Background Systemic lupus erythematosus is a common autoimmune disease occurring predominantly in women during reproductive age. Antiphospholipid syndrome (APS) is a prothrombotic, systemic autoimmune disease. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a recently identified proinflammatory cytokine of the TNF superfamily. The available evidences have indicated that TWEAK might be a target for therapeutic intervention in renal, vascular injury and neuropathy in systemic lupus erythematosus SLE. Hyperleptinaemia in the general population is also associated with atherosclerosis, hypertension and metabolic syndrome.
Objectives Aim of the study was to evaluate the correlation between IMTand serum level of soluble TWEAK (sTWEAK), adipokine Leptin and traditional risk factors of atherosclerosis. Comparison between (sTWEAK) and Leptin in different studied groups.
Methods The study is a case control study which conducted on 30 patients with SLE (A), 26 patients with secondry antiphospholipid syndrome (B), 14 patints with primary antiphospholipid syndrome (C) and 20 healthy volunteers with matched age and sex (D). All the study persons underwent full clinical assessment and investigations including Complete blood picture, ESR, kidney function tests, Lipid profile,body mass index.carotid duplex measuring intima media thickness (IMT). Serum soluble TWEAK and leptin using ELISA.
Results The results showed high statistically signficant difference (P value <0.001) between group C and D, group B and C amd high statistically signficant difference (P value: 0.006) between group A and C as regards IMT. High statistically signficant difference (P value <0.001) between all groups as regards sTWEAK and leptin. With high level in those with antiphospholipid syndrome. There was no significant correlation btween (sTWEAK) and Leptin and IMT in different studied groups.
Conclusions sTWEAK and leptin with other traditional risk factors can be a useful markers to predict and evaluate the presence of atherosclerosis in SLE and antiphospholipid patients.These findings should be taken into consideration as leptin contributes to increased oxidation, but further studies are required to determine whether hyperleptinaemia in patients with SLE contributes directly to increased oxidative stress.
Brian J. Skaggs, Bevra H. Hahn, and Maureen McMahon: The role of the immune system in atherosclerosis: molecules, mechanisms and implications for management of cardiovascular risk and disease in patients with rheumatic diseases, Nat Rev Rheumatol.; 8(4): 214–223, 2012.
Davies RJ, Sangle SR, Khamashta MA and D'Cruz DP: Antiphospholipid (Hughes) syndrome and atheroma. Lupus; 15, 55–58, 2006.
Frédéric A. Houssiau, M.D., Ph.D.:Toward better treatment forlupus nephritis,N Engl J Med; 365:1929–1930, November 17,2011.
Katarzyna Fischer, Marek Brzosko: Diagnosis of early atherosclerotic lesions, and selected atherosclerotic risk factors, in patients with systemic lupus erythematosus. Pol Arch Med Wewn; 119 (11): 736–742, 2009.
Acknowledgement Many thanks for our dear patients, hoping for better health and life
Disclosure of Interest None declared