Post-transplant Lymphoproliferative Disorder, Early Lesions and Polymorphic

Post-transplant Lymphoproliferative Disorder, Early Lesions and Polymorphic

C. Cameron Yin, MD, PhD

Pei Lin, MD

Polymorphic post-transplant lymphoproliferative disorder (PTLD) involving the rectum. Note the mixture of cell types present.

Polymorphic PTLD involving the rectum. In situ hybridization for Epstein-Barr virus (EBV) encoded small RNA (EBER) is positive in many cells.



  • Post-transplant lymphoproliferative disorder (PTLD)


  • Plasmacytic or lymphoid proliferations occurring as result of immunosuppression following solid organ or bone marrow transplantation

    • Early lesions are PTLDs characterized by architectural preservation of involved site

    • Polymorphic lesions are PTLDs that efface architecture but are morphologically heterogeneous and do not fulfill criteria for any known lymphoma type


Infectious Agents

  • Epstein-Barr virus plays a central role

    • 80% of all PTLDs are EBV(+)

      • Usually type A

    • Serum EBV antibody titers and blood EBV DNA load increase prior to onset of PTLD

    • Number of EBV(+) cytotoxic T cells drops prior to onset of PTLD

    • Treatment with EBV-specific T cells induces remission or responses in some patients

    • Analysis of EBV terminal repeat regions by Southern blot analysis has shown monoclonal form of virus

      • Indicates presence of EBV before monoclonal expansion began

    • EBV can transform germinal center (GC) B cells

      • Extended half-life of EBV-infected B cells increases likelihood of acquiring additional molecular aberrations that confer a growth advantage


  • Arise from GC or post-GC B cells

    • In solid organ allograft recipients, most PTLDs are of host origin

    • In bone marrow or stem cell allograft recipients, most PTLDs are of donor origin

  • Iatrogenically decreased host immunosurveillance

  • Risk factors for PTLD in general

    • EBV seronegativity before transplant

    • Degree of overall immunosuppression

    • Type of immunosuppression

      • Higher risk with tacrolimus, OKT3 monoclonal antibody, or antithymocyte globulin

    • Type of organs transplanted

      • Most common in intestinal and multiorgan transplant recipients

      • Lowest in renal transplant recipients

      • May be attributable to differences in immunosuppressive regimens used

    • Age

      • Pediatric patients have a higher incidence of PTLD

      • Most likely related to more frequent EBV seronegativity prior to transplant

    • Additional risk factors for patients who receive autologous bone marrow or stem cell transplants

      • HLA-mismatched allograft

      • T-cell-depleted allograft

      • Immunosuppressive therapy for graft vs. host disease



  • Incidence

    • Frequency of PTLD is related to type of transplant and associated immunosuppression

      • Kidney: 1-3% of all transplant patients

      • Liver: 1-3% of all transplant patients

      • Heart: 1-6% of all transplant patients

      • Heart-lung: 2-6% of all transplant patients

      • Lung: 4-10% of all transplant patients

      • Small intestine: ˜ 20% of all transplant patients

  • Age

    • Predicted by age of patient population undergoing transplant

      • Younger patients are at increased risk of developing PTLD


  • Early lesions

    • Primarily involving lymph nodes

    • Tonsils, adenoids

  • Polymorphic

    • Lymph nodes

    • Extranodal masses can occur

Jul 8, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Post-transplant Lymphoproliferative Disorder, Early Lesions and Polymorphic

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