Posttransplantation lymphoproliferative disorders (PTLD) develop in the setting of iatrogenic immunosuppression following solid organ transplantation (SOT) or allogeneic bone marrow transplantation (BMT),with some differences evident (Table 34-5). The incidence of these lesions varies based on the type of organ transplanted as well as the type and amount of immunosuppression employed. In these immunosuppressed patients, morphology does not accurately predict clinical course, making molecular analysis particularly useful. In some SOT recipients, a lesion may regress completely following a reduction in immunosup-pression, while morphologically similar lesion(s) in other patients may progress despite aggressive clinical intervention, resulting in the patient's demise. Furthermore, institution of the correct therapy in patients with PTLD is crucial since a reduction in immunosuppression can potentially result in organ loss, while chemotherapy can lead to life-threatening infection in an already immunosuppressed individual. Although in some studies specific molecular events correlate well with biologic aggressiveness of the lesions, in other studies these findings cannot be confirmed. It may be that differences in the type of organ transplanted, the immunosuppressive regimens, as well as host and donor factors influence the pathogenesis and biologic behavior of PTLD. In contrast to SOT PTLD, patients who develop PTLD following allogeneic BMT usually have an aggressive, frequently fatal, clinical course. As with other immunodeficiency-related LPDs, the development of PTLD in both SOT and BMT recipients is highly associated with EBV infection. Furthermore, the relative incidence of these lesions is higher in patients who are EBV negative at the time of transplantation.
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