Abstract

The prognosis of patients suffering from severe hyperlipidemia, sometimes combined with elevated lipoprotein (a) levels, and coronary heart disease refractory to diet and lipid-lowering drugs is poor. For such patients, regular treatment with low-density lipoprotein (LDL) apheresis is the therapeutic option. Today, there are five different LDL-apheresis systems available: cascade filtration or lipid filtration, immunoadsorption, heparin-induced LDL precipitation, dextran sulfate LDL adsorption, and the LDL hemoperfusion. There is a strong correlation between hyperlipidemia and atherosclerosis. Besides the elimination of other risk factors, in severe hyperlipidemia therapeutic strategies should focus on a drastic reduction of serum lipoproteins. Despite maximum conventional therapy with a combination of different kinds of lipid-lowering drugs, sometimes the goal of therapy cannot be reached. Hence, in such patients, treatment with LDL-apheresis is indicated. Technical and clinical aspects of these five different LDL-apheresis methods are shown here. There were no significant differences with respect to or concerning all cholesterols, or triglycerides observed. With respect to elevated lipoprotein (a) levels, however, the immunoadsorption method seems to be most effective. The different published data clearly demonstrate that treatment with LDL-apheresis in patients suffering from severe hyperlipidemia refractory to maximum conservative therapy is effective and safe in long-term application.

Highlights

  • In 1985, Brown and Goldstein were awarded the Nobel Prize for medicine for their excellent work on the regulation of cholesterol metabolism

  • Membrane differential filtration (MDF) or double filtration plasmapheresis seems to be superior to conventional plasmapheresis but less effective than adsorption or precipitation techniques [118,119,120]

  • Coagulation factors such as factors XI and XII were reduced by dextran sulfate adsorption, but those coagulation factors returned to normal range within one or two days after the treatment

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Summary

Introduction

In 1985, Brown and Goldstein were awarded the Nobel Prize for medicine for their excellent work on the regulation of cholesterol metabolism. In patients with familial hypercholesterolemia, this receptor is changed, and the LDL particles can no longer be recognized. Their absorption can no longer be mediated, leading to an accumulation of LDL in blood. Brown and Goldstein determined the structure of the LDL receptor [42, 44, 45] They discovered structural defects in this receptor in many patients with familial hypercholesterolemia [43]. Familial hypercholesterolemia was the first metabolic disease that could be tracked back to the mutation of a receptor gene. Homozygotes may have cholesterol in the range of 650–1,000 mg/dL, xanthoma by the age of 4 years, and death from coronary heart disease by the age of 20. Year Authors 1967 De Gennes et al [2] 1975 Thompson et al [3] 1980 Agishi et al [4] 1981 Stoffel and Demant [5] 1983 Borberg et al [6] 1983 Wieland and Seidel [7]

Method Plasmapheresis Plasmapheresis
Epidemiology and Pathophysiology
LDL-Apheresis Therapy
Cascade Filtration
Immunoadsorption
Low-Density Lipoprotein Hemoperfusion
Findings
10. Conclusion of LDL-Apheresis
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