Schindler Christoph
Institute of Clinical Pharmacology, Medical Faculty, Technical University of Dresden, Fiedlerstrasse 27, 01307 Dresden, Germany. christoph.schindler@ tu-dresden.de
Ther Adv Cardiovasc Dis. 2007 Oct;1(1):7-26. doi: 10.1177/1753944707082662.
The metabolic syndrome (MetS) represents a combination of cardiovascular risk determinants such as obesity, insulin resistance and lipid abnormalities such as hypertriglyceridemia, increased free fatty acids, low high-density-cholesterol and hypertension. As a multiple component condition it imparts a doubling of relative risk for atherosclerotic cardiovascular disease (ASCVD). It is currently controversial which component of the syndrome carries what weight. There is even a considerable debate whether the risk for ASCVD is greater in patients diagnosed with MetS than that by the individual risk factors. At present, no unifying pathogenetic mechanism can explain the metabolic syndrome and there is no unique treatment for it. This review summarizes and critically reviews the currently available clinical and scientific evidence for the concept that the MetS is causally an endocrine disease and discusses pharmacotherapeutic strategies targeting the pathogenesis rather than single symptoms of the cluster.
代谢综合征（MetS）是多种心血管疾病风险决定因素的组合，如肥胖、胰岛素抵抗以及脂质异常，如高甘油三酯血症、游离脂肪酸增加、高密度脂蛋白胆固醇降低和高血压。作为一种多组分病症，它使动脉粥样硬化性心血管疾病（ASCVD）的相对风险加倍。目前，该综合征的哪个组分起何种作用仍存在争议。甚至对于诊断为代谢综合征的患者发生ASCVD的风险是否高于个体风险因素导致的风险也存在相当大的争论。目前，尚无统一的发病机制能够解释代谢综合征，也没有针对它的独特治疗方法。本综述总结并批判性地审视了目前关于代谢综合征本质上是一种内分泌疾病这一概念的临床和科学证据，并讨论了针对发病机制而非该综合征单个症状的药物治疗策略。
