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Epstein-Barr virus lymphoproliferation after bone marrow transplantation
MM Zutter, PJ Martin, GE Sale, HM Shulman, L Fisher, ED Thomas and DM Durnam
Division of Clinical Research, Fred Hutchinson Cancer Research Center,
Seattle, Washington 98104.
We review 15 cases of secondary B-cell lymphoproliferative disorders that
occurred among 2,475 patients who received allogeneic bone marrow
transplants (BMTs) at the Fred Hutchinson Cancer Research Center (Seattle)
between 1969 and 1987. The histopathologic findings in 14 of the 15
patients spanned a wide spectrum of lymphoproliferative lesions. One
patient had features characteristic of angioimmunoblastic lymphadenopathy.
Epstein-Barr virus (EBV) genomic sequences were identified by Southern blot
analysis in each of the 13 patients evaluated. Ten of the 12 lesions
evaluated originated in donor cells. In two patients, who had mixed
chimerism after transplantation, the lesions originated in host cells. The
combined evidence from immunoglobulin light chain staining and the analysis
of immunoglobulin heavy chain gene rearrangement indicated that the lesions
in most patients represented polyclonal proliferations that gave rise to
clonal subpopulations. The results indicate an overall actuarial incidence
of 0.6% for this complication in BMT recipients. Anti-CD3 monoclonal
antibody (MoAb) treatment of acute graft-v-host disease (GVHD) and T cell
depletion of the donor marrow were statistically significant risk factors,
and GVHD appeared to play a contributing role, particularly in the setting
of human leukocyte antigen (HLA) disparity. Two patients had no
identifiable risk factors. Prophylaxis or treatment with acyclovir had no
detectable effect in the patients; all but two died with uncontrolled
lymphoproliferation.
Volume 72,
Issue 2,
pp. 520-529,
08/01/1988
Copyright © 1988 by The American Society of Hematology
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