Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis

Introduction Multifunctional pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) has been implicated in a variety of inflammatory diseases including rheumatoid arthritis (RA). TNF-α polymorphisms are mostly located in its promoter region and play a significant role in disease susceptibility an...

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Autores principales: Tayyaba Sadaf, Peter John, Attya Bhatti, Javaid M. Malik
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Publicado: Termedia Publishing House 2019
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spelling oai:doaj.org-article:a0694443d9a44e6c90e0cbb7d82242012021-12-02T19:15:42ZLack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis1734-19221896-915110.5114/aoms.2018.76946https://doaj.org/article/a0694443d9a44e6c90e0cbb7d82242012019-03-01T00:00:00Zhttps://www.archivesofmedicalscience.com/Lack-of-association-of-863C-A-rs1800630-polymorphism-of-tumor-necrosis-factor-gene,68764,0,2.htmlhttps://doaj.org/toc/1734-1922https://doaj.org/toc/1896-9151Introduction Multifunctional pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) has been implicated in a variety of inflammatory diseases including rheumatoid arthritis (RA). TNF-α polymorphisms are mostly located in its promoter region and play a significant role in disease susceptibility and severity. We therefore sought to investigate TNFA –863C/A (rs1800630) polymorphism association with RA activity in our Pakistani study group. Material and methods A total of 268 human subjects were enrolled. Among them, 134 were RA patients and 134 were controls. In this study the physical parameters of RA patients were collected, and the disease activity was measured by DAS28. The genotypes were determined following the allele-specific PCR along with the pre-requisite internal amplification controls. Subsequently, data were analyzed statistically for any significant association including χ 2 /Fisher’s exact test using GraphPad prism 6 software. Results We found that the TNF-α –863 C/A (rs1800630) variant was not differentially segregated between cases and controls in either genotype frequency, with χ2 of 2.771 and a p-value of 0.2502, or allele frequency, with χ2 of 2.741 and a p-value of 0.0978, with an odds ratio (95% CI) of 0.7490 (0.5317–1.055). Conclusions The lack of positive association of TNF-α –863(rs1800630) polymorphism in our study group implies that TNF-α –863 polymorphism is not a susceptible marker to RA and cannot serve as a genetic factor for screening RA patients in Pakistan. There might be other factors that may influence disease susceptibility. However, further investigations on additional larger and multi-regional population samples are required to determine the consequences of genetic variations for disease prognosis.Tayyaba SadafPeter JohnAttya BhattiJavaid M. MalikTermedia Publishing Housearticlerheumatoid arthritispolymorphismassociation studytumor necrosis factor-alphaMedicineRENArchives of Medical Science, Vol 15, Iss 2, Pp 531-536 (2019)
institution DOAJ
collection DOAJ
language EN
topic rheumatoid arthritis
polymorphism
association study
tumor necrosis factor-alpha
Medicine
R
spellingShingle rheumatoid arthritis
polymorphism
association study
tumor necrosis factor-alpha
Medicine
R
Tayyaba Sadaf
Peter John
Attya Bhatti
Javaid M. Malik
Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
description Introduction Multifunctional pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) has been implicated in a variety of inflammatory diseases including rheumatoid arthritis (RA). TNF-α polymorphisms are mostly located in its promoter region and play a significant role in disease susceptibility and severity. We therefore sought to investigate TNFA –863C/A (rs1800630) polymorphism association with RA activity in our Pakistani study group. Material and methods A total of 268 human subjects were enrolled. Among them, 134 were RA patients and 134 were controls. In this study the physical parameters of RA patients were collected, and the disease activity was measured by DAS28. The genotypes were determined following the allele-specific PCR along with the pre-requisite internal amplification controls. Subsequently, data were analyzed statistically for any significant association including χ 2 /Fisher’s exact test using GraphPad prism 6 software. Results We found that the TNF-α –863 C/A (rs1800630) variant was not differentially segregated between cases and controls in either genotype frequency, with χ2 of 2.771 and a p-value of 0.2502, or allele frequency, with χ2 of 2.741 and a p-value of 0.0978, with an odds ratio (95% CI) of 0.7490 (0.5317–1.055). Conclusions The lack of positive association of TNF-α –863(rs1800630) polymorphism in our study group implies that TNF-α –863 polymorphism is not a susceptible marker to RA and cannot serve as a genetic factor for screening RA patients in Pakistan. There might be other factors that may influence disease susceptibility. However, further investigations on additional larger and multi-regional population samples are required to determine the consequences of genetic variations for disease prognosis.
format article
author Tayyaba Sadaf
Peter John
Attya Bhatti
Javaid M. Malik
author_facet Tayyaba Sadaf
Peter John
Attya Bhatti
Javaid M. Malik
author_sort Tayyaba Sadaf
title Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
title_short Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
title_full Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
title_fullStr Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
title_full_unstemmed Lack of association of –863C/A (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
title_sort lack of association of –863c/a (rs1800630) polymorphism of tumor necrosis factor-α gene with rheumatoid arthritis
publisher Termedia Publishing House
publishDate 2019
url https://doaj.org/article/a0694443d9a44e6c90e0cbb7d8224201
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