Ascaso Juan, Gonzalez Santos Pedro, Hernandez Mijares Antonio, Mangas Rojas Alipio, Masana Luis, Millan Jesus, Pallardo Luis Felipe, Pedro-Botet Juan, Perez Jimenez Francisco, Pintó Xavier, Plaza Ignacio, Rubiés Juan, Zúñiga Manuel
Endocrinolgy Service, Clinic University Hospital, University of Valencia, Valencia, Spain.
Am J Cardiovasc Drugs. 2007;7(1):39-58. doi: 10.2165/00129784-200707010-00004.
In order to characterize the metabolic syndrome it becomes necessary to establish a number of diagnostic criteria. Because of its impact on cardiovascular morbidity/mortality, considerable attention has been focussed on the dyslipidemia accompanying the metabolic syndrome. The aim of this review is to highlight the fundamental aspects of the pathophysiology, diagnosis, and the treatment of the metabolic syndrome dyslipidemia with recommendations to clinicians. The clinical expression of the metabolic syndrome dyslipidemia is characterized by hypertriglyceridemia and low levels of high-density lipoprotein-cholesterol (HDL-C). In addition, metabolic syndrome dyslipidemia is associated with high levels of apolipoprotein (apo) B-100-rich particles of a particularly atherogenic phenotype (small dense low-density lipoprotein-cholesterol [LDL-C]. High levels of triglyceride-rich particles (very low-density lipoprotein) are also evident both at baseline and in overload situations (postprandial hyperlipidemia). Overall, the 'quantitative' dyslipidemia characterized by hypertriglyceridemia and low levels of HDL-C and the 'qualitative' dyslipidemia characterized by high levels of apo B-100- and triglyceride-rich particles, together with insulin resistance, constitute an atherogenic triad in patients with the metabolic syndrome. The therapeutic management of the metabolic syndrome, regardless of the control of the bodyweight, BP, hyperglycemia or overt diabetes mellitus, aims at maintaining optimum plasma lipid levels. Therapeutic goals are similar to those for high-risk situations because of the coexistence of multiple risk factors. The primary goal in treatment should be achieving an LDL-C level of <100 mg/dL (or <70 mg/dL in cases with established ischemic heart disease or risk equivalents). A further goal is increasing the HDL-C level to >or=40 mg/dL in men or 50 mg/dL in women. A non-HDL-C goal of 130 mg/dL should also be aimed at in cases of hypertriglyceridemia. Lifestyle interventions, such as maintaining an adequate diet, and a physical activity program, constitute an essential part of management. Nevertheless, when pharmacologic therapy becomes necessary, fibrates and HMG-CoA reductase inhibitors (statins) are the most effective drugs in controlling the metabolic syndrome hyperlipidemia, and are thus the drugs of first choice. Fibrates are effective in lowering triglycerides and increasing HDL-C levels, the two most frequent abnormalities associated with the metabolic syndrome, and statins are effective in lowering LDL-C levels, even though hypercholesterolemia occurs less frequently. In addition, the combination of fibrates and statins is highly effective in controlling abnormalities of the lipid profile in patients with the metabolic syndrome.
为了对代谢综合征进行特征描述,有必要确立一些诊断标准。由于其对心血管发病率/死亡率的影响,代谢综合征伴发的血脂异常已受到相当多的关注。本综述的目的是强调代谢综合征血脂异常的病理生理学、诊断及治疗的基本方面,并向临床医生提出建议。代谢综合征血脂异常的临床表现特征为高甘油三酯血症和高密度脂蛋白胆固醇(HDL-C)水平降低。此外,代谢综合征血脂异常与富含载脂蛋白(apo)B-100的具有特别致动脉粥样硬化表型的颗粒(小而密的低密度脂蛋白胆固醇[LDL-C])水平升高有关。富含甘油三酯的颗粒(极低密度脂蛋白)在基线时以及负荷情况下(餐后高脂血症)水平也明显升高。总体而言,以高甘油三酯血症和HDL-C水平降低为特征的“定量”血脂异常以及以apo B-100和富含甘油三酯的颗粒水平升高为特征的“定性”血脂异常,连同胰岛素抵抗,在代谢综合征患者中构成了一个致动脉粥样硬化三联征。代谢综合征的治疗管理,无论体重、血压、高血糖或显性糖尿病是否得到控制,目标都是维持最佳血脂水平。由于存在多种危险因素,治疗目标与高危情况类似。治疗的首要目标应是使LDL-C水平<100 mg/dL(对于已确诊的缺血性心脏病或风险等同情况,目标为<70 mg/dL)。另一个目标是将男性HDL-C水平提高至≥40 mg/dL,女性提高至50 mg/dL。对于高甘油三酯血症患者,非HDL-C目标也应设定为130 mg/dL。生活方式干预,如保持适当饮食和进行体育活动计划,是管理的重要组成部分。然而,当需要药物治疗时,贝特类药物和HMG-CoA还原酶抑制剂(他汀类药物)是控制代谢综合征高脂血症最有效的药物,因此是首选药物。贝特类药物可有效降低甘油三酯并提高HDL-C水平,这是与代谢综合征相关的两种最常见异常情况,他汀类药物可有效降低LDL-C水平,尽管高胆固醇血症较少见。此外,贝特类药物与他汀类药物联合使用在控制代谢综合征患者的血脂异常方面非常有效。