title: Remission induction in Behçet's disease following lymphocyte depletion by the anti-CD52 antibody CAMPATH 1-H.
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 Immunosuppressives were withdrawn and prednisolone reduced according to clinical status.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.
authors.affiliation: Department of Medicine, School of Clinical Medicine, University of Cambridge, UK.
authors.forename: C M
authors.initials: CM
authors.lastname: Lockwood
authors.forename: G
authors.initials: G
authors.lastname: Hale
authors.forename: H
authors.initials: H
authors.lastname: Waldman
authors.forename: D R W
authors.initials: DR
authors.lastname: Jayne
mesh_terms: D000293:Adolescent; D000328:Adult; D000074323:Alemtuzumab; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001528:Behcet Syndrome / Q000188:drug therapy* / Q000276:immunology; D018791:CD4 Lymphocyte Count; D018572:Disease-Free Survival; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007166:Immunosuppressive Agents / Q000008:administration & dosage / Q000627:therapeutic use; D008212:Lymphocyte Depletion / Q000379:methods*; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000008:administration & dosage / Q000627:therapeutic use; D012074:Remission Induction; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D018501:Antirheumatic Agents; D007166:Immunosuppressive Agents; D000074323:Alemtuzumab; D011239:Prednisolone