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Changes of autoantibodies against oxidatively modified low density lipoproteins during long-term LDL-apheresis.
Diabetes Nutr Metab. 1999 Dec; 12(6):413-7.DN

Abstract

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.

Authors+Show Affiliations

University Clinic for Diabetes, Endocrinology and Metabolic Diseases, Zagreb Croatia.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10782563

Citation

Turk, Z, et al. "Changes of Autoantibodies Against Oxidatively Modified Low Density Lipoproteins During Long-term LDL-apheresis." Diabetes, Nutrition & Metabolism, vol. 12, no. 6, 1999, pp. 413-7.
Turk Z, Mrzljak V, Turk N, et al. Changes of autoantibodies against oxidatively modified low density lipoproteins during long-term LDL-apheresis. Diabetes Nutr Metab. 1999;12(6):413-7.
Turk, Z., Mrzljak, V., Turk, N., & Metelko, Z. (1999). Changes of autoantibodies against oxidatively modified low density lipoproteins during long-term LDL-apheresis. Diabetes, Nutrition & Metabolism, 12(6), 413-7.
Turk Z, et al. Changes of Autoantibodies Against Oxidatively Modified Low Density Lipoproteins During Long-term LDL-apheresis. Diabetes Nutr Metab. 1999;12(6):413-7. PubMed PMID: 10782563.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Changes of autoantibodies against oxidatively modified low density lipoproteins during long-term LDL-apheresis. AU - Turk,Z, AU - Mrzljak,V, AU - Turk,N, AU - Metelko,Z, PY - 2000/4/27/pubmed PY - 2000/4/27/medline PY - 2000/4/27/entrez SP - 413 EP - 7 JF - Diabetes, nutrition & metabolism JO - Diabetes Nutr. Metab. VL - 12 IS - 6 N2 - 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. SN - 0394-3402 UR - https://www.unboundmedicine.com/medline/citation/10782563/Changes_of_autoantibodies_against_oxidatively_modified_low_density_lipoproteins_during_long_term_LDL_apheresis_ DB - PRIME DP - Unbound Medicine ER -