engleski

Antioxidized L D L autoantibodies during long-term LDL apheresis

With regard to the well documented atherogenic role of LDL oxidation in the process of atherosclerosis, the aim of this study was to evaluate the effect of long-term LDL apheresis on antioxidized-LDL-autoantibodies generation and fluctuation. It is believed that measuring plasma level of oxLDLab might help in evaluating the impact of LDL oxidation. A patient suffering from severe combined hyperlipidemia underwent LDL apheresis biweekly and was followed for 2 yrs. The reduction of baseline total cholesterol (58%), total triglycerides (80%), LDL-cholesterol (48%), apo B (50%), and apo (a) (61%), may be considered as a good response to treatment. The level of lipoproteins was not related to oxLDLab either before LDL apheresis or after the treatment. Thus, no significant correlation was found between the titres of oxLDLab and total cholesterol (pre r=0.04 ; post r=0.2) or apo B (pre r=-0.26 ; post r=0.04), while actual LDL cholesterol was showed negative correlation in the pre-treatment (r=-0.32, p<0.001) but not after apheresis (r=0.24, p<0.001). The oxLDLab status was showed negative correlation with HDL cholesterol, both in the pre- and post-apheresis treatment (pre r=-0.27, post r=-0.26, p<0.001). Nevertheless, the titres of autoantibodies against oxLDL were influenced by LDL apheresis and showed a dynamic change. Contrary to what might be expected, and although the LDL level was markedly decreased, oxLDLab rose after every single LDL-apheresis. Thus, oxLDLab pre- (48.2ą4.8 AcU/ml) and post-LDL apheresis (70.8ą8.7 AcU/ml) differed significantly in the first six-month period (p<0.0002), since the mean circulating post-treatment oxLDLab level was higher by 48%. This apparent paradox may have resulted from the possible partial linkage of oxLDLab in the oxLDL-immune complexes masking the free antibodies and making them undetectable by ELISA measurement. In the second six-month period of the same year the mean oxLDLab pre- (41.3ą5.8 AcU/ml) and post-apheresis (59.3ą7.5 AcU/ml) level was lower, with a less significant difference (p<0.05). The titres of circulating oxLDLab were significantly lower in the second year of LDL-apheresis application (18mo: 34.6ą9.8 vs 37.4ą7.8 AcU/ml, NS ; 24mo: 30.3ą5.9 vs 33.9ą9.9 AcU/ml, NS), whereas differences between the pre- and post-treatment periods were not significant. However, if the level of antibodies against oxLDL followed throughout the study, the curve shows a continuous decline, which denotes a regression of the autoantibody production. In parallel to changes in this biochemical parameter, regression of numerous xanthomas was clinically observed. In conclusion, our findings provide evidence that long-term LDL apheresis treatment decreases the production of autoantibodies against oxLDL. This is an additional benefit of LDL-apheresis therapy, since minimalization of oxidized LDL and oxLDL autoantibody production lessens their involvement in the atherosclerotic processes.

Oxidized LDL; Autoantibodies; LDL-apheresis

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