Prevention and treatment of the metabolic syndrome.
The prevalence of the metabolic syndrome is increasing owing to lifestyle changes leading to obesity. This syndrome is a complex association of several interrelated abnormalities that increase the risk for cardiovascular disease and progression to diabetes mellitus (DM). Insulin resistance is the key factor for the clustering of risk factors characterizing the metabolic syndrome. The National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III defined the criteria for the diagnosis of the metabolic syndrome and established the basic principles for its management. According to these guidelines, treatment involves the improvement of the underlying insulin resistance through lifestyle modification (eg, weight reduction and increased physical activity) and possibly by drugs. The coexistent risk factors (mainly dyslipidemia and hypertension) should also be addressed. Since the main goal of lipid-lowering treatment is to achieve the NCEP low-density lipoprotein cholesterol (LDL-C) target, statins are a good option. However, fibrates (as monotherapy or in combination with statins) are useful for the treatment of the metabolic syndrome that is commonly associated with hypertriglyceridemia and decreased high-density lipoprotein cholesterol (HDL-C) levels. The blood pressure target is < 140/90 mm Hg. The effect on carbohydrate homeostasis should possibly be taken into account in selecting an antihypertensive drug. Patients with the metabolic syndrome commonly have other less well-defined metabolic abnormalities (eg, hyperuricemia and raised C-reactive protein levels) that may also be associated with an increased cardiovascular risk. It seems appropriate to manage these abnormalities. Drugs that beneficially affect carbohydrate metabolism and delay or even prevent the onset of DM (eg, thiazolidinediones or acarbose) could be useful in patients with the metabolic syndrome. Furthermore, among the more speculative benefits of treatment are improved liver function in nonalcoholic fatty liver disease and a reduction in the risk of acute gout.
Daskalopoulou
S S
SS
Department of Clinical Biochemistry (Vascular Disease Prevention Clinics), Royal Free Hospital, London, UK.
Mikhailidis
D P
DP
Elisaf
M
M
D017667:Adipocytes / Q000378:metabolism; D000328:Adult; D000367:Age Factors; D000428:Alcohol Drinking; D001809:Blood Viscosity; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000453:epidemiology; D008078:Cholesterol, LDL / Q000097:blood; D003920:Diabetes Mellitus / Q000453:epidemiology; D005006:Ethnicity; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006949:Hyperlipidemias / Q000628:therapy; D006973:Hypertension / Q000628:therapy; D015228:Hypertriglyceridemia / Q000453:epidemiology; D033461:Hyperuricemia / Q000453:epidemiology; D007249:Inflammation / Q000628:therapy; D007333:Insulin Resistance; D008019:Life Style; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D009765:Obesity / Q000453:epidemiology; D015995:Prevalence; D012307:Risk Factors; D012907:Smoking; D015431:Weight Loss
D008078:Cholesterol, LDL; D005230:Fatty Acids, Nonesterified; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D005340:Fibrinogen; D002097:C-Reactive Protein