Lee I-Te, Lee Wen-Jane, Ou Hsiu-Chung, Huang Chien-Ning, Sheu Wayne Huey-Herng
Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung 407, Taiwan.
Metabolism. 2009 Mar;58(3):416-20. doi: 10.1016/j.metabol.2008.10.019.
Statin, a potent lipid-lowering agent, ameliorates the interaction of monocytes and endothelium, a critical step in the atherosclerotic process. However, it remains unclear whether this effect of statin depends on different doses or the presence of metabolic syndrome. In this prospectively double-blind study, 21 hypercholesterolemia subjects, with low-density lipoprotein cholesterol between 130 and 170 mg/dL, received low-dose (10 mg/d) or high-dose (40 mg/d) pravastatin treatment for 8 weeks. We assessed the reduction of monocyte adhesion to cultured endothelium between different-dose groups and the relationship to metabolic syndrome. Total cholesterol and low-density lipoprotein cholesterol were significantly decreased after 40-mg pravastatin treatment (-23.3% +/- 3.7%, P < .001 and -28.8% +/- 3.0%, P < .001), and the reductions were greater than those in the 10-mg group (P = .041 and P = .045, respectively). There was no significant difference in monocyte adhesion between high-dose and low-dose pravastatin treatment. When all subjects were divided into an improvement group and a no improvement group, according to the median of change percentage of monocyte adhesion after pravastatin treatment, there were significantly more subjects with metabolic syndrome in the no improvement than the improvement group (6 vs 1 person, P =.024). Using logistic regression analysis, metabolic syndrome, rather than dose effect of pravastatin, was an independent predictor of interaction between monocytes and endothelium (95% confidence interval = 0.001-0.865, P = .041). Attenuating adhesion between monocytes and endothelium is altered by the presence of metabolic syndrome when hypercholesterolemia subjects receive pravastatin treatment.
他汀类药物是一种强效降脂药，可改善单核细胞与内皮细胞之间的相互作用，这是动脉粥样硬化过程中的关键步骤。然而，尚不清楚他汀类药物的这种作用是否取决于不同剂量或代谢综合征的存在。在这项前瞻性双盲研究中，21名低密度脂蛋白胆固醇在130至170mg/dL之间的高胆固醇血症患者接受了低剂量（10mg/d）或高剂量（40mg/d）普伐他汀治疗8周。我们评估了不同剂量组之间单核细胞对培养内皮细胞黏附的降低情况以及与代谢综合征的关系。40mg普伐他汀治疗后总胆固醇和低密度脂蛋白胆固醇显著降低（分别为-23.3%±3.7%，P<.001和-28.8%±3.0%，P<.001），且降低幅度大于10mg组（分别为P=.041和P=.045）。高剂量和低剂量普伐他汀治疗之间单核细胞黏附无显著差异。根据普伐他汀治疗后单核细胞黏附变化百分比的中位数将所有受试者分为改善组和未改善组，未改善组中患有代谢综合征的受试者明显多于改善组（6例对1例，P=.024）。使用逻辑回归分析，代谢综合征而非普伐他汀的剂量效应是单核细胞与内皮细胞之间相互作用的独立预测因素（95%置信区间=0.001-0.865，P=.041）。当高胆固醇血症患者接受普伐他汀治疗时，代谢综合征的存在会改变单核细胞与内皮细胞之间黏附的减弱情况。
