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The −308 G/A polymorphism in the tumor necrosis factor‐α gene is not associated with development and progression of rheumatoid arthritis in A rgentinean patients
Author(s) -
Aranda Federico,
Perés Wingeyer Silvia D.,
Schneeberger Emilce,
Valerio María,
Saint Martin Emilia,
Dal Pra Fernando,
Correa María de los Ángeles,
Citera Gustavo,
Martínez Liliana,
Mannucci Pablo,
Remondino Graciela,
Larrañaga Gabriela F.
Publication year - 2016
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.12343
Subject(s) - medicine , rheumatoid arthritis , allele , genotype , cohort , immunology , tumor necrosis factor alpha , rheumatology , gene polymorphism , allele frequency , gastroenterology , oncology , gene , genetics , biology
Aim A polymorphism in the tumor necrosis factor‐alpha ( TNF ‐α) promoter region has been associated with disease susceptibility and progression in rheumatoid arthritis ( RA ). The presence of an adenosine ( TNF 2 allele) instead of a guanine ( TNF 1 allele) at position −308 may be responsible for a general increase in the transcriptional activity of the TNF ‐α gene. Our aim was to evaluate the association of the TNF 2 allele with the risk of disease development and/or progression of RA in an Argentine population cohort. Methods Two hundred and twenty‐three consecutive patients with RA according to the 1987 criteria of the A merican C ollege of R heumatology were included in the study. Clinical variables, D isease A ctivity Score 28, H ealth A ssessment Q uestionnaire and R heumatoid A rthritis Q uality of L ife were recorded. The radiographic erosions were determined by the method of S harp/van der H eijde. A group of 111 healthy subjects matched by sex and age was used as a control. All samples were genotyped for the −308 G/A TNF ‐α polymorphism. Results No significant differences were observed either in the frequency of the TNF 2 allele or in the genotypic distributions of the −308 G/A TNF ‐α polymorphism ( P  >   0.05) between the control group and the RA patients. No association was found between the TNF 2 allele and the variables related to the course and outcome of the disease ( P  >   0.05). Conclusion In this cohort of Argentinean patients with RA , the TNF 2 allele was neither associated with susceptibility to the disease nor was it associated with the variables related to the course and outcome of the disease.

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