Tumour necrosis factor-α (TNF-α) levels and influence of -308 TNF-α promoter polymorphism on the responsiveness to infliximab in patients with rheumatoid arthritis

M. Cuchacovich, L. Ferreira, M. Aliste, L. Soto, Jimena Cuenca, A. Cruzat, H. Gatica, I. Schiattino, C. Pérez, A. Aguirre, F. Salazar-Onfray, J. C. Aguillón

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66 Scopus citations

Abstract

Objective: To investigate the influence of -308 tumour necrosis factor-α (TNF-α) promoter polymorphism and circulating TNF-α levels in the clinical response to the infliximab treatment in patients with rheumatoid arthritis (RA). Methods: One hundred and thirty-two RA patients were genotyped for TNF-α promoter by polymerase-chain reaction restriction fragment-length polymorphism (PCR-RFLP) analysis. Ten patients with the -308 TNF-α gene promoter genotype G/A, and 10 with the G/G genotype were selected and received 3 mg/kg of infliximab at Weeks 0, 2, 6, and 14. Results: Both groups showed a significant improvement with treatment in all variables studied. Total mean TNF-α levels increased significantly with respect to basal levels in most of patients after treatment [probability (p) = 0.04]. Only patients from G/A showed a statistically significant correlation between ACR 50 and the increase of TNF-α levels (p<0.03). Conclusion: A relationship was detected between ACR criteria of improvement and increased circulating TNF-α levels in RA patients subjected to anti-TNF-α therapy.

Original languageEnglish
Pages (from-to)228-232
Number of pages5
JournalScandinavian Journal of Rheumatology
Volume33
Issue number4
DOIs
StatePublished - 2004
Externally publishedYes

Bibliographical note

Funding Information:
This study was supported by FONDECYT Grant 1990936. The authors thank Schering-Plough for providing infliximab for this study.

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