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目的探讨脑白质疏松症发病的相关因素和脂质代谢异常及载脂蛋白 E 基因多态性与脑白质疏松症的关系。方法将脑白质疏松症、脑梗死和脑萎缩的277例病人进行 CT 与临床出院诊断的回顾性对比分析;采用聚合酶链反应一限制片段长度多态性技术对50例脑白质疏松症患者和108例正常对照者载脂蛋白 E 基因型进行分析并进行血脂水平测定。结果脑白质疏松症、脑梗死和脑萎缩三者的伴随疾病谱相似,但脑白质疏松症高血压、动脉粥样硬化和心脏病的伴随率分别为58.3～75%,66.7%和41.7～60%均明显高于脑梗死和脑萎缩组(P<0.05)。脑白质疏松症、脑梗死和脑萎缩三者之间的伴发率极高。脑白质疏松症患者 ApoE2等位基因频率为0.15,明显高于对照组的0.074(P<0.05);在脑白质疏松症患者中检测出携带有 Apoε2/2纯合子基因者4例,高于对照组。携带 ApoE2等位基因患者的甘油三酯,低密度脂蛋白;载脂蛋白 B 的含量均高于ApoE3等位基因患者。结论脑白质疏松症、脑梗死与脑萎缩三者存在着共同相似的病因。载脂蛋白 E2等位基因,尤其是ε2/2纯合子基因可能是脑白质疏松症的一种遗传易感因子。脑白质疏松症可能是通过以甘油三酯含量增高为主的高脂血症的途径而发病的。
Objective To investigate the related factors of leukoaraiosis and the abnormal lipid metabolism and the relationship between apolipoprotein E gene polymorphism and leukoaraiosis. Methods A retrospective analysis of 277 patients with leukoaraiosis, cerebral infarction and cerebral atrophy was performed. The diagnostic results of CT and clinical discharge were compared retrospectively. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect 50 cases of leukoaraiosis 108 cases of normal controls apolipoprotein E genotype analysis and determination of blood lipid levels. Results The concomitant disease spectrum of leukoaraiosis, cerebral infarction and brain atrophy were similar, but the rates of concomitant hypertension, atherosclerosis and heart disease were 58.3-75%, 66.7% and 41.7-60 respectively % Were significantly higher than cerebral infarction and brain atrophy group (P <0.05). Leukoaraiosis, cerebral infarction and brain atrophy between the high incidence of the three. The frequency of ApoE2 allele in patients with leukoaraiosis was 0.15, which was significantly higher than that in the control group (P <0.05). Four patients with Apoε2 / 2 homozygote were detected in patients with leukoaraiosis group. Patients with ApoE2 alleles had higher levels of triglycerides and low density lipoproteins and apolipoprotein B than those with ApoE3 alleles. Conclusion There is a common etiological factor in the pathogenesis of leukoaraiosis, cerebral infarction and brain atrophy. The apolipoprotein E2 allele, especially the ε2 / 2 homozygous gene, may be a genetic predisposition to leukoaraiosis. Leukoaraiosis may be through the pathogenesis of hyperlipidemia with predominantly triglyceride levels.