Davidoff P
Unidad de Nutrición y Diabetes, Hospital San Juan de Dios, Universidad de Chile, Santiago.
Rev Med Chil. 1991 Jan;119(1):64-8.
LP(a) lipoprotein, discovered by Berg, appears as an independent risk factor for atherogenesis with a weight similar to that of the total to HDL cholesterol ratio. It is probably synthesized in the liver and its metabolism is similar to that of LDL; however degradation is preferential mediated by monocytes and macrophages. It is structurally related to plasminogen and may interfere with fibrinolysis. In vitro, its atherogenic power surpasses that of LDL. Elevated levels of LP(a) are inherited as an autosomic codominant trait. Increased atherogenic risk, both at coronary and cerebrovascular sites, is associated to plasma LP(a) levels in excess of 20 mg/dl. Its plasma level increases during pregnancy, after menopause, with renal failure and in decompensated insulin dependent diabetes. Plasma levels are decreased by stanozolol and chronic alcoholism. Diet therapy is of no value for control of high LP(a) levels; only neomycin associated to nicotinic acid has proven effective.
由伯格发现的脂蛋白(a)[LP(a)]，是动脉粥样硬化形成的一个独立危险因素，其权重与总胆固醇与高密度脂蛋白胆固醇的比值相似。它可能在肝脏合成，其代谢与低密度脂蛋白相似；然而，其降解优先由单核细胞和巨噬细胞介导。它在结构上与纤溶酶原相关，可能干扰纤维蛋白溶解。在体外，其致动脉粥样硬化能力超过低密度脂蛋白。LP(a)水平升高作为常染色体共显性性状遗传。在冠状动脉和脑血管部位，动脉粥样硬化风险增加与血浆LP(a)水平超过20mg/dl有关。在怀孕期间、绝经后、肾衰竭以及失代偿性胰岛素依赖型糖尿病时，其血浆水平会升高。司坦唑醇和慢性酒精中毒会使血浆水平降低。饮食疗法对控制高LP(a)水平没有作用；只有新霉素与烟酸联合使用已被证明有效。
