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 titres) during long-term LDL-apheresis treatment. A patient suffering from severe combined hyperlipidaemia 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 titre 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 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 parallel to the changes in this biochemical parameter, regression of numerous xanthomas was clinically observed. In spite of this, the presence of oxidised-LDL (oxLDL) antibodies was enhanced in comparison to antibody titre detected 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 titre 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 oxLDL was reduced during the treatment, indicating a lower level of the atherogenic antigen.