Tumor necrosis factor inhibitors in patients with Takayasu arteritis: experience from a referral center with long-term followup.
OBJECTIVE
To report a single-center experience with the use of tumor necrosis factor (TNF) inhibitors in patients with Takayasu arteritis (TA).


METHODS
We retrospectively studied a cohort of patients with refractory TA evaluated at our institution and treated with TNF inhibitors. American College of Rheumatology criteria for TA were used for inclusion. Disease activity was assessed according to the National Institutes of Health criteria.


RESULTS
We included 20 patients (19 women, 17 white) with a mean ± SD age of 33 ± 10.2 years and a median disease duration of 15.9 months (interquartile range [IRQ] 2-32.7 months) prior to the use of TNF inhibitors. Before the use of TNF inhibitors, all 20 patients received prednisone. Other medication use included methotrexate (18 patients), azathioprine (5 patients), mycophenolate mofetil (3 patients), and cyclophosphamide (3 patients). Seventeen patients (85%) received infliximab, 2 patients (10%) received adalimumab, and 1 patient (5%) received etanercept. The median duration of treatment with TNF inhibitors was 23.0 months (IQR 8.7-38.9 months). Treatment with TNF inhibitors resulted in disease remission in 18 (90%) of 20 patients and sustained remission in 10 patients (50%). Ten (83%) of 12 patients were able to taper prednisone below 10 mg and 7 patients discontinued prednisone. However, 6 of the 18 patients achieving remission experienced relapse while receiving TNF inhibitors. Eleven patients (55%) discontinued TNF inhibitors for the following reasons: relapse, persistently active disease, lack of corticosteroid-sparing effect, adverse effects (4 patients), and other reasons (4 patients).


CONCLUSIONS
In this study, treatment with TNF inhibitors induced remission, including sustained remission in patients with refractory TA. However, 33% of patients experienced disease relapse while receiving TNF inhibitors and 20% discontinued treatment because of adverse events.
Mayo Clinic, Rochester, Minnesota, USA. schmidt.jean@chu-amiens.fr
Jean
J
Schmidt
Tanaz A
TA
Kermani
A Kirstin
AK
Bacani
Cynthia S
CS
Crowson
Eric L
EL
Matteson
Kenneth J
KJ
Warrington
D000068879:Adalimumab; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects / Q000627:therapeutic use*; D000069285:Infliximab; D008137:Longitudinal Studies; D008297:Male; D011241:Prednisone / Q000627:therapeutic use; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012008:Recurrence; D012074:Remission Induction; D012189:Retrospective Studies; D013625:Takayasu Arteritis / Q000188:drug therapy*; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D011241:Prednisone