Treatment With Anti–Tumor Necrosis Factor Biologic Agents in Human T Lymphotropic Virus Type I–Positive Patients With Rheumatoid Arthritis
Article first published online: 22 APR 2014
Copyright © 2014 by the American College of Rheumatology
Arthritis Care & Research
Volume 66, Issue 5, pages 788–792, May 2014
How to Cite
Umekita, K., Hidaka, T., Miyauchi, S., Ueno, S., Kubo, K., Takajo, I., Hashiba, Y., Kai, Y., Nagatomo, Y. and Okayama, A. (2014), Treatment With Anti–Tumor Necrosis Factor Biologic Agents in Human T Lymphotropic Virus Type I–Positive Patients With Rheumatoid Arthritis. Arthritis Care Res, 66: 788–792. doi: 10.1002/acr.22205
- Issue published online: 22 APR 2014
- Article first published online: 22 APR 2014
- Accepted manuscript online: 14 OCT 2013 11:32AM EST
- Manuscript Accepted: 8 OCT 2013
- Manuscript Received: 3 APR 2013
To investigate the response to and safety of anti–tumor necrosis factor (anti-TNF) therapy in human T lymphotropic virus type I (HTLV-I)–positive patients with rheumatoid arthritis (RA).
Therapeutic response was evaluated in 10 HTLV-I–positive and 20 HTLV-I–negative patients with RA (sex and age matched) at 3 months after the beginning of anti-TNF therapy using the European League Against Rheumatism improvement criteria. As secondary end points, the discontinuation rate of anti-TNF therapy and its safety, especially the development of adult T cell leukemia (ATL), were evaluated over a 2-year period.
Significantly higher baseline levels of C-reactive protein (CRP) were observed in HTLV-I–positive patients than in HTLV-I–negative patients (P = 0.0003). The response rate to anti-TNF therapy was lower in HTLV-I–positive patients than in HTLV-I–negative patients. The median CRP level, erythrocyte sedimentation rate, and Disease Activity Score in 28 joints at 3 months after anti-TNF treatment in HTLV-I–positive patients were significantly higher than in HTLV-I–negative patients (P = 0.003, P = 0.03, and P = 0.003, respectively). The discontinuation rate due to insufficient response was significantly higher in HTLV-I–positive patients than in HTLV-I–negative patients (P = 0.013). During the 2-year observation period, no patients developed ATL.
These data suggest that HTLV-I–positive patients with RA had higher inflammation and greater resistance to anti-TNF treatment than HTLV-I–negative patients. Further study is necessary to determine whether HTLV-I infection should be measured when anti-TNF agents are administered to patients with RA, especially in areas were HTLV-I is endemic.