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Mediators of Inflammation
Volume 2017, Article ID 3708250, 7 pages
Research Article

Methotrexate Reduced TNF Bioactivity in Rheumatoid Arthritis Patients Treated with Infliximab

1Department of Rheumatology, CHU Saint-Etienne, Saint-Etienne, France
2Immunology and Immunomonitoring Department, CHU de Saint-Etienne, Saint-Etienne, France
3INSERM 1059/SAINBIOSE, Université Jean Monet, Université de Lyon, Saint-Etienne, France

Correspondence should be addressed to Hubert Marotte; rf.enneite-ts-uhc@ettoram.trebuh

Received 12 October 2016; Accepted 6 February 2017; Published 2 March 2017

Academic Editor: Ronald Gladue

Copyright © 2017 Delphine Dénarié et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objectives. To evaluate methotrexate effect on tumor necrosis factor (TNF) alpha bioactivity during infliximab (IFX) therapy in rheumatoid arthritis (RA) patients and to correlate TNF bioactivity with antibody towards IFX (ATI) development and RA clinical response. Materials and Methods. Thirty-nine active women RA patients despite conventional synthetic disease modifying antirheumatic drugs (csDMARDs) requiring IFX therapy were enrolled, and clinical data and blood samples were recorded at baseline (W0) and at 6 weeks (W6), W22, and W54 of IFX treatment. TNF bioactivity as well as IFX trough and ATI concentrations were assessed on blood samples. Results. TNF bioactivity decreased from W0 to W54 with a large range from W22 at the time of ATI detection. From W22, TNF bioactivity was lower in presence of methotrexate as csDMARD compared to other csDMARDs. IFX trough concentration increased from W0 to W54 with a large range from W22, similarly to TNF bioactivity. Methotrexate therapy prevented ATI presence at W22 and reduced TNF bioactivity compared to other csDMARDs (). Conclusion. This suggests that methotrexate plays a key role in TNF bioactivity and against ATI development.