Treatment of dyslipoproteinemia in the metabolic syndrome

被引:1
作者
Steinmetz, A
Fenselau, S
Schrezenmeir, J
机构
[1] Univ Bonn, Teaching Hosp, St Nikolaus Stiftshosp GmbH Andernach, D-56626 Andernach, Germany
[2] Fed Res Ctr, Inst Physiol & Biochem, Kiel, Germany
关键词
metabolic syndrome; dyslipidemia; diabetes; drug therapy; statins; fibrates;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:S548 / S559
页数:12
相关论文
共 102 条
[1]  
ABRAMOWICZ M, 1996, MED LETT, V38, P67
[2]  
*AM DIAB ASS, 1998, DIABETES CARE, V21, P536
[3]  
[Anonymous], 1975, JAMA-J AM MED ASSOC, V231, P360
[4]   EFFECTS OF LOVASTATIN THERAPY ON VERY-LOW-DENSITY LIPOPROTEIN TRIGLYCERIDE-METABOLISM IN SUBJECTS WITH COMBINED HYPERLIPIDEMIA - EVIDENCE FOR REDUCED ASSEMBLY AND SECRETION OF TRIGLYCERIDE-RICH LIPOPROTEINS [J].
ARAD, Y ;
RAMAKRISHNAN, R ;
GINSBERG, HN .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1992, 41 (05) :487-493
[5]  
AUSTIN MA, 1988, JAMA-J AM MED ASSOC, V260, P1917
[6]   Hypertriglyceridemia as a cardiovascular risk factor [J].
Austin, MA ;
Hokanson, JE ;
Edwards, KL .
AMERICAN JOURNAL OF CARDIOLOGY, 1998, 81 (4A) :7B-12B
[7]  
BADRAWY HS, 1984, THERAPIEWOCHE, V34, P1122
[8]   MEVINOLIN AND COLESTIPOL STIMULATE RECEPTOR-MEDIATED CLEARANCE OF LOW-DENSITY LIPOPROTEIN FROM PLASMA IN FAMILIAL HYPERCHOLESTEROLEMIA HETEROZYGOTES [J].
BILHEIMER, DW ;
GRUNDY, SM ;
BROWN, MS ;
GOLDSTEIN, JL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1983, 80 (13) :4124-4128
[9]   ARTERIAL IMAGING AND ATHEROSCLEROSIS REVERSAL [J].
BLANKENHORN, DH ;
HODIS, HN .
ARTERIOSCLEROSIS AND THROMBOSIS, 1994, 14 (02) :177-192
[10]   COMPARISON OF PROPERTIES OF 4 INHIBITORS OF 3-HYDROXY-3-METHYLGLUTARYL-COENZYME-A REDUCTASE [J].
BLUM, CB .
AMERICAN JOURNAL OF CARDIOLOGY, 1994, 73 (14) :D3-D11