ABSTRACT
The receptor for advanced glycation end products [RAGE] has been implicated in the pathogenesis of RA through its ability to amplify inflammatory pathways. [1] To evaluate the levels of soluble receptors of advanced glycated end products [sRAGE] as well as the gene variant among patients with rheumatoid arthritis [RA]. [2] To assess the association between the sRAGE level and the RAGE gene variants and to correlate the findings with various clinical and laboratory data. All patients were fulfilling the criteria for RA described by the American College of Rheumatology. In all patients assessment of disease activity was done by DAS28-ESR. Soluble RAGE level was determined by enzymatic immunoassay. Molecular study of single nucleotide polymorphisms [SNP] in the glycine82serine [G82S] of the RAGE gene was performed. The data was collected and statistically analyzed. Serum levels of sRAGE were significantly lower in RA patients than controls [840.11 +/- 230.32 pg/ml versus 1111.59 +/- 143.20 pg/ml, p < 0.05]. Genotyping of the RAGE gene showed polymorphisms in the glycine82serine [G82S] allele which did not reach statistical significance between patients and controls. The sRAGE levels were significantly lower in RA patients with Sjogren's syndrome and in those with cardiac disease. Correlation analysis showed that the glycine82serine [G82S] allele is related to MS, CRP and sRAGE in RA patients. Also, the G82S allele was more common in patients with cardiac affection. Linear regression analysis detected CRP and gene polymorphism as significant predictors for sRAGE level. The levels of sRAGE were significantly lower in patients with RA and this reduction was correlated with the disease activity parameters and glycine82serine gene polymorphism. The sRAGE may be an important marker of disease activity. The correlation of sRAGE level and cardiac disease can suggest that RAGE activity influences the co-development of joint and vascular disease in rheumatoid arthritis patients