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Original Article

Oxidized LDL and anti‐oxLDL antibody levels in peripheral atherosclerotic disease

, , , , &
Pages 473-478 | Received 17 Sep 2007, Accepted 02 Dec 2007, Published online: 08 Jul 2009
 

Abstract

Objective. Oxidative modification of LDL (oxLDL) is important in atherogenesis and is proposed as a useful marker for identifying patients with coronary artery disease. Antibody to oxLDL (oxLDL Ab) is detected in human sera, although its biological significance is not well established. We aimed to measure oxLDL and oxLDL Ab in peripheral atherosclerotic disease (PAD) patients, and to examine the relation between them in an attempt to understand the role of oxLDL Ab. Total risk of atherosclerosis was estimated using the global risk assessment score (GRAS) calculated on the basis of age, total cholesterol, HDL cholesterol (HDL‐Chol), diabetes, hypertension and smoking. Material and methods. Twenty‐one patients aged 63.05±9.13 years, diagnosed by peripheric angiography as PAD, and 21 healthy controls aged 47.67±13.61 years took part in the study. Total LDL and HDL cholesterol levels were determined by enzymatic methods. Levels of circulating oxLDL were measured by monoclonal antibody 4E6‐based competition ELISA. IgG class oxLDL Ab titre was measured by ELISA. Results. Compared to healthy controls, PAD patients had higher levels of oxLDL (p<0.05), oxLDL Ab (p<0.05), LDL cholesterol (LDL‐Chol) (p<0.05), total cholesterol (p<0.05) and lower HDL‐Chol (p<0.05). OxLDL was found to be positively correlated with total cholesterol (r = 0.471, p<0.05) and LDL‐Chol (r = 0.614, p<0.01) and GRAS (r = 0.435, p<0.05) and negatively with HDL‐Chol (r = −0.459, p<0.05), but not with oxLDL Ab in PAD patients. Conclusions. These findings might indicate that high LDL‐Chol levels influence the oxidation of LDL and that oxLDL is a possible marker of PAD. However, the role of oxLDL Ab in atherosclerosis remains controversial.

Acknowledgement

This study was supported by the Research Fund of İstanbul University (project no. UDP‐1194/01062007).

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