Abstract
We conducted 2 sequential studies of donor leukocyte infusion (DLI) in 26 patients with chronic myeloid leukemia in hematologic relapse after unmodified allogeneic bone marrow transplantation. In the first study, cells for DLI were collected from 13 donors who were not treated with granulocyte colony-stimulating factor (G-CSF) (group 1). In the second study, cells were collected from 13 donors who received G-CSF before apheresis (group 2) in an attempt to avoid aplasia after DLI. Patients in group 2 received 550-fold more CD34+ cells than those in group 1. We found no significant difference in the incidence (31% versus 22%), onset time (41 vs. 48 days), or duration (15 vs. 14 days) of cytopenia after DLI in the 2 groups. G-CSF given to donors before collection of cells did not prevent aplasia. These findings support the hypothesis that the pathogenesis of aplasia after DLI is not restricted to the destruction of recipient hematopoietic cells but also involves failure of donor hematopoiesis by undefined mechanisms.
Publication types
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Comparative Study
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Evaluation Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adolescent
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Adult
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Anemia, Aplastic / etiology
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Anemia, Aplastic / prevention & control*
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Biomarkers, Tumor / analysis
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Blood Component Removal*
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Blood Donors*
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Bone Marrow Transplantation*
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Child
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Combined Modality Therapy
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Female
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Fusion Proteins, bcr-abl / blood
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Graft Rejection*
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Graft vs Host Disease / etiology
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Granulocyte Colony-Stimulating Factor / administration & dosage
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Granulocyte Colony-Stimulating Factor / therapeutic use*
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Hematopoietic Stem Cell Mobilization*
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Hematopoietic Stem Cell Transplantation*
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Humans
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Interferon-alpha / therapeutic use
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / blood
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy*
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Leukocyte Transfusion / adverse effects*
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Male
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Middle Aged
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Neoplasm Proteins / blood
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Premedication*
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Recurrence
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Salvage Therapy*
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Treatment Outcome
Substances
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Biomarkers, Tumor
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Interferon-alpha
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Neoplasm Proteins
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Granulocyte Colony-Stimulating Factor
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Fusion Proteins, bcr-abl