Abstract
Background
The full etiology of RA remains unclear; in addition to the contributions of infectious, hormonal, and environmental factors, several lines of evidence have suggested that the disease has a genetic basis. The VEGF gene is also an independent risk factor for RA severity and correlates with multiple disease parameters, such as disease activity, joint damage, and functional disability. This case-control study aimed to investigate the impact of a common genetic polymorphism in the vascular endothelial growth factor (VEGF) gene on disease activity and synovial lesions in patients with rheumatoid arthritis (RA).
Results
T allele was present in the RA group more frequently (22.5% vs. 10% respectively in controls). The C allele was less frequent in the RA group (77.7% vs. 90% respectively in controls) (P = 0.002). Homozygous genotype (CC) was found in 61.2% of patients and 82.5% of controls, homozygous genotype (TT) in 6.3% of patients, and 2.5% of controls while heterozygous (CT) genotype in 32.5% of patients and 15% of controls (P = 0.011). Grade 1 PDUS was found in 30.6% of CC and 11.5% of CT and not found in TT genotypes. The grade 2 was found in 69.4%, 65.4%, and only 20% of CC, CT, and TT genotypes, respectively. The grade 3 was found in 80% of TT, 23.1% of CT, and none of CC genotypes (P < 0.001).
Conclusion
An association between VEGF gene SNP rs3025039 and increased risk for RA among a sample of Egyptian population was noticed. VEGF gene polymorphism appears to be a potential diagnostic activity indicator and a promising therapeutic target for RA patients.
Study of active controlled tocilizumab monotherapy for rheumatoid arthritis patients with an inadequate response to methotrexate (SATORI): significant reduction in disease activity and serum vascular endothelial growth factor by IL-6 receptor inhibition therapy
