Objective Dyslipidemia with higher inflammatory states disease activity and longer disease

Objective Dyslipidemia with higher inflammatory states disease activity and longer disease duration in juvenile idiopathic arthritis (JIA) patients AGAP1 seemed to increase the risks of atherosclerosis. their serum lipid profiles at baseline and 2 4 6 12 months later and decided whether there were differences in total blood counts inflammatory mediators lipid levels and atherogenic indices between patients who experienced inactive disease (responders) and those who were poor responders (non-responders) to etanercept treatment. Results Analysis of dynamic change in total JIA patients before and after TNF inhibitor therapy showed modest increases in hemoglobin levels (P?=?0.02) and decreases in WBC counts Platelet and CRP levels progressively (p?=?0.002 p?=?0.006 and p?=?0.006 respectively).Twelve of the 23 patients achieved inactive disease status (responders) after 12-months of treatment. In responders compared to non-responders total cholesterol (TC) low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) increased significantly (P?=?0.007 P?=?0.044 P<0.001) whereas triglyceride and atherogenic index (TC/HDL-C ratio) significantly decreased (P?=?0.04 P?=?0.01 respectively) after etanercept treatment. Conclusion Disease severity was associated with triglyceride level atherogenic index and was inversely associated with total cholesterol HDL-C and LDL-C levels and can be improved substantially by using anti TNF-α treatment. Such treatment may have a beneficial effect on the cardiovascular risk in patients with JIA. Introduction Chronic inflammatory diseases such as rheumatoid arthritis systemic lupus erythematosus had been proven to have a higher risk of premature coronary artery disease [1]. Abnormal lipoprotein levels play an important role in atherosclerotic processes that can be related to autoimmune disease. The risk to develop atherosclerosis increases progressively with increasing low-density lipoprotein cholesterol (LDL-C) and hypertriglyceridemia levels and declines with increased MLN9708 levels of high-density lipoprotein cholesterol (HDL-C) [2] [3]. In adult patients with rheumatoid arthritis cardiovascular disease is the leading cause of shortened life expectancy relative to the general population and nearly half of these deaths can be attributed to cardiovascular disease that is usually linked to inflammation and elevated C-reactive protein (CRP) levels [4]. However data regarding dyslipidemia prevalence and related impact are seldom seen and do not conclusively define the role of JIA in this metabolic disturbance. JIA is the most common rheumatic disease in child years and represents a major cause of functional disability in children. JIA is also a heterogeneous and multi-factorial autoimmune MLN9708 disease characterized by chronic joint inflammation [5]-[7]. In JIA studies have exhibited an imbalance favoring the production of pro-inflammatory cytokines including interleukin-1β (IL-1β) interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) that are important contributors to the perpetuation of the inflammatory response [8]. Non-steroidal anti-inflammatory drug methotrexate and glucocorticoid are the standard and first collection treatment regimen for JIA [9]. Such traditional MLN9708 therapy is not usually effective and has unknown harmful side effects. Most patients with systemic or polyarticular-onset JIA need other second-line medications. Etanercept is usually a soluble fusion protein comprised of the extracellular domain name of the MLN9708 TNF receptor (p75) and Fc portion of human immunoglobulin G1 and is the drug of choice for disease-modifying antirheumatic drugs refractory RA [10] [11]. It also has a beneficial effect in patients with JIA that experienced previously experienced no response or were refractory to standard therapy [12] [13]. Disease activity and inflammatory status are inversely correlated with changes in plasma total and HDL cholesterol levels and positively correlated with the variance of atherogenic index in RA patients after anti-TNF therapy [14]. Dyslipidemia was also observed in JIA patients with higher disease activity and longer disease duration seemed to increase the risks of atherosclerosis [15]. However the correlation of lipid profile changes and disease activity before and after anti-TNF therapy has seldom been examined. To clarify the relationship between disease activity and the dynamic changes of complete blood.