Lack of association between TNFα gene polymorphism at position –308 and risk of acute rheumatic fever in Turkish patients

Abstract

Objective: Acute rheumatic fever (ARF) is a multisystem inflammatory disease process that follows nasopharyngeal infection caused by group A streptococcus (GAS) (Streptococcus pyogenes). Recent studies have demonstrated that allelic variations at the tumour necrosis factor alpha (TNFα) locus are involved in the nature of rheumatic diseases such as juvenile idiopathic arthritis and rheumatic heart disease. Thus, TNFα polymorphisms at –308 in ARF patients might be useful in contributing to identification of the primary factors associated with pathogenesis of ARF.

Methods: We performed a case–control association study between the common G/A promoter polymorphism at position –308 in the TNFα gene and ARF in Turkish patients, investigating whether this locus acts as a risk factor or has a modifying effect.

Results and Conclusion: Previous studies have reported that TNFα plays a major role in the pathogenesis of a number of autoimmune and inflammatory diseases. Moreover, significantly elevated TNFα levels were reported in patients with ARF. However, in our sample of patients with ARF (n = 66), no such association was found. No interactive effect was found between the TNFα polymorphism at position –308 and no association was detected with disease progression. These findings suggest that the role of TNFα in ARF may be in linkage disequilibrium with some other severity genes not yet genetically determined.