Background Chronic inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus had been proven to have a higher risk of atherosclerosis and premature coronary artery disease. On the other hand, the role of inflammation on dyslipidemia in patients with juvenile idiopathic arthritis (JIA), is not yet well established.
Objectives We have investigated whether etanercept (tumor necrosis factor-α receptor blocking agent) has the influence on inflammation markers and lipid profile in patients with JIA, after 1 year of treatment.
Methods A total of 50 patients with active polyarticular JIA and 31 healthy children were enrolled in the study. JIA patients donated paired blood samples prior to and 12 months after etanercept therapy. Inflammation markers (erythrocite sedimentation rate (ESR), white blood cells count (WBC) and C-reactive protein (CRP) level), as well as serum cholesterol, triacylglycerol, LDL-C and HDL-C levels were determined using standard biochemical analysis.
Results ESR, WBC count and CRP levels were significanly higher in JIA patients before treatment in comparison to control (p=0.001, p=0.048, p<0.001, respectively). Etanercept treatment significantly decreased ESR, WBC count and CRP levels in JIA patients in comparison to the values from before (p=0.011, p=0.039, p=0.016). Serum levels of cholesterol, triacylglycerol and LDL-C in JIA patients before treatment showed increase compared to control values (p=0.013, p=0.001, p=0.044). On the other hand HDL-C levels were lower in JIA patients in comparison to control (p<0.001). Etanercept treatment significantly decreased triacylglycerol levels and increased HDL-C levels in JIA patients compared to baseline values (p=0.020, p=0.007). There is a negative correlation between ESR and HDL-C levels either before or after etanercept treatment (p=0.001, p=0.041).
Conclusions Patients with JIA showed disturbances in serum lipid profile. Etanercept treatment in JIA patients increased the levels of HDL-C and lowered triacylglycerol levels in comparison to baseline values.
Kuo-Wei Yeh et al. PLoS One 2014;9(3):1-7.
Breda L et al. Clin Res Cardiol 2013;102:63–71.
Disclosure of Interest None declared
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