PTLD occurring in allogeneic BMT recipients are biologically distinct from those occurring in SOT recipients. BMT PTLD are of donor origin, often have an explosive clinical presentation, and are frequently fatal. Furthermore, BMT PTLD tend to occur in the first 6 months following transplantation, since the level of anti-EBV cytotoxic T-cell precursors returns to normal only approximately 6 months after transplantation. In comparison to SOT PTLD, the incidence of BMT PTLD is relatively low (cumulative incidence of 1% at 10 years). As with SOT PTLDs, the vast majority of BMT PTLD cases are associated with EBV infection.
Morphologically, BMT PTLD consists of lesions exhibiting the histologic features of PH and polymorphic PTLD, as seen in SOT recipients.10 However, none of the PTLD studied from 27 allogeneic BMT recipients showed the morphologic features of monomorphic PTLD,11 although other investigators have identified such lesions.12 Although morphology correlates with clinical outcome, B-cell clon-ality status does not correlate with morphology or with clinical outcome, based on polymerase chain reaction (PCR) analysis of the early-onset PTLD.11 Specifically, both patients with monoclonal/oligoclonal PTLD as well as those with polyclonal PTLD died of PTLD. In contrast to SOT PTLD, examination of the BMT PTLD for BCL6 mutations did not identify any correlation of this genetic alteration with patient outcome.13 All BMT PTLD in this study exhibited EBV latency patterns type II or III (expressed LMP1 with or without EBNA2), indicating that these lesions are EBV driven.11 The clinical outcome of BMT PTLD patients is largely related to the number and competence of EBV-specific cytotoxic T cells rather than to intrinsic differences in BMT PTLD subtypes.
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