1,721,198 research outputs found
The Plurimetabolic Syndrome: qualitative lipoprotein abnormalities and atherosclerosis
No full textHypercholesterolemia with increased LDL-C levels is associated with higher risk of coronary artery disease (CAD). However, over 50% of patients with CAD do not present with increased plasma LDL-C, but their lipoprotein profile is rather characterized by qualitative lipoprotein abnormalities such as LDL particles that are small, dense and more atherogenic, mild hypertriglyceridemia and low HDL-C, particularly HDL2-C. This lipoprotein profile is often found in patients with insulin resistance and increased intra-abdominal adipose tissue, hallmarks of the plurimetabolic syndrome. Smaller, denser LDL particles are more susceptible to oxidative modifications. Oxidized LDL are potent inflammatory agents when they reach the sub-endothelial space. In addition, low levels of HDL2-C may be a marker of an impaired reverse cholesterol transport. Indeed, this lipid profile is associated with a three- to six-fold increased risk of both cardiovascular and cerebrovascular disease. It is interesting to..
IDENTIFICAZIONE E VALUTAZIONE DEI SOGGETTI A RISCHIO DI OSTEOPOROSI. ASPETTI EPIDEMIOLOGICI
No full text
Review article: the metabolic syndrome--a chronic cardiovascular inflammatory condition.
No full textThe atherosclerotic process is regulated by inflammatory mechanisms, which also appear to be involved in the modulation of insulin-resistance, a key player in the pathogenesis of the metabolic syndrome (MS). The interaction between components of the clinical phenotype of the MS with its biological phenotype (insulin resistance, dyslipidaemia, etc.) contributes to the development of a pro-inflammatory state characterized by an increased oxidative stress (i.e. oxidized lipoproteins) and a chronic, subclinical vascular inflammation, as also suggested by the increased C reactive protein (CRP) concentration found in patients with MS. The subclinical inflammatory state peculiar of the MS modulates the atherosclerotic process at different stages, resulting in: (i) endothelial dysfunction and increased expression of endothelial adhesion molecules; (ii) an enhanced recruitment of monocytes within the arterial wall, in the early stages of the atherosclerotic process; leading to (iii) the formation of an unstable atherosclerotic plaque, rich in inflammatory cells, which is the culprit lesion in the vast majority of both coronary and cerebrovascular events observed in with MS
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