Influence of TNF-α gene polymorphisms in coronary artery calcification in psoriasis patients

Psoriasis is a systemic inflammatory disorder associated with numerous medical comorbidities and increased risk of cardiovascular disease (CVD. Psoriasis’ systemic inflammation may play an important role in the accelerated atherosclerosis observed in these patients2 as inflammatory processes play a key role in atherogenesis. Psoriasis and atherosclerosis share some pathological features including endothelial dysfunction, alteration in angiogenesis and some inflammatory pathways. TNF-a is a potent pro-inflammatory cytokine that has been implicated in psoriasis and atherosclerosis pathogenesis and its synthesis is tightly regulated at gene transcription level. TNF-a gene promoter region contains several single-nucleotide polymorphisms (SNP) that influence TNF-a production. Several TNF-a gene polymorphisms have been associated with psoriasis and CVD. A recent meta-analysis suggested that TNF-a rs1800629(308G/A) polymorphism was associated with decreased risk of psoriasis, whereas TNF-a rs361525(238G/A) was associated with increased risk. Regarding TNF-a rs1799964 (1031T/C) polymorphism, existing data are limited and contradictory.8 Since psoriasis morbidity and mortality are strongly linked to accelerated atherosclerosis, determining the genetic contribution for cardiovascular morbidity in psoriasis patients becomes an issue of major importance. The aim of this study was to evaluate the contribution of TNF-a rs361525(238G/A), TNF-a rs1800629(308G/A) and TNFa rs1799964(1031T/C) gene polymorphisms to coronary artery calcification (CAC) in severe psoriasis patients.