Changes of autoantibodies against oxidatively modified low density lipoproteins during long-term LDL-apheresis

The oxidation of low-density lipoproteins (LDL) is considered a key event i n the initiation of atherosclerosis. The aim of this study was to follow-up the biological marker of in vivo LDL oxidation (oxidatively modified LDL a utoantibody titres) during long-term LDL-apheresis treatment. A patient suf fering from severe combined hyperlipidaemia underwent LDL-apheresis biweekl y and was followed for two years. The significant reduction of baseline tot al cholesterol (58%), total triglycerides (80%), LDL-cholesterol (48%), apo protein B (50%) and apolipoprotein (a) (61%) may be considered as a good re sponse to the treatment. The titre of autoantibodies (IgG) against oxidativ ely modified LDL (malondialdehyde-derived LDL) was followed throughout the study and showed dynamic changes. The measured values were multiple compare d as mean+/-SD over each semester of apheresis application: I semester 70.0 +/-8.3 U/ml, n=12; II semester 58.0+/-13.8 U/ml, n=12; III semester 37.6+/- 6.0 U/ml, n=12; IV semester 34.3+/-7.0 U/ml, n=12; ANOVA: I vs II semester p<0.083, II vs III semester p<0.00053, III vs IV semester p<0.248. In paral lel to the changes in this biochemical parameter, regression of numerous xa nthomas was clinically observed. In spite of this, the presence of oxidised -LDL (oxLDL) antibodies was enhanced in comparison to antibody titre detect ed in a group of age-matched normolipaemic healthy controls (n=15; 19.4+/-8 .6; p<0.01). Classical lipoprotein parameters were correlated with the titr e of autoantibodies against oxLDL and showed low correlation coefficients: total cholesterol vs oxLDLab, r=0.36; triglycerides vs oxLDLab, r=0.43; LDL cholesterol vs oxLDLab, r=0.14; HDL cholesterol vs oxLDLab, r=-0.33; apo B vs oxLDLab, r=0.25; apo (a) vs oxLDLab, r=-0.05. Our study showed an addit ional benefit of LDL-apheresis therapy. The production of autoantibodies ag ainst oxLDL was reduced during the treatment, indicating a lower level of t he atherogenic antigen. (C) 1999, Editrice Kurtis.