title: Decreased low-density lipoprotein oxidation after repeated selective apheresis in homozygous familial hypercholesterolemia.
abstract: Familial hypercholesterolemia was the first genetic disorder recognized to cause myocardial infarction. Patients with homozygous familial hypercholesterolemia have rapidly progressive coronary atherosclerosis with angina pectoris, myocardial infarction, or sudden death at a young age. Selective apheresis on dextran sulfate cellulose columns reduces mortality and may induce regression of coronary lesions. These patients have both increased levels and prolonged circulation residence time of low-density lipoprotein (LDL), which is not removed by cellular receptor. LDL oxidation may play a pivotal role in atherogenesis. LDL undergoes oxidation before being taken up by macrophages and then transformed into arterial wall foam cells. The aim of this study was to investigate LDL oxidation in eight homozygous patients with familial hypercholesterolemia during repeated LDL apheresis. LDL lipid peroxidation, estimated by conjugated-diene absorbance at 234 nm, lipid peroxides, and malondialdehyde showed an increased resistance against oxidation after repeated LDL apheresis. This phenomenon was also observed in the oxidative indexes of protein moiety of LDL (apolipoprotein-B100 fragmentation, trinitrobenzenesulfonic acid reactivity, and electrophoresis agarose mobility). Similarly, cholesteryl esterification was decreased after LDL apheresis. Thus selective LDL apheresis not only decreases the pool of LDL, but it also induces changes that render LDL less susceptible to oxidation. This phenomenon might contribute to reduce coronary atherosclerosis and thus mortality of these particular patients.
authors.affiliation: Department of Clinical and Experimental Medicine, Federico II School of Medicine, University of Naples, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Napoli
authors.forename: G
authors.initials: G
authors.lastname: Ambrosio
authors.forename: N
authors.initials: N
authors.lastname: Scarpato
authors.forename: G
authors.initials: G
authors.lastname: Corso
authors.forename: G
authors.initials: G
authors.lastname: Palumbo
authors.forename: F P
authors.initials: FP
authors.lastname: D'Armiento
authors.forename: F P
authors.initials: FP
authors.lastname: Mancini
authors.forename: A
authors.initials: A
authors.lastname: Malorni
authors.forename: S
authors.initials: S
authors.lastname: Formisano
authors.forename: A
authors.initials: A
authors.lastname: Ruocco
authors.forename: A
authors.initials: A
authors.lastname: Calí
authors.forename: M
authors.initials: M
authors.lastname: Chiariello
mesh_terms: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B / Q000097:blood; D001781:Blood Component Removal; D002788:Cholesterol Esters / Q000097:blood; D005609:Free Radicals; D008401:Gas Chromatography-Mass Spectrometry; D006720:Homozygote; D006801:Humans; D006938:Hyperlipoproteinemia Type II / Q000097:blood* / Q000235:genetics / Q000628:therapy*; D015227:Lipid Peroxidation; D008077:Lipoproteins, LDL / Q000097:blood* / Q000378:metabolism; D008315:Malondialdehyde / Q000097:blood; D010084:Oxidation-Reduction; D010743:Phospholipids / Q000097:blood; D014280:Triglycerides / Q000097:blood
chemical_list: D053299:Apolipoprotein B-100; D001055:Apolipoproteins B; D002788:Cholesterol Esters; D005609:Free Radicals; D008077:Lipoproteins, LDL; D010743:Phospholipids; D014280:Triglycerides; D008315:Malondialdehyde