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Rheumatology Advance Access published online on August 29, 2003
Rheumatology, doi:10.1093/rheumatology/keg424
Rheumatology © British Society for Rheumatology 2003; all rights reserved
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© 2003 Rheumatology 42 © British Society for Rheumatology 2003; all rights reserved

Original Papers

Remission induction in Behçet's disease following lymphocyte depletion by the anti-CD52 antibody CAMPATH 1-H

C. M. Lockwood 1, G. Hale 2, H. Waldman 3, and D. R. W. Jayne 1*

1 Department of Medicine, School of Clinical Medicine, University of Cambridge, Cambridge, UK
2 Therapeutic Antibody Centre, Oxford, UK
3 Dunn School of Pathology, University of Oxford, Oxford, UK

* Corresponding author. E-mail: dj106{at}cam.ac.uk.

Received 19 December 2002 ; accepted 28 April 2003

Abstract

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 Immunosuppressives were withdrawn and prednisolone reduced according to clinical status.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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