Abstract
Problem statement: Associations between serum levels of fetuin-A, C3 complement, calcium × phosphate product and calcification risk index and lipid profile in SLE patients were established. However, the mechanism of accelerated atherosclerosis accompanied with SLE remains elusive. We therefore turned to investigate the association between Fetuin-A, disease activity and accelerated atherosclerosis in patients with SLE. Approach: Serum blood samples were taken from 100 female SLE patients. All Patient samples were analyzed by ELISA for determination of Fetuin-A level. Calcium, Phosphate, C3 compelement, Lipid profile, Creatinine and urea were measured also in SLE patients compared with healthy control volunteers. Results: We found that Serum fetuin-A had been positively associated with carotid arterial stiffness, independent of known atherogenic factors in healthy subjects. Furthermore, Fetuin-A was correlated negatively with IMT, SLEDAI, CRI, CaxP product, Triglycerdies, VLDL and LDL. While it was correlated positively with C3 complement. Conclusion: Fetuin-A deficiency accompanied with increasing levels of calcium and phosphate gave an evidence that there was a key role of fetuin-A as a strong inhibitor of Cardio Vascular Calcification (CVC) by formation of a complex called (calciprotein) with calcium and phosphate in blood stream. So, Identification of biologic markers of disease activity associated with atherosclerosis may help to optimize therapy for this important manifestation of systemic autoimmune disease.
Highlights
SLE is an autoimmune disease in which immune system attacks the body cells and tissues, resulting in inflammation and tissue damage
Recruitment were: diagnosis of SLE according to the American College of Rheumatology (ACR) criteria and the absence of any concomitant Cardio Vascular Calcification (CVC) traditional risk factors' Disease Activity was assessed the time of enrollment in the study using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)
Significant negative correlations were found between fetuin-A (g/l), Intima-Media Thickness (IMT) and SLEDAI [r = 0.898 p
Summary
SLE is an autoimmune disease in which immune system attacks the body cells and tissues, resulting in inflammation and tissue damage. Accelerated Atherosclerotic Vascular Disease (ASVD) is a major problem in SLE and is one of its major causes of death (Urowitz and Gladman, 2007). J. 3 (2): 249-254, 2012 therapeutics for prevention of Coronary Vascular Disease (CVD) in SLE (Harley et al, 2006). Fetuin-A (Alpha 2-Heremans-Schimd glycoprotein, AHSG), is a glycoprotein secreted by adult liver into the peripheral circulation. This protein is commonly present in the cortical plate of immature cerebral cortex and bone marrow hemopoietic matrix (Kazama et al, 2005). Reduced fetuin-A levels associated with inflammation and increased CVC (Cozzolino et al, 2006; Selim et al, 2006)
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