OBJECTIVE: Rheumatoid arthritis (RA) is chronic inflammatory disease in which cytokines play an important role. The aim of present study was to evaluate the exon 5 +3953 IL-1beta and IL-2 -330 promoter polymorphisms in patients with RA in association with disease activity and severity. METHODS: In the study 93 patients with rheumatoid arthritis diagnosed according to the criteria of American College of Rheumatology were included. Polymerase chain reaction amplification was used for analysis of the polymorphisms studied. RESULTS: The distribution of IL-1beta and IL-2 genotypes in RA patients did not differ from control subjects. Nevertheless in patients with A2 allele of IL-1beta and GG genotype of IL-2, the active form of RA was more frequently diagnosed. Moreover in these patients the measurements of disease activity (DAS 28 score, ESR, number of swollen and tender joints) were significantly increased. CONCLUSION: We suggest that exon 5 +3953 IL1beta and IL-2 -330 promoter polymorphisms may be a genetic risk factor for RA severity.
OBJECTIVE:Rheumatoid arthritis (RA) is chronic inflammatory disease in which cytokines play an important role. The aim of present study was to evaluate the exon 5 +3953 IL-1beta and IL-2 -330 promoter polymorphisms in patients with RA in association with disease activity and severity. METHODS: In the study 93 patients with rheumatoid arthritis diagnosed according to the criteria of American College of Rheumatology were included. Polymerase chain reaction amplification was used for analysis of the polymorphisms studied. RESULTS: The distribution of IL-1beta and IL-2 genotypes in RApatients did not differ from control subjects. Nevertheless in patients with A2 allele of IL-1beta and GG genotype of IL-2, the active form of RA was more frequently diagnosed. Moreover in these patients the measurements of disease activity (DAS 28 score, ESR, number of swollen and tender joints) were significantly increased. CONCLUSION: We suggest that exon 5 +3953 IL1beta and IL-2 -330 promoter polymorphisms may be a genetic risk factor for RA severity.