Jenner J L, Ordovas J M, Lamon-Fava S, Schaefer M M, Wilson P W, Castelli W P, Schaefer E J
Lipid Metabolism Laboratory, USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111.
Circulation. 1993 Apr;87(4):1135-41. doi: 10.1161/01.cir.87.4.1135.
Lipoprotein(a) [Lp(a)] is an atherogenic particle that structurally resembles a low density lipoprotein (LDL) particle but contains a molecule of apolipoprotein(a) attached to apolipoprotein B-100 by a disulfide bond. Because elevated plasma levels of Lp(a) have been shown to be an independent risk factor for coronary artery disease, it is important to define normal ranges for this lipoprotein.
We have measured Lp(a) in 1,284 men (mean age, 48 +/- 10 years) and 1,394 women (mean age, 48 +/- 10 years) free of cardiovascular and cerebrovascular disease and not on medications known to affect lipids who were seen at the third examination cycle of the Framingham Offspring Study. Plasma Lp(a) levels were measured by an enzyme-linked immunosorbent assay, which uses a "capture" monoclonal anti-apo(a) antibody that does not cross-react with plasminogen, and a polyclonal anti-apo(a) antibody conjugated to horseradish peroxidase. The assay was calibrated to total Lp(a) mass. The Lp(a) frequency distribution was highly skewed to the right, with 56% of the values in the 0-10-mg/dL range. Mean plasma Lp(a) concentrations were 14 +/- 17 mg/dL in men and 15 +/- 17 mg/dL in women. Values of more than 38 mg/dL were above the 90th percentile and values of more than 22 mg/dL were above the 75th percentile in both men and women.
We have determined mean Lp(a) levels for men and women participating in the Framingham Offspring Study. In this population, there was an inverse association between plasma levels of Lp(a) and triglycerides for both sexes (p < 0.006), but triglycerides accounted for only approximately 0.5% of the variation in Lp(a) levels. Associations of Lp(a) levels with total and LDL cholesterol levels were not significant after correction for the estimated contribution of Lp(a) cholesterol to total and LDL cholesterol. After controlling for age, Lp(a) values were 8% greater in postmenopausal women than in premenopausal women, but this difference was not statistically significant. Body mass index, alcohol consumption, cigarette smoking, use of beta-blockers or cholesterol-lowering medications, and use of drugs for the treatment of diabetes and hypertension were not correlated with Lp(a) levels.
脂蛋白(a)[Lp(a)]是一种致动脉粥样硬化颗粒,其结构类似于低密度脂蛋白(LDL)颗粒,但含有一个通过二硫键与载脂蛋白B-100相连的载脂蛋白(a)分子。由于血浆Lp(a)水平升高已被证明是冠状动脉疾病的独立危险因素,因此确定这种脂蛋白的正常范围很重要。
我们在弗雷明汉后代研究的第三个检查周期中,对1284名男性(平均年龄48±10岁)和1394名女性(平均年龄48±10岁)进行了Lp(a)测量,这些人无心血管和脑血管疾病,且未服用已知会影响血脂的药物。血浆Lp(a)水平通过酶联免疫吸附测定法测量,该方法使用一种不与纤溶酶原发生交叉反应的“捕获”抗载脂蛋白(a)单克隆抗体,以及一种与辣根过氧化物酶偶联的抗载脂蛋白(a)多克隆抗体。该测定法根据总Lp(a)质量进行校准。Lp(a)频率分布高度右偏,56%的值在0-10mg/dL范围内。男性血浆Lp(a)平均浓度为14±17mg/dL,女性为15±17mg/dL。男性和女性中,Lp(a)水平超过38mg/dL的值高于第90百分位数,超过22mg/dL的值高于第75百分位数。
我们确定了参与弗雷明汉后代研究的男性和女性的Lp(a)平均水平。在该人群中,两性的血浆Lp(a)水平与甘油三酯之间均呈负相关(p<0.006),但甘油三酯仅占Lp(a)水平变异的约0.5%。在校正Lp(a)胆固醇对总胆固醇和低密度脂蛋白胆固醇的估计贡献后,Lp(a)水平与总胆固醇和低密度脂蛋白胆固醇水平之间的关联不显著。在控制年龄后,绝经后女性Lp(a)值比绝经前女性高8%,但这种差异无统计学意义。体重指数、饮酒、吸烟、使用β受体阻滞剂或降胆固醇药物以及使用治疗糖尿病和高血压的药物与Lp(a)水平均无相关性。