Galetta F, Sampietro T, Basta G, Bionda A
Istituto di Clinica Medica II, Università di Pisa.
Minerva Med. 1994 Jun;85(6):321-6.
The efficacy of pravastatin as reducing plasma cholesterol, LDL-CH and Apo B is widely proved. Other molecules within the Apolipoprotein family are recently emerging to have a predictive and/or causative role in atherosclerosis such as particularly Lp(a). The aim of this study was to evaluate the effects of pravastatin therapy in patients affected by primary hypoercholesterolemia on apoprotein and Lp(a) plasma levels. We investigated the effects of pravastatin on 15 patients, seven female and eight male patients, mean age 50.23 +/- 17.2 (range 21-71 years) with primary hypercholesterolemia, of which 7 patients affected by familial hypercholesterolemia and 8 patients by polygenic hypercholesterolemia, were selected. Five weeks after suspension of lipid-lowering drugs and on a normocaloric-fat diet, were given 20 mg pravastatin/day for 12 weeks. The following parameters were measured basally, on the 6th week and the 12th week on pravastatin therapy and after five weeks from drug withdrawal: cholesterol (CH), triglicerides (TG), high density and low density lipoprotein cholesterol (HDL-CH and LDH-CH) measured enzymatically, apoproteins A1, B, C2, C3, E measured radial immunodiffusion technique (RID) and Lp(a), measured as apoprotein(a) with immunoradiometric assay (RIA). Our data confirm pravastatin efficacy in decreasing CH (from 305.6 +/- 43.4 mg/dl to 266.2 +/- 47.7 mg/dl, p < 0.01) LDL-CH (from 223.9 +/- 56.4 mg/dl to 187.2 +/- 59.8 mg/dl, p < 0.01) and Apo B (from 170.4 +/- 27.5 to 152.4 +/- 25.2, p < 0.02); non influence was observed on HDL-CH and apoproteins A1, C2, E and Lp(a). Pravastatin determined a significant increase only on Apo C3 (from 8.35 +/- 2.7 to 10.3 +/- 3.1, p < 0.04). The above data confirm the beneficial effect of pravastatin in greatly decreasing CH and LDL-CH considered as major risk factors for coronary artery disease, but also point to a role of pravastatin in regulating the apoproteins equilibrium, an aspect that surely merits further studies.
普伐他汀降低血浆胆固醇、低密度脂蛋白胆固醇(LDL-CH)和载脂蛋白B的功效已得到广泛证实。载脂蛋白家族中的其他分子最近开始在动脉粥样硬化中发挥预测和/或致病作用,特别是脂蛋白(a)[Lp(a)]。本研究的目的是评估普伐他汀治疗对原发性高胆固醇血症患者载脂蛋白和血浆Lp(a)水平的影响。我们调查了普伐他汀对15例原发性高胆固醇血症患者的影响,其中7例女性和8例男性,平均年龄50.23±17.2岁(范围21-71岁),其中7例为家族性高胆固醇血症患者,8例为多基因高胆固醇血症患者。在停用降脂药物并采用正常热量-脂肪饮食5周后,给予患者每天20mg普伐他汀,持续12周。在普伐他汀治疗的第0周、第6周和第12周以及停药5周后,测定以下参数:采用酶法测定胆固醇(CH)、甘油三酯(TG)、高密度和低密度脂蛋白胆固醇(HDL-CH和LDL-CH),采用放射免疫扩散技术(RID)测定载脂蛋白A1、B、C2、C3、E,采用免疫放射分析(RIA)测定Lp(a),以载脂蛋白(a)表示。我们的数据证实普伐他汀在降低CH(从305.6±43.4mg/dl降至266.2±47.7mg/dl,p<0.01)、LDL-CH(从223.9±56.4mg/dl降至187.2±59.8mg/dl,p<0.01)和载脂蛋白B(从170.4±27.5降至152.4±25.2,p<0.02)方面有效;未观察到对HDL-CH以及载脂蛋白A1、C2、E和Lp(a)有影响。普伐他汀仅使载脂蛋白C3显著升高(从8.35±2.7升至10.3±3.1,p<0.04)。上述数据证实了普伐他汀在大幅降低被视为冠状动脉疾病主要危险因素的CH和LDL-CH方面的有益作用,但也指出了普伐他汀在调节载脂蛋白平衡方面的作用,这方面肯定值得进一步研究。