INVESTIGATION OF THE FREQUENCY OF FC GAMMA RECEPTOR IIIA V/158/F GENE POLYMORPHISM AND COMPARISON OF CLINICAL AND LABORATORY FINDINGS IN RHEUMATOID ARTHRITIS (RA)

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<div><!--block-->Objective: Rheumatoid Arthritis (RA) is a chronic multisystem disease with unknown etiology that progressively affects peripheral joints. Receptors, which serve as links between humoral and cellular immune responses, recognize the Fc region of immunoglobulin G (FcR) and have become the focus of many research studies concerning the etiology and pathogenesis of autoimmune diseases. This region displays extensive genetic variation, which has been associated with susceptibility to various chronic inflammatory disorders including RA. This study aimed to investigate the frequency of the FcγRIIIA V158F genetic polymorphism and compare clinical and laboratory findings in RA.&nbsp;<br><br>Materials and Methods: Between April 2010 and June 2011, 105 patients, who had been diagnosed with RA according to the American Rheumatology Association (ARA) diagnostic criteria, were admitted to the Cukurova University Department of Rheumatology outpatient clinic and 110 healthy controls were included in this study. Patient groups were divided into stages using the ARA functional classification. The FcγRIIIA V158F gene polymorphism of patients was investigated from blood samples using the real-time Polymerase Chain Reaction (PCR) method.&nbsp;<br><br>Results: There was no significant difference in the distribution of the FcγRIIIA polymorphism between patients and controls (p=.106). There were no significant differences between the distribution of age at diagnosis of patients with the gene polymorphism (p=.919) or in the gene polymorphism (p=.552). No association was found between the gene polymorphism and clinical signs of disease such as eye involvement and the presence of rheumatoid nodules. There was also no significant association between the gene polymorphism with rheumatoid factor, anticyclic citrullinated peptide, and antinuclear antibodies (p=.625, p=.136, p=.716, respectively).&nbsp;<br><br>Conclusion: In our study, no significant relationship was found between the FcγRIIIA V158F gene polymorphism and the pathogenesis of RA.&nbsp;</div>