S. BLANCHE, M.D.; F. Le DEIST, M.D.; F. VEBER, M.D.; G. LENOIR, M.D.; A.M. FISCHER, M.D.; J. BROCHIER, Ph.D.; C. BOUCHEIX, Ph.D.; M. DELAAGE, M.D.; C. GRISCELLI, M.D.; A. FISCHER, M.D.
We treated two children who developed Epstein-Barr virus-induced polyclonal B-cell proliferation after HLA-mismatched bone marrow transplantation for congenital immunodeficiency with two monoclonal anti-B-cell antibodies. Lymphoproliferative syndrome occurred between 50 and 60 days after bone marrow infusion, and was diagnosed by the presence of spontaneously growing B cells containing Epstein-Barr nuclear antigen in the blood and bone marrow. The mouse monoclonal anti-B-cell antibodies used were a CD21-specific antibody recognizing the CR2 receptor on B cells (BL13, lgG1) and a CD24-specific antibody binding B cells at all steps of differentiation (ALB9 lgG1). Both antibodies were given intravenously (0.2 mg/kg/body weight · d for 10 days). All clinical and biological manifestations resolved within 3 weeks of treatment. Recurrence was not seen at 18- and 15-month follow-ups. T-cell function developed normally; B-cell function remained partially deficient in one patient 21 months after bone marrow transplantation. These results suggest that monoclonal anti-B-cell antibodies could be useful in controlling severe polyclonal lymphoproliferative syndrome in profoundly immunodeficient patients after bone marrow transplantation.
BLANCHE S, Le DEIST F, VEBER F, LENOIR G, FISCHER A, BROCHIER J, et al. Treatment of Severe Epstein-Barr Virus-Induced Polyclonal B-Lymphocyte Proliferation by Anti-B-Cell Monoclonal Antibodies: Two Cases After HLA-Mismatched Bone Marrow Transplantation. Ann Intern Med. 1988;108:199–203. doi: 10.7326/0003-4819-108-2-199
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Published: Ann Intern Med. 1988;108(2):199-203.
Hematology/Oncology, Infectious Disease.
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