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, J. Cuenca, A. Cruzat, H. Gatica, I. Schiattino, C. Pérez, A. Aguirre, F. Salazar-Onfray, J. C. Aguillón

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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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