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他汀类药物对 HDL-C 的影响:与 LDL-C 变化无关的复杂过程:VOYAGER 数据库分析。

Effect of statins on HDL-C: a complex process unrelated to changes in LDL-C: analysis of the VOYAGER Database.

机构信息

Heart Research Institute, Sydney, Australia.

出版信息

J Lipid Res. 2010 Jun;51(6):1546-53. doi: 10.1194/jlr.P002816. Epub 2009 Dec 2.

DOI:10.1194/jlr.P002816
PMID:19965573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3035518/
Abstract

The relationship between statin-induced increases in HDL cholesterol (HDL-C) concentration and statin-induced decreases in LDL cholesterol (LDL-C) is unknown. The effects of different statins on HDL-C levels, relationships between changes in HDL-C and changes in LDL-C, and predictors of statin-induced increases in HDL-C have been investigated in an individual patient meta-analysis of 32,258 dyslipidemic patients included in 37 randomized studies using rosuvastatin, atorvastatin, and simvastatin. The HDL-C raising ability of rosuvastatin, and simvastatin was comparable, with both being superior to atorvastatin. Increases in HDL-C were positively related to statin dose with rosuvastatin and simvastatin but inversely related to dose with atorvastatin. There was no apparent relationship between reduction in LDL-C and increase in HDL-C, whether analyzed overall for all statins (correlation coefficient = 0.005) or for each statin individually. Percentage increase in apolipoprotein A-I was virtually identical to that of HDL-C at all doses of the three statins. Baseline concentrations of HDL-C and triglyceride (TG) and presence of diabetes were strong, independent predictors of statin-induced elevations of HDL-C. Statins vary in their HDL-C raising ability. The HDL-C increase achieved by all three statins was independent of LDL-C decrease. However, baseline HDL-C and TGs and the presence of diabetes were predictors of statin-induced increases in HDL-C.

摘要

他汀类药物引起的高密度脂蛋白胆固醇(HDL-C)浓度升高与他汀类药物引起的低密度脂蛋白胆固醇(LDL-C)降低之间的关系尚不清楚。本个体患者荟萃分析纳入了 37 项随机研究中的 32258 例血脂异常患者,旨在评估不同他汀类药物对 HDL-C 水平的影响、HDL-C 变化与 LDL-C 变化之间的关系,以及他汀类药物引起 HDL-C 升高的预测因素。结果显示,瑞舒伐他汀和辛伐他汀升高 HDL-C 的能力与阿托伐他汀相当,且均优于阿托伐他汀。瑞舒伐他汀和辛伐他汀的 HDL-C 升高与他汀类药物剂量呈正相关,但阿托伐他汀的 HDL-C 升高与剂量呈负相关。总体上分析所有他汀类药物(相关系数=0.005)或单独分析每种他汀类药物,HDL-C 降低与 HDL-C 升高之间均无明显关系。三种他汀类药物在所有剂量下,载脂蛋白 A-I 的百分比增加与 HDL-C 几乎相同。HDL-C 和三酰甘油(TG)的基线浓度以及糖尿病的存在是他汀类药物引起 HDL-C 升高的强有力独立预测因素。他汀类药物在升高 HDL-C 的能力方面存在差异。三种他汀类药物均可独立于 LDL-C 降低来升高 HDL-C。然而,基线 HDL-C 和三酰甘油以及糖尿病的存在是他汀类药物引起 HDL-C 升高的预测因素。

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本文引用的文献

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Cholesteryl ester transfer protein: at the heart of the action of lipid-modulating therapy with statins, fibrates, niacin, and cholesteryl ester transfer protein inhibitors.胆固醇酯转移蛋白:他汀类药物、贝特类药物、烟酸和胆固醇酯转移蛋白抑制剂调脂治疗作用的核心。
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Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.瑞舒伐他汀预防C反应蛋白升高的男性和女性发生血管事件。
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Efficacy and tolerability of rosuvastatin and atorvastatin when force-titrated in patients with primary hypercholesterolemia: results from the ECLIPSE study.瑞舒伐他汀和阿托伐他汀在原发性高胆固醇血症患者中强制滴定剂量时的疗效和耐受性:ECLIPSE研究结果
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Sterol regulatory element-binding protein-2- and liver X receptor-driven dual promoter regulation of hepatic ABC transporter A1 gene expression: mechanism underlying the unique response to cellular cholesterol status.固醇调节元件结合蛋白2和肝脏X受体驱动的肝脏ABC转运蛋白A1基因表达的双启动子调控:对细胞胆固醇状态独特反应的潜在机制
J Biol Chem. 2007 Jul 20;282(29):21090-9. doi: 10.1074/jbc.M701228200. Epub 2007 May 27.
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Comparison of the effects of high doses of rosuvastatin versus atorvastatin on the subpopulations of high-density lipoproteins.高剂量瑞舒伐他汀与阿托伐他汀对高密度脂蛋白亚群影响的比较
Am J Cardiol. 2007 Mar 1;99(5):681-5. doi: 10.1016/j.amjcard.2006.09.117. Epub 2007 Jan 4.
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Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis.他汀类药物、高密度脂蛋白胆固醇与冠状动脉粥样硬化的消退
JAMA. 2007 Feb 7;297(5):499-508. doi: 10.1001/jama.297.5.499.
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Coronary atherosclerosis can regress with very intensive statin therapy.冠状动脉粥样硬化可以通过非常强化的他汀类药物治疗而消退。
Cleve Clin J Med. 2006 Oct;73(10):937-44. doi: 10.3949/ccjm.73.10.937.
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The effect of atorvastatin therapy on lecithin:cholesterol acyltransferase, cholesteryl ester transfer protein and the antioxidant paraoxonase.阿托伐他汀治疗对卵磷脂胆固醇酰基转移酶、胆固醇酯转运蛋白及抗氧化对氧磷酶的影响。
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