Posttransplantation plasma cell dyscrasias

Lymphoproliferative disorders that occur in patients receiving cyclosporine for immunosuppression after solid organ transplantation typically are B-cell neoplasms associated with Epstein-Barr virus (EBV), which may be polyclonal or monoclonal in origin. Although these tumors may have partial B-cell differentiation, (manifested as plasmacytoid features), terminal differentiation to plasma cells that secrete a monoclonal immunoglobulin is rare. The case of a patient who developed a posttransplantation lymphoproliferative disorder that was composed of multiple plasmacytomas located in the abdomen and urinary bladder after liver transplantation is presented. The patient also had high levels of an immunoglobulin-G kappa monoclonal paraprotein.

The plasmacytoma was examined for the presence of EBV by both polymerase chain reaction and in situ hybridization, and the possibility of a codon-12 mutation in the ras gene was investigated by digestion of DNA amplification products with the HpaII-restriction endonuclease.

Epstein-Barr virus genomes were demonstrated by DNA amplification of sequences in the long, internal, direct repeat region, and in situ hybridization showed expression of EBV RNA transcripts that annealed to an EBER-1 probe. Immunohistochemistry showed clonally restricted expression of kappa light chains but failed to reveal evidence of expression of the latent membrane protein 1 encoded by EBV. Mutations of codon-12 in the H-ras gene were not detected.

Resolution of the tumor and the paraprotein after radiation and reduction of immunosuppression indicates that terminal plasmacytic differentiation does not necessarily portend an unfavorable prognosis, even in a clonal lesion.