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代谢综合征的大血管并发症:早期干预势在必行。

Macrovascular complications of metabolic syndrome: an early intervention is imperative.

作者信息

Tenenbaum Alexander, Motro Michael, Schwammenthal Ehud, Fisman Enrique Z

机构信息

Cardiac Rehabilitation Institute, Chaim Sheba Medical Center, 52621 Tel-Hashomer, Israel.

出版信息

Int J Cardiol. 2004 Nov;97(2):167-72. doi: 10.1016/j.ijcard.2003.07.033.

Abstract

The metabolic syndrome is a widespread clinical condition and an important cluster of atherothrombotic disease risk factors. The inclusion of this syndrome in the recently published Adult Treatment Panel III (ATP III) guidelines focused the attention of the physicians on this entity. Abdominal obesity, PPAR modulation, insulin resistance (with or without glucose intolerance), atherogenic dyslipidemia, elevated blood pressure, prothrombotic and proinflammatory states are the principal factors of this multifaceted syndrome. There are two major pathways of metabolic syndrome progress: (1) With preserved pancreatic beta cells function and insulin hypersecretion, which can recompense for insulin resistance. This pathway leads mostly to the macrovascular complications of metabolic syndrome. (2) With substantial injure of pancreatic beta cells leading to gradually reduced insulin secretion and to hyperglycemia (e.g. overt type 2 diabetes). This pathway leads to both microvascular and macrovascular complications. Because macrovascular complications of insulin resistance state precede the onset of hyperglycemia, early intervention in patients with metabolic syndrome is particularly important. Since central obesity (accompanied by insulin resistance even in the absence of hyperglycemia) is the key factor leading to development of metabolic syndrome and its future macrovascular complications, we assume that next logical step is the recognition of central obesity itself as a major risk factor for cardiovascular diseases.

摘要

代谢综合征是一种广泛存在的临床病症,是动脉粥样硬化血栓形成疾病危险因素的重要集合。最近发布的成人治疗小组第三次报告(ATP III)指南中纳入了该综合征,这引起了医生们对这一实体的关注。腹型肥胖、过氧化物酶体增殖物激活受体(PPAR)调节、胰岛素抵抗(伴或不伴葡萄糖不耐受)、致动脉粥样硬化血脂异常、血压升高、血栓前状态和促炎状态是这一多方面综合征的主要因素。代谢综合征进展有两条主要途径:(1)胰腺β细胞功能保留且胰岛素分泌过多,可代偿胰岛素抵抗。此途径主要导致代谢综合征的大血管并发症。(2)胰腺β细胞严重受损,导致胰岛素分泌逐渐减少并出现高血糖(如显性2型糖尿病)。此途径导致微血管和大血管并发症。由于胰岛素抵抗状态的大血管并发症先于高血糖的发生,因此对代谢综合征患者进行早期干预尤为重要。由于中心性肥胖(即使在无高血糖情况下也伴有胰岛素抵抗)是导致代谢综合征及其未来大血管并发症发生的关键因素,我们认为接下来合理的步骤是将中心性肥胖本身视为心血管疾病的主要危险因素。

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