Meta-analysis of SLC22A4 and RUNX1 polymorphisms Associations with rheumatoid arthritis susceptibility
- Authors
- Lee, Y. H.; Bae, S. -C.; Kim, J. -H.; Seo, Y. H.; Choi, S. J.; Ji, J. D.; Song, G. G.
- Issue Date
- May-2015
- Publisher
- SPRINGER HEIDELBERG
- Keywords
- Ethnicity; Gene frequency; Inflammation; Autoimmune diseases; Literature review
- Citation
- ZEITSCHRIFT FUR RHEUMATOLOGIE, v.74, no.4, pp 351 - 358
- Pages
- 8
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- ZEITSCHRIFT FUR RHEUMATOLOGIE
- Volume
- 74
- Number
- 4
- Start Page
- 351
- End Page
- 358
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/7915
- DOI
- 10.1007/s00393-014-1447-3
- ISSN
- 0340-1855
1435-1250
- Abstract
- Objective. The aim in this study was to determine whether solute carrier family 22, member 4 (SLC22A4), and runt-related transcription factor 1 (RUNX1) polymorphisms are associated with susceptibility to rheumatoid arthritis (RA) in populations of different ethnicities. Methods. We conducted a literature search using the MEDLINE and EMBASE, and performed a meta-analysis using a fixed or random effects model. Results. A total of 26 comparative studies from 14 articles met the study inclusion criteria. Studies on the SLC22A4 polymorphism involved 12,458 RA patients and 9283 controls, and studies on the RUNX1 polymorphism involved 3958 RA patients and 3773 controls. The meta-analysis showed no association be-tween the 22+21 genotype of the SLC22A4 F1 and RA in overall group [odds ratio (OR) 1.074, 95% confidence interval (CI) 0.952-1.212, p=0.245]. After stratification by ethnicity, the meta-analysis indicated that the 22+21 genotype of the SLC22A4 F1 was associated significantly with RA in the East Asian population, but not in the European population (OR 1.124, 95% CI 1.018-1.240, p=0.021; OR 0.981, 95% CI 0.773-1.243, p=0.871). Conclusion. This meta-analysis demonstrates that the SLC22A4 F1 polymorphism is associated with susceptibility to RA in East Asians, but not in Europeans.
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- Appears in
Collections - 2. Clinical Science > Department of Rheumatology > 1. Journal Articles
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