Nakajima K, Hata Y
Department of Medicine and Gerontology, Kyorin University School of Medicine, Tokyo, Japan.
J Atheroscler Thromb. 1996;2(2):96-106. doi: 10.5551/jat1994.2.96.
Lp(a) levels are genetically determined and remain stable without major changes throughout lives. However, when an individual's Lp(a) levels are observed over a one-year period, they show spontaneous variation. The rate of intraindividual variation in Lp(a) was observed in 16 patients with hypertension, hyperlipidemia and/or glucose intolerance in a chronic stable state who regularly visited the hospital clinic once a month, at least 10 times during the year, and in whom a total of 42 blood and clinical chemistry tests including serum lipids, Lp(a) and apoproteins were performed. The rate of annual intraindividual variation of Lp(a) averaged out as 16.6%. The rate was 18.8% for isoform S4 (n = 10), 18.6% for S3 (n = 3), and although small in number of subjects, other isoforms showed minor variation rates. There was a significant negative correlation between the rate of variation (y%) and LP(a) level (xmg/dl) r = -0.605, p < 0.05, y = -0.461 x +29.8). Therefore, when Lp(a) was high, the rate of variation (SD%) was low. This was consistent with the finding that the rates of variation were low for isoforms S2, S3S4 and F, whose molecular weights were low, accompanied by high Lp(a) levels. On the other hand, when the relationship between Lp(a) level and the amount of variation (SD mg/dl) was examined, there was no correlation between the two, since the amounts of variation were almost constant at a level of 3.8 mg/dl, regardless of Lp(a) level. The annual variation of Lp(a) level was found to be related to three groups of factors based on comparison of the variations among WHO phenotypes of hyperlipidemias, univariate correlation analysis with the clinical parameters tested, and multivariate analysis: the first group of factors was related to structure and metabolism of very low-density lipoprotein such as triglycerides, phospholipids, apo C-II, C-III, E, A-II and uric acid; the second group was related to thrombosis centering on platelets; and the third group involved those in the acute phase reactions represented by 1 hr and 2 hr erythrocyte sedimentation rates.
脂蛋白(a)[Lp(a)]水平由基因决定，在一生中保持稳定，无重大变化。然而，当观察个体的Lp(a)水平在一年期间的变化时，会发现其呈现自发波动。在16例患有高血压、高脂血症和/或糖耐量异常且处于慢性稳定状态的患者中观察了Lp(a)的个体内变异率。这些患者每月定期到医院门诊就诊一次，一年至少就诊10次，期间共进行了42次血液和临床化学检测，包括血脂、Lp(a)和载脂蛋白检测。Lp(a)的年个体内变异率平均为16.6%。异构体S4（n = 10）的变异率为18.8%，S3（n = 3）的变异率为18.6%，尽管研究对象数量较少，但其他异构体的变异率较小。变异率（y%）与Lp(a)水平（xmg/dl）之间存在显著负相关[r = -0.605，p < 0.05，y = -0.461x + 29.8]。因此，当Lp(a)水平较高时，变异率（标准差%）较低。这与以下发现一致，即分子量较低的异构体S2、S3S4和F，其Lp(a)水平较高，变异率较低。另一方面，当研究Lp(a)水平与变异量（标准差mg/dl）之间的关系时，两者之间无相关性，因为无论Lp(a)水平如何，变异量在3.8mg/dl水平时几乎恒定。基于高脂血症WHO表型之间变异的比较、与所测临床参数的单变量相关分析以及多变量分析，发现Lp(a)水平的年度变异与三组因素有关：第一组因素与极低密度脂蛋白的结构和代谢有关，如甘油三酯、磷脂、载脂蛋白C-II、C-III、E、A-II和尿酸；第二组与以血小板为中心的血栓形成有关；第三组涉及以1小时和2小时红细胞沉降率为代表的急性期反应中的因素。
