ABSTRACT
Systemic lupus erythematosus [SLE], rheumatoid arthritis [RA] and systemic sclerosis [SSc] are inflammatory diseases of unknown etiology. Vascular endothelial growth factor [VEGF] is a cytokine participating in the inflammatory process. Antiphospholipid [APL] antibodies may have a role in the development of thrombosis. To investigate the role of APL antibodies and VEGF in different rheumatic diseases and their relation to clinical manifestations and disease activity scores. Forty four patients were included in this study, 15 with SLE, 15 with RA and 15 with SSc, in addition to 15 apparently healthy controls. All patients were subjected to complete history, clinical and joint examination and calculation of disease activity scores. Lupus anticoagulant [LAC], anticardiolipin [ACL] anti beta-2 glycoprotein antibodies [anti beta2 GPI] IgM and IgG isotypes and VEGP were measured in all subjects. Also complete blood picture, prothrombin time and concentration, activated partial thromboplastin time, rheumatoid factor and antinuclear factor were performed. The frequency of LAC was 13.3% in RA, 53.3% in SLE and 0% in SSc. The frequency of ACL was 53.3% in RA, 86.7% in SLE and 13.3% in SSc. The frequency of anti beta2-GP1 [IgG] was 26.7% in RA, 40% in SLE and 0% in SSc. The titer of LAC and ACL were higher in all groups than controls while IgG anti beta2-GPI antibody were higher in SLE than controls. The titer of these antibodies were higher in SLE with manifestations of antiphospholipid syndrome than without [p<0.001 for LAC and <0.05 for and IgG anti beta2-GP1. Also, the presence of three-fold APL increased the risk of APS OR/6 [1.09-234]. VEGF was significantly higher in all studied groups than controls [p<0.001]. By bivariate analysis positive correlations were found between VEGF and disease activity scores while no correlations were found between VEGF and APL. A full positive profile with high titers is more likely to identify patients at higher risk of PAS related events. VEGF may play a role in the pathogenesis and activity of rheumatic diseases. However, its role in the development of APS requires further studies