CAMPATH-1H in the treatment of autoimmune cytopenias.
BACKGROUND
The autoimmune cytopenias encompass the disorders of immune thrombocytopenia purpura (ITP), pure red-cell aplasia (PRCA), autoimmune hemolytic anemia (AIHA), autoimmune neutropenia and various combinations of these conditions. T lymphocytes are thought to play an important role in the pathogenesis of autoimmune cytopenias, and the presence of autoantibody may represent an epiphenomenon, rather than the primary pathogenetic mechanism. The majority of patients usually respond to standard immunosuppressive therapy and can mostly be treated as out-patients. A small proportion, however, have severe, resistant and life-threatening disease, or may experience major morbidity from side effects of drugs given to treat their disease.


METHODS
We have treated 21 patients with autoimmune cytopenias with the MAb Campath-1H, and for later patients in this series, in combination with low dose CYA.


RESULTS
Responses were seen in 14 of 20 evaluable patients, although relapse occurred in seven patients. In many patients corticosteroid therapy could be discontinued or greatly reduced.


CONCLUSIONS
We conclude that Campath-1H can induce remissions in autoimmune cytopenias and we critically review its role in the treatment of these disorders.
Marsh
J C
JC
Department of Haematology, St George's Hospital Medical School, London, UK.
Gordon-Smith
E C
EC
D000293:Adolescent; D000328:Adult; D000368:Aged; D000074323:Alemtuzumab; D000743:Anemia, Hemolytic / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm / Q000008:administration & dosage / Q000009:adverse effects / Q000627:therapeutic use*; D015703:Antigens, CD / Q000187:drug effects / Q000276:immunology; D000951:Antigens, Neoplasm / Q000187:drug effects / Q000276:immunology; D001323:Autoantibodies / Q000187:drug effects / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D000074301:CD52 Antigen; D005260:Female; D006023:Glycoproteins / Q000187:drug effects / Q000276:immunology; D006402:Hematologic Diseases / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007165:Immunosuppression Therapy / Q000009:adverse effects / Q000379:methods* / Q000639:trends; D008297:Male; D008875:Middle Aged; D009026:Mortality; D009503:Neutropenia / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D010865:Pilot Projects; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D012010:Red-Cell Aplasia, Pure / Q000276:immunology / Q000503:physiopathology / Q000628:therapy; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000912:Antibodies, Neoplasm; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D001323:Autoantibodies; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D000074323:Alemtuzumab