Short- and long-term effects on serum lipoproteins by three different techniques of apheresis.
Low-density lipoprotein (LDL) apheresis is applied in patients with coronary heart disease because of severe inherited forms of hypercholesterolemia, for which dietary and combined drug treatment cannot lower LDL cholesterol concentrations less than 130 mg/dl. The following article describes the changes in lipoprotein levels in a total of 19 patients undergoing weekly LDL apheresis. Immunoadsorption, operating with polyclonal antibodies against apolipoprotein B-100, was used in 6 patients. Five patients were put on heparin-induced extracorporeal LDL precipitation (HELP) therapy; 6 received dextran sulfate adsorption treatments. Under steady-state conditions a single treatment reduced LDL cholesterol by 149 + or - 3 mg/dl with immunoadsorption, 122 + or - 2 mg/dl with HELP, and 124 + or - 18 mg/dl with dextran sulfate adsorption. Lipoprotein (a) (Lp[a]) declined by 52 to 65%. Very low density lipoprotein (VLDL) cholesterol and VLDL triglycerides declined by 45 to 55% because of the activation of lipoprotein lipase and precipitation during the HELP procedure. In all procedures, there was a small reduction in the different high-density lipoprotein fractions, which had returned to normal after 24 h. The long-term HDL3 cholesterol levels increased significantly. During all procedures there was a decrease in the molar esterification rate of lecithin cholesterol acyltransferase activity. All changes in lipid fractions were paralleled by changes in the corresponding apolipoprotein levels. It is concluded that all three techniques described are powerful tools capable of lowering LDL cholesterol in severe hereditary forms of hypercholesterolemia. In HELP and dextran sulfate adsorption, the amount of plasma is limited by the elimination of other plasma constituents. Immunoadsorption may thus be preferred in very severe forms of hypercholesterolemia.
Richter
W O
WO
Medical Department II, Klinikum Grosshadern, Ludwig-Maxmilians-University of Munich, Germany.
Donner
M G
MG
Schwandt
P
P
D000214:Acyl Coenzyme A / Q000037:antagonists & inhibitors; D000327:Adsorption; D001054:Apolipoproteins A / Q000097:blood / Q000302:isolation & purification; D008078:Cholesterol, LDL / Q000097:blood / Q000302:isolation & purification*; D015243:Cholesterol, VLDL / Q000097:blood / Q000302:isolation & purification*; D017023:Coronary Angiography; D016264:Dextran Sulfate / Q000737:chemistry / Q000378:metabolism; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000628:therapy*; D007164:Immunosorbents; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D010956:Plasmapheresis / Q000379:methods* / Q000592:standards
D000214:Acyl Coenzyme A; D001054:Apolipoproteins A; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D007164:Immunosorbents; C008047:3-hydroxy-3-methylglutaryl-coenzyme A; D016264:Dextran Sulfate; D007862:Phosphatidylcholine-Sterol O-Acyltransferase