Severe hypertriglyceridemia with insulin resistance is associated with systemic inflammation: Reversal with bezafibrate therapy in a randomized controlled trial

American Journal of Medicine

Volumn 112, Issue 4, 2002, Pages 275-280

  Jonkers, Iris J ^a   Mohrschladt, Martina F ^a   Westendorp, Rudi G ^a   Van Der Laarse, Arnoud ^a   Smelt, Augustinus H ^a  

^a LEIDEN UNIVERSITY MEDICAL CENTER   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

APOLIPOPROTEIN B; BEZAFIBRATE; FIBRINOGEN; GLUCOSE; HIGH DENSITY LIPOPROTEIN CHOLESTEROL; INSULIN; INTERLEUKIN 6; LIPOPOLYSACCHARIDE; LOW DENSITY LIPOPROTEIN CHOLESTEROL; TRIACYLGLYCEROL; TUMOR NECROSIS FACTOR ALPHA; VERY LOW DENSITY LIPOPROTEIN CHOLESTEROL;

ADULT; ARTICLE; BODY MASS; CARDIOVASCULAR DISEASE; CARDIOVASCULAR RISK; CHOLESTEROL BLOOD LEVEL; CLINICAL ARTICLE; CLINICAL TRIAL; CONTROLLED CLINICAL TRIAL; CONTROLLED STUDY; CROSSOVER PROCEDURE; CYTOKINE PRODUCTION; DOUBLE BLIND PROCEDURE; DRUG EFFECT; FEMALE; GLUCOSE BLOOD LEVEL; HUMAN; HYPERTRIGLYCERIDEMIA; INFLAMMATION; INSULIN BLOOD LEVEL; INSULIN RESISTANCE; MALE; PRIORITY JOURNAL; PROTEIN SECRETION; RANDOMIZED CONTROLLED TRIAL; TRIACYLGLYCEROL BLOOD LEVEL;

ANTILIPEMIC AGENTS; BEZAFIBRATE; BLOOD GLUCOSE; C-REACTIVE PROTEIN; CROSS-OVER STUDIES; DOUBLE-BLIND METHOD; FEMALE; FIBRINOGEN; HUMANS; HYPERTRIGLYCERIDEMIA; INFLAMMATION; INFLAMMATION MEDIATORS; INSULIN; INSULIN RESISTANCE; INTERLEUKIN-6; LIPIDS; MALE; MIDDLE AGED; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0036121471     PISSN: 00029343     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0002-9343(01)01123-8     Document Type: Article

References (38)

1. Atherosclerosis - An inflammatory disease
2. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators
3. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris
4. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men
5. Measuring plasma fibrinogen to predict stroke and myocardial infarction: An update
6. Hypertriglyceridemia as a cardiovascular risk factor
7. Hypertriglyceridaemia and hypercoagulability
8. Fibrinolysis in hypertriglyceridaemic subjects in response to venous occlusion
9. Hyperlipoproteinemia affects cytokine production in whole blood samples ex vivo. The influence of lipid-lowering therapy
10. Role of cytokines in the acute phase response
11. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol
12. Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)
13. Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: A randomized controlled trial
14. The PPAR alpha-leukotriene B4 pathway to inflammation control
15. Not acute but chronic hypertriglyceridemia is associated with impaired endothelium-dependent vasodilation: Reversal after lipid-lowering therapy by atorvastatin
16. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man
17. Gerinnungsphysiologische schnellmethode zur bestimmung des fibrinogens
18. Determination of tumor necrosis factor α and interleukin 10 production in a whole blood stimulation system: Assessment of laboratory error and individual variation
19. Direct stimulation of cytokines (IL-1β, TNF-α, IL-6, IL-2, INF-γ and GM-CSF) in whole blood. I. Comparison with isolated PMBC stimulation
20. Effects of fenofibrate on plasma cytokine concentrations in patients with atherosclerosis and hyperlipoproteinemia IIb
21. Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators
22. Effects of fluvastatin and bezafibrate combination on plasma fibrinogen, t-plasminogen activator inhibitor and C reactive protein levels in coronary artery disease patients with mixed hyperlipidaemia (FACT study). Fluvastatin Alone and in Combination Treatment
23. Hypertriglyceridemia, insulin resistance, and the metabolic syndrome
24. Chronic subclinical inflammation as part of the insulin resistance syndrome: The Insulin Resistance Atherosclerosis Study (IRAS)
25. C-reactive protein in healthy subjects: Associations with obesity, insulin resistance, and endothelial dysfunction: A potential role for cytokines originating from adipose tissue?
26. Elevated C-reactive protein: Another component of the atherothrombotic profile of abdominal obesity
27. In vivo protection against endotoxin by plasma high density lipoprotein
28. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules
29. HDL, its enzymes and its potential to influence lipid peroxidation
30. Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells
31. Changes of lipolytic enzymes cluster with insulin resistance syndrome
32. Altering triglyceride concentrations changes insulin-glucose relationships in hypertriglyceridemic patients. Double-blind study with gemfibrozil with implications for atherosclerosis
33. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events
34. Effect of statin therapy on C-reactive protein levels
35. Inhibition of proinflammatory cytokine production by pravastatin
36. Lipophilic HMG-CoA reductase inhibitor has an anti-inflammatory effect: Reduction of MRNA levels for interleukin-1beta, interleukin-6, cyclooxygenase-2, and p22phox by regulation of peroxisome proliferator-activated receptor alpha (PPARalpha) in primary endothelial cells
37. Statin-induced inhibition of the Rho-signaling pathway activates PPARalpha and induces HDL apoA-I
38. Peroxisome proliferator-activated receptor α negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-κB and AP-1