Extracorporeal Plasma Therapy in the Treatment of Severe Hyper-β-Lipoproteinemia: The HELP System

  • D. Seidel
Conference paper

Abstract

A large and convincing body of evidence links coronary risk with elevated plasma levels of both low density lipoprotein (LDL) cholesterol and fibrinogen. Cholesterol of atherosclerotic lesions originates mainly from cholesterol circulating in the blood which is bound to LDL. Most forms of hyper-β-lipoproteinemia result from a defect in extraction of LDL from plasma by the liver and the LDL receptor is now recognized as a crucial element in the control of cholesterol homeostasis [1]. Elevated levels of fibrinogen, a common phenomenon in hypercholesterolemia, increase blood viscosity and erythrocyte aggregation, thereby altering tissue perfusion in severe atherosclerotic disease. In addition, fibrinogen and its degradation products can influence prostaglandin metabolism of endothelial and vascular smooth muscle cells, facilitating platelet aggregation; it can also injure endothelial cells.

Keywords

Cholesterol Filtration Heparin Polysaccharide Bicarbonate 

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Copyright information

© Springer-Verlag Berlin Heidelberg 1989

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  • D. Seidel

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