title: Lymphoproliferative disease of donor origin arising in patients after orthotopic liver transplantation.
abstract: BACKGROUND
  Lymphoproliferative disease is a well recognized complication of organ transplantation and in many cases is associated with Epstein-Barr virus (EBV) infection. It is widely though that posttransplantation lymphoproliferative disease (PTLPD) arises from recipient lymphoid cells. However, solid organ allografts are likely to include donor lymphoid tissue around or within the transplanted organ. Therefore, it is possible that transplanted donor lymphocytes may proliferate to form PTLPD:
  
  
  METHODS
  The genetic origin of tumor cells was determined by microsatellite DNA fingerprinting using the polymerase chain reaction (PCR). Their EBV association and clonality were established by PCR amplification of DNA extracted from formalin fixed, paraffin embedded tissue using primers to conserved regions of the EBV genome and the immunoglobulin heavy chain gene, respectively.
  
  
  RESULTS
  The authors have demonstrated two cases of lymphoproliferative disease that were derived from donor lymphocytes in orthotopic liver transplant recipients. In both cases, the proliferating cells were EBV DNA positive. Furthermore, the PTLPD was restricted to allograft tissue around the porta hepatis. However, the two cases differed in their clonal properties and response to treatment: one case was oligoclonal and regressed after antiviral therapy and a modest reduction of immunosuppression, whereas the other contained two clonal populations and was controlled only after treatment with antineoplastic chemotherapy.
  
  
  CONCLUSIONS
  This study has demonstrated two cases of PTLPD that were derived from donor lymphoid tissue. Although both cases were associated with EBV and remained localized to allograft tissue, their clonality and response to therapy differed.
authors.affiliation: Department of Anatomical Pathology, Austin Hospital, Heidelberg, Victoria, Australia.
authors.forename: J E
authors.initials: JE
authors.lastname: Armes
authors.forename: P
authors.initials: P
authors.lastname: Angus
authors.forename: M C
authors.initials: MC
authors.lastname: Southey
authors.forename: S E
authors.initials: SE
authors.lastname: Battaglia
authors.forename: B C
authors.initials: BC
authors.lastname: Ross
authors.forename: R M
authors.initials: RM
authors.lastname: Jones
authors.forename: D J
authors.initials: DJ
authors.lastname: Venter
mesh_terms: D000328:Adult; D001483:Base Sequence; D004279:DNA, Viral / Q000235:genetics; D015321:Gene Rearrangement; D006566:Herpesviridae Infections / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D004854:Herpesvirus 4, Human / Q000235:genetics / Q000276:immunology; D006801:Humans; D007143:Immunoglobulin Heavy Chains / Q000235:genetics; D008107:Liver Diseases / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D016031:Liver Transplantation / Q000009:adverse effects* / Q000276:immunology / Q000473:pathology; D008214:Lymphocytes / Q000821:virology; D008232:Lymphoproliferative Disorders / Q000209:etiology* / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D016133:Polymerase Chain Reaction; D014019:Tissue Donors; D014412:Tumor Virus Infections / Q000209:etiology* / Q000276:immunology / Q000473:pathology
chemical_list: D004279:DNA, Viral; D007143:Immunoglobulin Heavy Chains