Skip Navigation



Rheumatology Advance Access published online on October 15, 2007

Rheumatology, doi:10.1093/rheumatology/kem235
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
46/11/1662    most recent
kem235v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Chang, S.-J.
Right arrow Articles by Ko, Y.-C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chang, S.-J.
Right arrow Articles by Ko, Y.-C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The polymorphism -863C/A in tumour necrosis factor-{alpha} gene contributes an independent association to gout

S.-J. Chang, P.-C. Tsai1, C.-J. Chen2, H.-M. Lai2 and Y.-C. Ko

Department of Public Health, Faculty of Medicine, College of Medicine, 1Institute of Public Health, College of Health Science, Kaohsiung Medical University and 2Division of Rheumatology, Allergy and Immunology, Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan

Correspondence to: S.-J. Chang, PhD, Department of Public Health, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, No. 100, Shih-Chuan 1st Road, Kaohsiung 807, Taiwan. E-mail: changsj{at}kmu.edu.tw


   Abstract

Objective. To investigate the associations between polymorphisms in the promoter of the tumour necrosis factor-{alpha} (TNF-{alpha}) gene and gout.

Methods. The polymorphisms -308G/A and -863C/A in the TNF-{alpha} gene were determined in 106 gout patients and 159 healthy controls among male Taiwanese using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) method. The biochemical markers, including Glutamic-oxaloacetic transaminase (GOT), Glutamic-pyruvic transaminase (GPT), uric acid, creatinine, total cholesterol (TC), triglycerides (TG), body mass index (BMI) and hypertension, as well as alcohol consumption were measured.

Results. The gout patients had 9.43% (10/106) with genotype AA at polymorphism -863C/A showing a significantly higher fraction than controls (0.63%; 1/159, P < 0.001). The crude results also showed that the gout patients had significantly higher portions of abnormal GOT, GPT, creatinine, TC, TG, alcohol consumption, hypertension and hyperuricaemia than controls (P < 0.05), but the -308G/A, BMI and genotype CA at -863C/A did not show the same significant difference (P > 0.05). After adjustment by a stepwise logistic regression method, the hyperuricaemia, creatinine, GPT, TG and alcohol consumption as well as genotype AA at polymorphism -863C/A were found to be significantly associated with gout.

Conclusion. The genotype AA at polymorphism -863C/A in a recessive model showed a significant association with developing gout independent of hyperuricaemia, abnormal creatinine, higher TG, GPT and alcohol consumption.

KEY WORDS: Gout, Tumour necrosis factor, Hyperuricaemia, Creatinine

Submitted 11 May 2007; revised version accepted 3 August 2007.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Rheumatology (Oxford)Home page
S.-J. Chang, C.-J. Chen, F.-C. Tsai, H.-M. Lai, P.-C. Tsai, M.-H. Tsai, and Y.-C. Ko
Associations between gout tophus and polymorphisms 869T/C and -509C/T in transforming growth factor {beta}1 gene
Rheumatology, May 1, 2008; 47(5): 617 - 621.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.