TNF-α-308 promoter polymorphism in patients with rheumatoid arthritis.
A Pawlik, M Florczak, L Ostanek… - Scandinavian …, 2005 - search.ebscohost.com
A Pawlik, M Florczak, L Ostanek, M Brzosko, I Brzosko, BG Szklarz
Scandinavian journal of rheumatology, 2005•search.ebscohost.comObjectives: Rheumatoid arthritis (RA) is a chronic inflammatory disease in which tumour
necrosis factor-α (TNF-α) plays an important role. There are, however, controversial reports
that TNF-α promoter polymorphism may be an independent marker of susceptibility and
severity of RA. The aim of the present study was to examine the TNF-α-308 promoter
polymorphism in patients with RA. Methods: We examined 91 patients with RA diagnosed
according to the criteria of the American College of Rheumatology. Polymerase chain …
necrosis factor-α (TNF-α) plays an important role. There are, however, controversial reports
that TNF-α promoter polymorphism may be an independent marker of susceptibility and
severity of RA. The aim of the present study was to examine the TNF-α-308 promoter
polymorphism in patients with RA. Methods: We examined 91 patients with RA diagnosed
according to the criteria of the American College of Rheumatology. Polymerase chain …
Abstract
Objectives: Rheumatoid arthritis (RA) is a chronic inflammatory disease in which tumour necrosis factor-α (TNF-α) plays an important role. There are, however, controversial reports that TNF-α promoter polymorphism may be an independent marker of susceptibility and severity of RA. The aim of the present study was to examine the TNF-α-308 promoter polymorphism in patients with RA. Methods: We examined 91 patients with RA diagnosed according to the criteria of the American College of Rheumatology. Polymerase chain reaction (PCR) amplification was used for analysis of the polymorphism at position-308 in promoter of TNF-α gene. Results: Distribution of TNF-α genotypes in RA patients did not differ from that in control subjects. Moreover, there was no association between TNF-α genotypes and age at disease diagnosis, disease activity in global physician's assessment, and joint and extra-articular involvement. There was also no correlation between TNF-α polymorphism and disease activity measures, including erythrocyte sedimentation rate (ESR), CRP, number of swollen and tender joints, and morning stiffness duration. Conclusions: We suggest that TNF-α-308 promoter polymorphism is not a genetic risk factor for RA susceptibility and severity.
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