FRI0022 EVALUATION OF DYSFUNCTIONAL HIGH-DENSITY LIPOPROTEIN LEVELS WITH MYELOPEROXIDASE/PARAOXONASE1 RATIO IN RHEUMATOID ARTHRITIS

Abstract

Background: Rheumatoid arthritis (RA) is a chronic, systemic and autoimmune disease with inflammatory arthritis. Atherosclerosis and cardiovascular diseases are common in RA patients. Although chronic systemic inflammation in RA patients is considered to be the main cause of this condition, the relationship between systemic inflammation and vascular pathophysiology is not clear [1]. While high-density lipoprotein (HDL) is known to be a negative risk factor for atherosclerosis by reverse cholesterol transport, recent studies show that HDL can be pro-atherogen (dysfunctional, inflammatory) by losing this characteristic in cases of inflammation and oxidative stress. Myeloperoxidase (MPO)/paraoxonase 1 (PON1) ratio is a valuable marker that can be routinely used as an indicator of dysfunctional HDL. PON1 is a lipoprotein-derived enzyme which provides antioxidant properties of HDL. Although MPO is a bactericidal enzyme derived from granular leukocytes, it causes oxidative modification of circulating lipoproteins [2]. Objectives: The aim of this study is to evaluate the levels of dysfunctional HDL in RA patients and to explore the relationship between dysfunctional HDL and coronary artery disease (CAD) in RA patients. Methods: Sixty seven healthy individuals and 130 RA patients without diabetes mellitus, hypertension and hyperlipidemia were included to study. Blood samples taken from patients and healthy volunteers were centrifuged to separate serum and these serum samples were stored at -80 °C until the study day. Total cholesterol (TC), triglyceride (TG), HDL, Low-density lipoprotein cholesterol (LDL), MPO and PON1 levels were measured. The MPO/PON1 ratio was calculated as a dysfunctional HDL marker. Cardiology notes of the patients were examined to detect patients who also have CAD. Results: The mean age of the patient and control groups were 54.6 ± 11.3 and 52.0 ± 10.0, respectively (p:0.107). The mean DAS28 score of the patients was 2.77 ± 0.96. There were no significant differences between two groups in TC, TG, HDL and LDL (p> 0.05). MPO, PON1 and dysfunctional HDL levels were significantly higher in the RA group compared to control group (p Dysfunctional HDL levels were higher in 44 RA patients with CAD compared to 86 RA patients without CAD (p = 0.002). 58 patients with active RA had higher dysfunctional HDL levels compared to 72 patients with remission (p = 0.002). There was a positive correlation between DAS28 scores and dysfunctional HDL levels (rho: 0.357, p Conclusion: Our study shows that, although there is no abnormality in lipid profile parameters, dysfunctional HDL levels were higher in patients with active disease than patients with RA in remission and RA patient with CAD than without CADs. This condition could be associated with CAD in RA patients. Disturbance as a result of inflammation on HDL functions such as inhibition of LDL oxidation and reverse cholesterol transport, could be the cause of CAD in RA patients. As a result screening of conventional cardiovascular risk factors in RA patients with normal lipid panel might be inadequate. Therefore as an additional parameter, dysfunctional HDL are promising to evaluate cardiovascular risk of RA patients.