Rheumatology Advance Access originally published online on August 29, 2003
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Rheumatology 2003; 42: 1539-1544
© 2003 British Society for Rheumatology
Remission induction in Behçet’s disease following lymphocyte depletion by the anti-CD52 antibody CAMPATH 1-H
Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, 1Therapeutic Antibody Centre and 2Dunn School of Pathology, University of Oxford, Oxford, UK.
Correspondence to:
D. R. W. Jayne, Box 157 Department of Medicine, School of Clinical Medicine, Hills Road, Cambridge CB2 2SP, UK. E-mail: dj106{at}cam.ac.uk
Objective. Behçet’s disease (BD) is a multisystem vasculopathy of unknown cause with variable clinical presentation and the outcome of current treatments is often unsatisfactory. There is evidence for T-cell autoreactivity in BD and this study explores the therapeutic response to lymphocyte depletion with a humanized anti-CD52 antibody, CAMPATH-1H.
Methods. Eighteen patients with active BD received a single course of 134 mg of CAMPATH-1H. Immunosuppressives were withdrawn and prednisolone reduced according to clinical status. Treatment response was assessed by remission of clinical features of disease activity, erythrocyte sedimentation rate, C-reactive protein, prednisolone dose, the need for subsequent immunosuppressives and disease relapse.
Results. By 6 months, 13/18 (72%) had entered remission and average, daily prednisolone dose was reduced from 17.7 to 6.7 mg/day (P < 0.005). At patient follow-up after 37 (6–60) months, seven had relapsed after an average of 25 months, five had required the introduction of an immunosuppressive drug and two had been retreated with CAMPATH-1H; 10 were in stable remission and six were receiving no therapy. Moderate infusion-related adverse effects occurred in five and two developed hypothyroidism. Circulating CD4+ T cells fell to low levels after CAMPATH-1H and remained depressed for at least 1 yr; no opportunistic infections were seen.
Conclusions. The therapeutic response to CAMPATH-1H suggests a central role for autoreactive lymphocytes in BD. The potential of CAMPATH-1H to induce sustained treatment-free remission in BD poorly controlled by conventional therapy requires further evaluation.
KEY WORDS: Behçet’s disease, Lymphocyte depletion, T cell, Monoclonal antibody, CAMPATH-1H, CD52, Therapy.
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