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Drs. Hoffman and Merkel have also been investigators of studies evaluating anti–tumor necrosis factor (anti-TNF) therapies in Wegener's granulomatosis and giant cell arteritis, which were partially funded by Centocor, Immunex, and Amgen. Dr. Brasington has also been an investigator of a study evaluating the role of anti-TNF therapy in rheumatoid arthritis, which was funded by Amgen, and has received speaker's fees from Immunex, Amgen, and Centocor.
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Research Article
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Anti–tumor necrosis factor therapy in patients with difficult to treat Takayasu arteritis
Article first published online: 6 JUL 2004
DOI: 10.1002/art.20300
Copyright © 2004 by the American College of Rheumatology
Additional Information
How to Cite
Hoffman, G. S., Merkel, P. A., Brasington, R. D., Lenschow, D. J. and Liang, P. (2004), Anti–tumor necrosis factor therapy in patients with difficult to treat Takayasu arteritis. Arthritis & Rheumatism, 50: 2296–2304. doi: 10.1002/art.20300
Publication History
- Issue published online: 6 JUL 2004
- Article first published online: 6 JUL 2004
- Manuscript Accepted: 1 MAR 2004
- Manuscript Received: 13 NOV 2003
Funded by
- National Institute of Arthritis and Musculoskeletal and Skin Diseases. Grant Number: K24 AR-2224-01A1
- Abstract
- Article
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- Cited By
Abstract
Objective
Granulomatous inflammation is a typical feature of Takayasu arteritis (TA), and tumor necrosis factor (TNF) is important in the formation of granulomas. In this study, we assessed therapy with anti-TNF agents in patients with TA that was not controlled by glucocorticoid therapy or other immunosuppressants.
Methods
We conducted an open-label trial of anti-TNF therapy at 3 academic medical centers over a period of 4.25 years. Fifteen patients with active, relapsing TA (median 6 years) were selected. Seven received etanercept (later changed to infliximab in 3 patients), and 8 received infliximab. Relapses had occurred in all patients while they were receiving glucocorticoids and, in 13 patients, additional immunosuppressive drugs. No other agents were added to the treatment regimen concurrently with anti-TNF. If patients were receiving cytotoxic agents, the dosage was not increased. Clinical symptoms were recorded, and physical examinations, laboratory studies, and serial magnetic resonance imaging were performed.
Results
The median daily dose of prednisone required to maintain remission prior to anti-TNF therapy was 20 mg. Ten of the 15 patients achieved complete remission that was sustained for 1–3.3 years without glucocorticoid therapy. Four patients achieved partial remission, with a >50% reduction in the glucocorticoid requirement. At a median of 12 months of followup, the median dose of prednisone was 0. Therapy failed in 1 patient. In 9 of the 14 responders, an increase in the anti-TNF dosage was required to sustain remission. Two relapses occurred during periods when anti-TNF therapy (etanercept) was interrupted, but remission was reestablished upon reinstitution of therapy.
Conclusion
In this pilot study of relapsing TA, addition of anti-TNF therapy resulted in improvement in 14 of 15 patients and sustained remission in 10 of 15 patients, who were able to discontinue glucocorticoid therapy. Anti-TNF may be a useful adjunct to glucocorticoids in the treatment of TA. Our results justify a randomized, controlled clinical trial of anti-TNF therapy for TA.