Seed M, O'Connor B, Perombelon N, O'Donnell M, Reaveley D, Knight B L
Department of Medicine, Charing Cross and Westminster Medical School, London, UK.
Atherosclerosis. 1993 Jun;101(1):61-8. doi: 10.1016/0021-9150(93)90102-z.
This study examines the effect of nicotinic acid (1 g t.d.s.) on serum Lp(a) concentration in a group of patients with type II hyperlipidaemia selected on the basis of a plasma Lp(a) concentration greater than 30 mg/dl. Reductions in total cholesterol, triglyceride, LDL-cholesterol and Lp(a) were 16.3%, 25.5%, 23.7% and 36.4%, respectively, with an increase in HDL cholesterol of 37.3%. The reduction in Lp(a) concentration did not correlate with any other lipoprotein changes. In order to establish the mechanism of the fall in Lp(a) concentration, in vivo turnover of autologous Lp(a) was studied in three subjects before and whilst taking nicotinic acid. The fractional catabolic rate in Lp(a) was unaltered in the subjects on therapy, indicating that nicotinic acid did not increase catabolism of Lp(a) but decreased the synthetic rate. Since nicotinic acid was poorly tolerated we examined the effect of acipimox, an analogue of nicotinic acid on lipoproteins using a placebo controlled double-blind crossover design in a group of hyperlipidaemic patients again selected with plasma Lp(a) concentration greater than 30 mg/dl. Acipimox was better tolerated than nicotinic acid but the percentage changes in lipoprotein concentrations were smaller.
本研究在一组基于血浆Lp(a)浓度大于30mg/dl入选的II型高脂血症患者中，检测了烟酸（每日3次，每次1g）对血清Lp(a)浓度的影响。总胆固醇、甘油三酯、低密度脂蛋白胆固醇和Lp(a)分别降低了16.3%、25.5%、23.7%和36.4%，高密度脂蛋白胆固醇升高了37.3%。Lp(a)浓度的降低与其他任何脂蛋白变化均无相关性。为了确定Lp(a)浓度下降的机制，在3名受试者服用烟酸之前及期间，对自体Lp(a)的体内周转率进行了研究。接受治疗的受试者中Lp(a)的分数分解代谢率未改变，这表明烟酸并未增加Lp(a)的分解代谢，而是降低了合成率。由于烟酸耐受性较差，我们采用安慰剂对照双盲交叉设计，在另一组同样基于血浆Lp(a)浓度大于30mg/dl入选的高脂血症患者中，检测了烟酸类似物阿昔莫司对脂蛋白的影响。阿昔莫司的耐受性优于烟酸，但脂蛋白浓度的变化百分比更小。
