title: Low density lipoprotein immunoapheresis does not increase plasma lipid peroxidation products in vivo.
abstract: Extracorporeal elimination of low density lipoprotein (LDL) is frequently used in drug-resistant hypercholesterolemia. LDL-immunoapheresis selectively removes LDL and lipoprotein(a) [Lp(a)] from plasma. Lipid peroxidation is one unwanted side effect, that occurs during extracorporeal plasma treatment. The purpose of this study was to investigate the effect of LDL immunoapheresis on lipid peroxidation. Before and after a single LDL-immunoapheresis treatment, plasma concentrations of lipid hydroperoxides, determined with two different spectophotometric assays, thiobarbituric acid-reacting substances (TBARS), determined spectrophotometrically and malondialdehyde (MDA), determined by an MDA-TBA/HPLC method, were measured in 13 hypercholesterolemic patients. In addition MDA was also determined in the eluate of the apheresis column. Before treatment, plasma cholesterol and LDL cholesterol concentrations were significantly higher in patients than in healthy control subjects, as were the lipid peroxidation products. LDL-immunoapheresis treatment of the patients led to significant decreases in total cholesterol (69+/-8%), LDL-cholesterol (79+/-7%), HDL-cholesterol (35+/-17%), triglycerides (38+/-21%), apolipoprotein-B (77+/-6%), apolipoprotein-A1 (25+/-5%) and Lp(a) concentrations (76+/-10%). Changes in plasma lipid peroxide concentrations (17+/-8 nmol/l before vs. 14+/-5 nmol/l after treatment) were not significant, neither were those in TBARS (3. 0+/-2.6 micromol/l vs. 2.3+/-1.3 micromol/l) or MDA concentrations (1.03+/-0.17 micromol/l vs. 1.0+/-0.20 micromol/l). Patients with high baseline values showed a decrease, whereas others did not. MDA was present (0.57+/-0.13 micromol/l) in the eluate of the apheresis column, suggesting that, along with LDL, lipid peroxidation products are also removed. From these results we conclude that a single LDL-immunoapheresis treatment effectively reduces LDL and Lp(a) in the absence of increases in plasma lipid peroxidation products.
authors.affiliation: Department of Cardiology, University of Vienna, Waehringerguertel 18-20, A-1090, Vienna, Austria. kkostner@pop3.kard.akh-wien.ac.at
authors.forename: K
authors.initials: K
authors.lastname: Kostner
authors.forename: S
authors.initials: S
authors.lastname: Banyai
authors.forename: M
authors.initials: M
authors.lastname: Jansen
authors.forename: G
authors.initials: G
authors.lastname: Khoschsorur
authors.forename: W H
authors.initials: WH
authors.lastname: Hörl
authors.forename: G
authors.initials: G
authors.lastname: Maurer
authors.forename: B
authors.initials: B
authors.lastname: Winklhofer-Roob
authors.forename: K
authors.initials: K
authors.lastname: Derfler
mesh_terms: D000328:Adult; D001781:Blood Component Removal / Q000379:methods*; D016022:Case-Control Studies; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood; D015227:Lipid Peroxidation; D008054:Lipid Peroxides / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood / Q000302:isolation & purification*; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D008054:Lipid Peroxides; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; D008315:Malondialdehyde