Extracorporal Plasma Therapy in the Treatment of Severe Hyper-β-lipoproteinemia: The HELP System
A large and convincing body of evidence links coronary risk with elevated plasma levels of both low-density lipoprotein (LDL) cholesterol and fibrinogen. Cholesterol in atherosclerotic lesions originates mainly from cholesterol circulating in the blood 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 being recognized as the crucial element in the control of cholesterol homeostasis . Elevated levels of fibrinogen, a common phenomenon in hypercholesterolemia increases the viscosity of the blood and thereby further alters perfusion of tissues in severe atherosclerotic disease. Furthermore, fibrinogen and its degradation products can both influence prostaglandin metabolism by inhibiting PGI2 synthesis by endothelial and vascular smooth muscle cells, thereby facilitating platelet aggregation, and can also cause injury to endothelial cells.
KeywordsCholesterol Filtration Heparin Assure Bicarbonate
Unable to display preview. Download preview PDF.
- 1.Goldstein JL, Brown MS (1983) Familial hypercholesterolemia. In: Stanbury JB, Wyngaarden JB, Frederickson DS, Goldstein JL, Brown MS (eds) The metabolic basis of inherited disease, 5th edn. McGraw Hill, New YorkGoogle Scholar
- 2.Seidel D, Wieland H (1982) Ein neues Verfahren zur selektiven Messung und extrakorporalen Elimination von Low Density Lipoproteinen. J Clin Chem Clin Biochem 20: 684–685Google Scholar