Lipid Disorders Clinic and Metabolic Research Centre, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, PO Box X2213, Perth, WA 6847, Australia.
Nat Rev Cardiol. 2013 Nov;10(11):648-61. doi: 10.1038/nrcardio.2013.140. Epub 2013 Sep 24.
Hypertriglyceridaemia (typical triglyceride level 1.7-5.0 mmol/l) is caused by interactions between many genetic and nongenetic factors, and is a common risk factor for atherosclerotic cardiovascular disease (CVD). Patients with hypertriglyceridaemia usually present with obesity, insulin resistance, hepatic steatosis, ectopic fat deposition, and diabetes mellitus. Hypertriglyceridaemia reflects the accumulation in plasma of proatherogenic lipoproteins, triglyceride-rich lipoprotein (TRL) remnants, and small, dense LDL particles. Mendelian randomization studies and research on inherited dyslipidaemias, such as type III dysbetalipoproteinaemia, testify that TRLs are causally related to atherosclerotic CVD. Extreme hypertriglyceridaemia (a triglyceride level >20 mmol/l) is rare, often monogenic in aetiology, and frequently causes pancreatitis. Treatment of hypertriglyceridaemia relies on correcting secondary factors and unhealthy lifestyle habits, particularly poor diet and lack of exercise. Pharmacotherapy is indicated for patients with established CVD or individuals at moderate-to-high risk of CVD, primarily those with metabolic syndrome or diabetes. Statins are the cornerstone of treatment, followed by fibrates and n-3 fatty acids, to achieve recommended therapeutic levels of plasma LDL cholesterol, non-HDL cholesterol, and apolipoprotein (apo) B-100. The case for using niacin has been weakened by the results of clinical trials, but needs further investigation. Extreme hypertriglyceridaemia requires strict dietary measures, and patients with a diagnosis of genetic lipoprotein lipase deficiency might benefit from LPL gene replacement therapy. Several therapies for regulating TRL metabolism, including inhibitors of diacylglycerol O-acyltransferase and microsomal triglyceride transfer protein, and apoC-III antisense oligonucleotides, merit further investigation in patients with hypertriglyceridaemia.
高甘油三酯血症（典型甘油三酯水平为 1.7-5.0mmol/L）是由许多遗传和非遗传因素相互作用引起的，是动脉粥样硬化性心血管疾病（CVD）的常见危险因素。高甘油三酯血症患者通常表现为肥胖、胰岛素抵抗、肝脂肪变性、异位脂肪沉积和糖尿病。高甘油三酯血症反映了致动脉粥样硬化脂蛋白、富含甘油三酯的脂蛋白（TRL）残基和小而密的 LDL 颗粒在血浆中的积累。孟德尔随机化研究和遗传性血脂异常（如 III 型β脂蛋白血症）的研究表明，TRLs 与动脉粥样硬化性 CVD 有因果关系。极端高甘油三酯血症（甘油三酯水平>20mmol/L）较为罕见，通常为单基因病因，常引起胰腺炎。高甘油三酯血症的治疗依赖于纠正继发因素和不健康的生活方式习惯，特别是不良的饮食和缺乏运动。对于已确诊 CVD 的患者或 CVD 中-高风险个体（主要是代谢综合征或糖尿病患者），药物治疗是指征。他汀类药物是治疗的基石，其次是贝特类药物和 n-3 脂肪酸，以达到推荐的血浆 LDL 胆固醇、非-HDL 胆固醇和载脂蛋白（apo）B-100 的治疗水平。烟酸的应用案例因临床试验结果而减弱，但仍需要进一步研究。极端高甘油三酯血症需要严格的饮食措施，对于确诊为脂蛋白脂肪酶缺乏症的患者，脂蛋白脂肪酶基因替代治疗可能会受益。几种调节 TRL 代谢的治疗方法，包括二酰基甘油 O-酰基转移酶和微粒体甘油三酯转移蛋白抑制剂，以及 apoC-III 反义寡核苷酸，在高甘油三酯血症患者中值得进一步研究。
