Background: An increased incidence of posttransplant lymphoproliferative disorders (PTLD) as a result of immunosuppression has been suggested in combined heart-lung transplantation compared with other solid organ transplants, and represents a significant source of morbidity and mortality among lung transplant patients. Although infection with the Epstein-Barr virus has been implicated in the pathogenesis of PTLD, it is unclear if the PTLD is of donor or recipient origin in lung transplant patients.
Methods: The case histories and histologic, immunophenotypic, and molecular genetic findings for the three patients who developed PTLD in the authors' transplantation program are presented.
Results: All three patients developed PTLD of B-cell immunophenotype with two patients having evidence of monoclonality by Southern blotting DNA gene rearrangement analysis. The site of involvement by PTLD was the lung in two patients and the small bowel in the third. In one patient, two separate pulmonary lesions were found to be comprised of distinct clonal populations, one exhibiting kappa and the other lambda light chain restriction and each having different immunoglobulin heavy chain gene rearrangements. The Epstein-Barr virus genome was present in the PTLD from all three patients. Polymerase chain reaction (PCR) amplification of a polymorphic huntington gene or annexin III locus was used to identify the PTLD in all three patients as being of recipient origin.
Conclusions: PCR amplification of polymorphic genetic loci demonstrated the recipient origin of PTLD in these three pulmonary transplant patients.