THE RECIPIENT ORIGIN OF POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDERS IN PULMONARY TRANSPLANT PATIENTS - A REPORT OF 3 CASES

BACKGROUND. An increased incidence of posttransplant lymphoproliferati ve disorders (PTLD) as a result of immunosuppression has been suggeste d in combined heart-lung transplantation compared with other solid org an transplants, and represents a significant source of morbidity and m ortality among lung transplant patients. Although infection with the E pstein-Barr virus has been implicated in the pathogenesis of PTLD, it is unclear if the PTLD is of donor or recipient origin in lung transpl ant patients. METHODS. The case histories and histologic, immunophenot ypic, and molecular genetic findings for the three patients who develo ped PTLD in the authors' transplantation program are presented. RESULT S. All three patients developed PTLD of B-cell immunophenotype with tw o patients having evidence of monoclonality by Southern blotting DNA g ene rearrangement analysis. The site of involvement by PTLD was the lu ng in two patients and the small bowel in the third. In one patient, t wo separate pulmonary lesions were found to be comprised of distinct c lonal populations, one exhibiting kappa and the other lambda light cha in restriction and each having different immunoglobulin heavy chain ge ne rearrangements. The Epstein-Barr virus genome was present in the PT LD from all three patients. Polymerase chain reaction (PCR) amplificat ion 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 demonstrate d the recipient origin of PTLD in these three pulmonary transplant pat ients. (C) 1996 American Cancer Society.