title: Treatment of dyslipoproteinemia in the metabolic syndrome.
abstract: The metabolic syndrome consists of a cluster of metabolic disorders, many of which promote the development of atherosclerosis and increase the risk to develop cardiovascular disease. The metabolic syndrome is characterized by atherogenic dyslipidemia (elevated triglycerides, increased small dense low-density lipoproteins, and decreased high-density lipoproteins), hypertension, insulin resistance and obesity. To decrease the risk of cardiovascular disease events decreasing body weight by ingesting a healthy diet, increasing physical activity, cessation of smoking and managing dyslipidemia are recommended. Pharmacological treatment of dyslipidemia is based on different drug classes. For LDL-cholesterol-lowering mainly statins and for triglyceride-lowering mainly fibrates are used. In primary and secondary prevention trials of heart disease they have shown to reduce the incidence of coronary artery disease or coronary events by 25-60 percent. Statins reduce mainly LDL-cholesterol levels by competitive inhibition of HMG-CoA reductase but have also shown to reduce fasting and postprandial triglyceride levels. Fibrates effectively reduce fasting and postprandial lipemia, shift the distribution of LDL particles towards less dense particles and increase HDL-cholesterol. Thus fibrates particularly address components of the metabolic syndrome and features of diabetic dyslipidemia. However studies still are needed showing definite evidence on differential therapy in lipid lowering based on prospective controlled trials with endpoints of macro- and microangiopathy in diabetic patients.
authors.affiliation: St. Nikolaus-Stiftshospital, Teaching Hospital, University of Bonn at Andernach, Germany. Armin.Steinmetz@Stiftshospital-Andernach
authors.forename: A
authors.initials: A
authors.lastname: Steinmetz
authors.forename: S
authors.initials: S
authors.lastname: Fenselau
authors.forename: J
authors.initials: J
authors.lastname: Schrezenmeir
mesh_terms: D001161:Arteriosclerosis / Q000209:etiology; D002995:Clofibric Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use; D003327:Coronary Disease / Q000209:etiology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000628:therapy; D015248:Gemfibrozil / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006951:Hyperlipoproteinemias / Q000150:complications / Q000188:drug therapy / Q000628:therapy*; D015228:Hypertriglyceridemia / Q000150:complications; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D024821:Metabolic Syndrome
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; C009746:etofibrate; D002995:Clofibric Acid; D015248:Gemfibrozil