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

  • D. Seidel
Conference paper


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.


Familial Hypercholesterolemia Erythrocyte Aggregation Disposable Material Plasma Protein Fraction Severe Coronary Heart Disease 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 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. 2.
    De Gennes J-L, Touraine R, Maunand B et al. (1967) Formes homozygotes cutaneoten-dineuses de xanthomatose hypercholesterolemique dans une observation familiale exemplaire. Essai de Plasmapherese à titre de traitment heroique. Bull Mem Soc Hop (Paris) 118:1137–1402Google Scholar
  3. 3.
    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
  4. 4.
    Eisenhauer T, Armstrong VW, Wieland H, Fuchs C, Scheler F, Seidel D (1987) Selective removal of low density lipoproteins (LDL) by precipitation at low pH: first clinical application of the HELP system. Klin Wochenschr 65:161–168PubMedCrossRefGoogle Scholar
  5. 5.
    Armstrong VW, Seidel D (1987) A novel technique for the extracorporeal treatment of familial hypercholesterolemia. In: Schlierf G, Mörl H (eds) Expanding horizons in atherosclerosis research. Springer, Berlin Heidelberg New YorkGoogle Scholar
  6. 6.
    Schuff-Werner P, Schütz E, Seyde WC, Eisenhauer T, Janning G, Armstrong VW, Seidel D (1988) Improved hemorheology associated with a reduction in plasma fibrinogen and LDL in patients being treated by heparin-induced extracorporeal LDL precipitation (HELP). Eur J Clin Invest (Submitted)Google Scholar
  7. 7.
    Endo A, Kuroda M, Tsujita Y (1976) ML-236A, ML-236B and ML-236C, new inhibitors of cholesterogenesis produced by penicillium citrinum. J Antibiot 29:1346–1348PubMedGoogle Scholar
  8. 8.
    Havel RJ et al. (1987) Lovastatin (mevinolin) in the treatment of heterozygous familial hypercholesterolemia. A multicenter study. Ann of Intern Med 107:607–615Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1989

Authors and Affiliations

  • D. Seidel

There are no affiliations available

Personalised recommendations