此外,将载脂蛋白E基因型与血脂水平相关联,以了解特定基因型与可能导致高血压的血脂谱之间的可能相互作用。
采用聚合酶链反应继以Hha I酶切法,对185例患者和200例对照进行载脂蛋白E基因型检测。使用逻辑回归分析计算高血压的多变量校正比值比。发现ε4等位基因在患者中的发生率(12.16%)显著高于对照组(5.75%,χ2 = 10.87;p < 0.05),并且与家族史阴性者(8.87%,χ2 = 8.45;p < 0.1)相比,家族史阳性患者中ε4等位基因的发生率(16.7%)也更高。此外,观察到与其他等位基因携带者相比,ε4等位基因携带者患高血压的风险高两倍(p < 0.05)。与非ε4等位基因携带者相比,携带ε4等位基因的患者总胆固醇和低密度脂蛋白胆固醇水平显著更高(p < 0.05)。ε4和ε2等位基因相对于ε3等位基因的校正比值比分别为2.2(95%置信区间1.2至3.8,p < 0.05)和1.2(95%CI,0.75至1.77,p < 0.514)。
我们的研究揭示了载脂蛋白E位点与高血压及血脂谱之间存在强关联。然而,需要开展基于大规模人群的研究来了解该位点在引发该病中的确切作用。