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DOI 10.1093/rheumatology/kem235

Медицинская библиотека · Rheumatology (Oxford, England) · 2007

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

Chang S-J, Tsai P-C, Chen C-J, Lai H-M, Ko Y-C

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Аннотация

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.

Для цитирования: Chang S-J, Tsai P-C, Chen C-J, Lai H-M, Ko Y-C. The polymorphism -863C/A in tumour necrosis factor-alpha gene contributes an independent association to gout.. Rheumatology (Oxford, England). 2007. DOI: 10.1093/rheumatology/kem235.

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