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

The oxidation of low-density lipoproteins (LDL) is considered a key event in the initiation of atherosclerosis. The aim of this study was to follow-up the biological marker of in vivo LDL oxidation (oxidatively modified LDL autoantibody titers) during long-term LDL-apheresis treatment. A patient suffering from severe combined hyperlipidemia underwent LDL-apheresis biweekly and was followed for two years. The significant reduction of baseline total cholesterol (58%), total triglycerides (80%), LDL cholesterol (48%), apoprotein B (50%) and apolipoprotein (a) (61%) may be considered as a good response to the treatment. The titer of autoantibodies (IgG) against oxidatively modified LDL (malondialdehyde-derived LDL) was followed throughout the study and showed dynamic changes. The measured values were multiple compared as means?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 parallel to the changes in this biochemical parameter, regression of numerous xanthomas was clinically observed. In spite of this, the presence of ox-LDL antibodies was enhanced in comparison to antibody titer detected in a group of age-matched normolipemic healthy controls (n=15 ; 19.4?8.6 ; p<0.01). Classical lipoprotein parameters were correlated with the titer 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 additional benefit of LDL-apheresis therapy. The production of autoantibodies against oxidized-LDL was reduced during the treatment, indicating a lower level of the atherogenic antigen.

hyperlipidemia; LDL-apheresis; antibodies to oxidized-LDL

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