Dr. Fabrizio Montecucco, MD, PhD, Cardiology Division, Foundation for Medical Researches, Department of Internal Medicine, University of Geneva, 64 Avenue Roseraie, 1211 Geneva, Switzerland, Tel: +41 22 382 72 38, Fax: +41 22 382 72 45, E-mail:
Thromb Haemost. 2013 Nov;110(5):940-58. doi: 10.1160/TH13-06-0499. Epub 2013 Aug 22.
The increased atherothrombotic risk in patients with metabolic syndrome (MetS) has been classically explained by the multiplicative effect of systemic concomitant pro-atherosclerotic factors. In particular, centripetal obesity, dyslipidaemia, glucose intolerance, hypertension (differently combined in the diagnosis of the disease) would be expected to act as classical cardiovascular risk conditions underlying accelerated atherogenesis. In order to better understand specific atherosclerotic pathophysiology in MetS, emerging evidence focused on the alterations in different organs that could serve as both pathophysiological targets and active players in the disease. Abnormalities in adipose tissue, heart and arteries have been widely investigated in a variety of basic research and clinical studies in MetS. In this narrative review, we focus on pathophysiological activities of the liver and kidney. Considering its key role in metabolism and production of soluble inflammatory mediators (such as C-reactive protein [CRP]), the liver in MetS has been shown to be altered both in its structure and function. In particular, a relevant amount of the fat accumulated within this organ has been shown to be associated with different degrees of inflammation and potential insulin resistance. In humans, non-alcoholic fatty liver disease (NAFLD) has been described as the hepatic manifestation of MetS. In an analogous manner, epidemiological evidence strongly suggested a "guilty" association between MetS and chronic kidney disease (CKD). Some biomarkers of hepatic (such as C-reactive protein, TNF-alpha or other cytokines) and renal diseases (such as uric acid) associated with MetS might be particularly useful to better manage and prevent the atherothrombotic risk.
代谢综合征（MetS）患者的动脉粥样硬化血栓形成风险增加，通常可以用全身性促动脉粥样硬化因素的倍增效应来解释。具体来说，向心性肥胖、血脂异常、葡萄糖耐量异常、高血压（在疾病诊断中不同组合）预计会作为加速动脉粥样硬化形成的经典心血管风险条件。为了更好地理解 MetS 中的特定动脉粥样硬化病理生理学，新出现的证据集中在不同器官的改变上，这些改变既可以作为病理生理学靶点，也可以作为疾病的活跃参与者。在 MetS 的各种基础研究和临床研究中，已经广泛研究了脂肪组织、心脏和动脉的异常。在这篇叙述性综述中，我们重点关注肝脏和肾脏的病理生理学活动。考虑到肝脏在代谢和产生可溶性炎症介质（如 C 反应蛋白[CRP]）方面的关键作用，MetS 中的肝脏在结构和功能上都发生了改变。特别是，在这个器官中积累的大量脂肪与不同程度的炎症和潜在的胰岛素抵抗有关。在人类中，非酒精性脂肪性肝病（NAFLD）被描述为 MetS 的肝脏表现。类似地，流行病学证据强烈表明 MetS 与慢性肾脏病（CKD）之间存在“有罪”关联。一些与 MetS 相关的肝脏（如 C 反应蛋白、TNF-α 或其他细胞因子）和肾脏疾病（如尿酸）的生物标志物可能特别有助于更好地管理和预防动脉粥样硬化血栓形成风险。
