|Home | About | Journals | Submit | Contact Us | Français|
Aberrant T cell function,1 subsequently accompanied by increased tumour necrosis factor α (TNFα) levels, induces inflammatory symptoms in patients with Behçet's disease (BD).2 Subsequently, treatment usually involves T cell‐directed immunosuppressive or anti‐TNFα treatment in patients with severe disease.3,4,5,6,7 Administration of the new human monoclonal TNFα antibody adalimumab has only been described in three patients with BD with uveitis.8 We analysed the effects of adalimumab on severe and often chronic disease in six heavily pretreated patients with BD in whom immunosuppressive therapy had failed (table 11).
These patients were treated in the past with infliximab.9 Indications for anti‐TNFα treatment were uveitis (patients 2 and 4), CNS disease (patients 3 and 5), colitis (patient 6) and severe oral ulcers and arthritis (patient 1), and are further presented in table 11.. Symptoms were scored retrospectively since no official scoring system such as the Behcet's Disease Current Activity Form (BDCAF) was available at the start of anti‐TNFα treatment in our centre.
It is unknown how long anti‐TNFα treatment must be given, but anti‐TNFα treatment in patients with rheumatic arthritis is continued for >2 years and continued until there is a settled response.10 In our patients, infliximab was discontinued after complete response of >3 months or acceptable improvement of (eye) symptoms. In five of the six patients, relapses after infliximab did not necessitate immediate restart of anti‐TNFα treatment. In this period (mean duration 562, range 136–1093 days), immunosuppressive therapy could be adjusted until the symptoms required a restart of anti‐TNFα treatment. Adalimumab was considered to be equal potential, but more convenient, and was added in cases of severe relapse with patients' informed consent. In addition, formation of autoantibodies to infliximab when restarted was considered. All patients responded and most of them showed dramatic and quick improvement. Subsequently, immunosuppressive therapy could again be tapered (table 11).
Patient 6 had a severe BD‐associated colitis and was periodically treated with infliximab and other immunosuppressive agents for nearly 3 years. Despite intensified immunosuppressive therapy, the colitis worsened and became refractory and life threatening. Subsequently, a high dose of adalimumab 40 mg/week was started subcutaneously, yielding a complete response of >1 year. Adalimumab was briefly combined with 30 mg of prednisone, which was tapered rapidly to prevent central retinal serosa ablation that developed in a previous period in which steroids had been used. Later, mesalazine and rectal budenoside were also given. Apart from some minor flares, the patient remained stable for nearly 2 years. Until now, all patients are receiving adalimumab, except patient 5 who discontinued 4 months after complete remission was achieved (table 11).). In general, few side effects were observed. Three patients (1, 3 and 6) developed lichenoid‐like lesions that were treated with local steroids by a dermatologist.
This report on patients with treatment refractory BD indicates that adalimumab treatment is promising and can be prescribed safely for a prolonged period. To our knowledge, this is the first case series in which patients with BD with systemic disease treated with adalimumab are presented. More studies on this subject are warranted.
Competing interests: PMvH has cooperated in a European study on patients with uveitis treated with infliximab that was sponsored by Centocor. JAMvL and PMvH were in part sponsored to visit the 12th international Behçet's congress in Lisbon by Abbott BV where JAMvL presented these data to the international investigators on Behçet's disease.