Endocrine and Metabolic Diseases Research Center, University of Zulia, School of Medicine, Maracaibo, Venezuela.
Am J Ther. 2010 May-Jun;17(3):263-73. doi: 10.1097/MJT.0b013e3181e00bf1.
Lipoprotein (a) [Lp(a)] was discovered by Kare Berg in 1963 from the study of low-density lipoprotein genetic variants. Lp(a) contains a unique protein, apolipoprotein(a), which is linked to the Apo B-100 through a disulfide bond that gives it a great structural homology with plasminogen, and confers it atherogenic and atherothrombotic properties. Interest in Lp(a) has increased because an important association between high plasma levels of Lp(a) and coronary artery disease and cerebral vascular disorders has been demonstrated. Numerous case control studies have confirmed that hyper-Lp(a) is a risk factor for premature cardiovascular disease. Lp(a) is identified as a genetic trait with autosomal transmission, codified by one of the most studied polymorphic genes in humans. It has been demonstrated that variations in this gene are a major factor in the serum levels of Lp(a). Variations differ considerably between individuals and sex across populations. Various approaches to drug treatment using fibric acid derivatives, growth hormone, insulin-like growth factor-1, alcohol extracted soy protein, niacin, and exercise have been proven to decrease Lp(a) in high risk patients, but none has really been an effective therapeutic option for successfully reducing Lp(a) plasma levels.
脂蛋白(a) [Lp(a)]是由 Kare Berg 于 1963 年在研究低密度脂蛋白遗传变异时发现的。Lp(a) 含有一种独特的蛋白质，载脂蛋白(a)，它通过二硫键与 Apo B-100 连接，使其与纤溶酶原具有高度的结构同源性，并赋予其动脉粥样硬化和动脉血栓形成的特性。人们对 Lp(a) 的兴趣增加，是因为已经证明高血浆 Lp(a)水平与冠状动脉疾病和脑血管疾病之间存在重要关联。大量病例对照研究证实，高 Lp(a)血症是导致早发性心血管疾病的危险因素。Lp(a)被确定为一种具有常染色体遗传的遗传特征，由人类研究最多的多态性基因之一编码。已经证明，该基因的变异是血清 Lp(a)水平的主要因素。个体之间和人群之间的性别差异很大。使用纤维酸衍生物、生长激素、胰岛素样生长因子-1、酒精提取大豆蛋白、烟酸和运动等各种药物治疗方法已被证明可以降低高危患者的 Lp(a)水平，但没有一种方法真正成为成功降低 Lp(a)血浆水平的有效治疗选择。
