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Remission of Behçet's syndrome with TNFα blocking treatment
  1. M Rozenbaum,
  2. I Rosner,
  3. E Portnoy
  1. Department of Rheumatology, Bnai Zion Medical Centre, Technion Faculty of Medicine, Haifa, Israel
  1. Correspondence to:
    Dr Rosner;
    rosner{at}tx.technion.ac.il

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Goossens et al reported on a patient in whom a remission of Behçet's syndrome was induced with tumour necrosis factor (TNF) blocking treatment.1 We would like to add our experience in a patient with Behçet's disease associated with rheumatoid arthritis (RA), treated with infliximab (Remicade).

A 47 year old male patient, born in Morocco, living in Israel, was diagnosed 14 years earlier with severe, progressive polyarthritis of hands, feet, and knees. Radiography showed articular bone erosions; rheumatoid factor was positive, with a high erythrocyte sedimentation rate and C reactive protein. In parallel, the patient reported recurrent buccal and genital ulcers two to three times a month with papulopustular skin lesions on the feet. HLA-B5 (51) was positive. There was no eye involvement. A diagnosis of Behçet's disease associated with erosive, seropositive RA was suggested. The patient was treated with sulfasalazine and colchicine without improvement; steroid treatment with auranofin was added. The disease was poorly controlled, with progressive erosions in hands, knees, and feet. Later, pulse steroids, methotrexate, azathioprine, and cyclosporin were added serially, either singly or in combination.

In subsequent years he became dependent on steroids and never achieved complete remission. In December 2000 the patient was admitted to hospital with severe active polyarthritis, flexion contractures of the elbows, and an especially swollen left knee with Baker's cyst and severe erosive disease. The patient additionally had buccal and penile ulcers. Because of the lack of response to conventional treatment we decided to treat him with infliximab (remicade; schering), a chimeric IgG monoclonal antibody directed against TNF. He received 300 mg intravenously (3 mg/kg) at intervals of two weeks, six weeks, and then every eight weeks. Two weeks after the first infusion the ulcers of mouth, penis, and other skin lesions were already considerably smaller and later disappeared. The polyarthritis improved considerably, except for the left knee, which required total replacement. Infliximab was given with continued colchicine and azathioprine. Our case, as in Goossens' report, suggests that infliximab may have a beneficial therapeutic effect in mucoserosal and cutaneous lesions as well as synovitis in Behçet's disease, in our case in association with RA.

Controlled studies will be needed to assess adequately the full effect of TNF antagonists in Behçet's disease.

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