Oropharyngeal plasmacytic hyperplasia in a post-liver transplant recipient: morphologic and histologic signs.

Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030, USA.
Liver Transplantation (Impact Factor: 3.79). 02/2007; 13(1):170-2.
Source: PubMed
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    ABSTRACT: Posttransplant lymphoproliferative disorders (PTLDs) represent a morphologic, immunophenotypic, and genotypic spectrum of disease. Most recently, Knowles et al divided PTLDs into 3 distinct categories: (1) plasmacytic hyperplasia, (2) polymorphic B-cell hyperplasia and polymorphic B-cell lymphoma, and (3) immunoblastic lymphoma and multiple myeloma. Although one form of PTLD may progress to another form, only 1 previous case has been reported in which multiple myeloma developed 14 months after an original diagnosis of plasmacytic hyperplasia. The type of solid organ transplant was not specified in that case. We report a post--cardiac transplant plasmacytic hyperplasia developing 7 years posttransplant. Six years subsequent to the plasmacytic hyperplasia, the patient developed a posttransplant plasmacytic malignancy, supported by morphology, flow cytometric immunophenotyping, and genotypic studies. Since we have no data to support disseminated bony disease or an abnormal serum protein, we have not used the term "multiple myeloma" for this case.
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    ABSTRACT: Posttransplant lymphoproliferative disorder (PTLD) is a well-known complication of both solid organ and bone marrow transplantation. It includes a wide spectrum of proliferative changes ranging from reactive hyperplasia, borderline lesions to malignant lymphomas. PTLD develops in 1% to 10% of transplant recipients. We present 10 cases of PTLD. Five developed after renal, four after liver, and one after heart transplantation. Among the early lesions, we diagnosed two reactive plasmacytic hyperplasias; one infectious mononucleosis-like PTLD; one polymorphic lesion; and one "mixed" case of plasmacytic hyperplasia in one tonsil with a polymorphic PTLD in the second one. Among the lymphomas, we observed three diffuse large B-cell lymphoma (DLBCL); one mantle lymphoma; and one Hodgkin lymphoma-like PTLD. The morphological pictures of six PTLD cases were typical and posed no diagnostic problems. In the one case of plasmacytic hyperplasia, the lymph node morphology was atypical with atrophy of lymphoid components accompanying plasma cell proliferation. Contrary to a good prognosis of early, reactive PTLD, this patient experienced a rapid course and succumbed to sepsis. The most difficult case was a rare Hodgkin lymphoma-like PTLD, which was diagnosed only by a bone marrow biopsy. Because of its noncharacteristic immunophenotype, it was primarily diagnosed as an anaplastic lymphoma of the T-cell type. After additional immunohistochemical studies (BOB and OCT2), we established the final diagnosis of Hodgkin lymphoma-like PTLD. Due to the increasing number of organ transplantations, doctors of various specialties may encounter PTLD.
    Transplantation Proceedings 01/2006; 38(1):168-72. · 0.95 Impact Factor
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    ABSTRACT: Twenty cases of posttransplant lymphoproliferative disorders arising in solid organ allograft recipients (18 patients) or bone marrow allograft recipients (2 patients: 1 autologous; 1 allogeneic) were selected for presentation at the Society for Hematopathology Workshop. In the course of the Workshop discussions, based both on the submitted cases and the combined experience of the participants, it was possible to agree on several distinctive categories of PTLD. These include (1) early lesions, (2) polymorphic posttransplant lymphoproliferative disorders (PTLDs), (3) monomorphic PTLDs (B- and T-cell lymphomas), (4) plasmacytoma-like lesions, and (5) T-cell-rich large B-cell lymphoma/Hodgkin's disease-like lesions. Monomorphic lesions should be classified according to a recognized classification of non-Hodgkin's lymphoma, although specified in the report as PTLD. Polymorphic lesions should be carefully evaluated for clonality; by immunophenotyping; and, if necessary, analysis of antigen-receptor and Epstein-Barr virus (EBV) genomes. Minimal pathological evaluation should include routine morphology, immunophenotyping on fresh tissue (flow cytometry or frozen section), and preservation of tissue for molecular genetic analysis. Analysis of the presence of EBV can be useful in establishing whether early or equivocal lesions represent PTLD (EBV+) or unrelated processes, but is not required in most cases. The pathologist can make an important contribution to the management of patients with PTLD by providing a complete diagnostic evaluation of the biopsy specimens (this is the least expensive part of the care of a transplant patients, not a place to try to cut costs) and making sure the attending physicians understand the special issues in management of PTLD.
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