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Epstein-Barr virus associated B cell lymphoproliferative disorders
following bone marrow transplantation
RS Shapiro, K McClain, G Frizzera, KJ Gajl-Peczalska, JH Kersey, BR Blazar, DC Arthur, DF Patton, JS Greenberg and B Burke
Department of Pediatrics, University of Minnesota Hospital and Clinic,
Minneapolis 55455.
B cell lymphoproliferative disorders (BLPD) developed in eight patients
following bone marrow transplantation (BMT) for leukemia (five patients) or
immunodeficiency (three patients). Recipients of T depleted marrow from a
mismatched donor were at particularly high risk of this complication. Six
of 25 (24%) recipients of mismatched T depleted bone marrow developed BLPD.
In contrast, none of 47 matched T depleted transplants, one of ten (10%)
who received non-depleted marrow from an unrelated donor, and only one of
424 matched non-depleted transplants were associated with BLPD.
Epstein-Barr virus (EBV) specific serology and DNA hybridization studies
demonstrating five to 50 copies of EBV genome/cell in involved tissues
implicate this virus as an associated etiologic agent. Restriction fragment
length polymorphism (RFLP) and cytogenetic analysis of involved tissue
demonstrated donor origin (five of seven) or host origin (two of seven).
Histologic appearance was similar to EBV-induced polymorphic B cell
proliferations described following solid organ transplantation, or which
occur de novo in primary immunodeficiency. Six of seven patients with
adequate tissue available for study were found to have monoclonal
proliferations by: in situ immunofluorescence (six of seven), and/or
immunoglobulin gene rearrangement, (four of six). Cytogenetic analysis of
involved tissues from four patients showed a normal karyotype, whereas two
had multiple clonal chromosomal abnormalities. Seven patients died despite
aggressive attempts at therapy with combinations of antiviral, immunologic,
and chemotherapeutic agents.
Volume 71,
Issue 5,
pp. 1234-1243,
05/01/1988
Copyright © 1988 by The American Society of Hematology
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