THE CLINICAL DIVERSITY AND ROLE OF CHEMOTHERAPY IN LYMPHOPROLIFERATIVE DISORDER IN LIVER-TRANSPLANT RECIPIENTS

Background/Aims: Post-transplant lymphoproliferative disorder is a wel l-documented complication with an incidence ranging from 2 to 10%, dep ending on the organ transplanted. Yet despite our increased understand ing of the pathophysiology of this disease and the various treatments available, the mortality remains high at 60-80%. We present the clinic al and histological features of ten adult liver transplant recipients with post-transplant lymphoproliferative disorder presenting over a 15 -year period and review the therapeutic options. Methods: CD20/CD45RO immunostaining was used for T/B-cell markers; polymerase chain reactio n and is-sits hybridisation for Epstein-Barr virus genome detection; k appa/lambda, immunostaining and gene rearrangement analysis for clonal ity. Results: There mere six females and four males (age range 24-56) with onset of post-transplant lymphoproliferative disorder-symptoms ra nging from 3 to 72 months post transplant. Sites of post-transplant ly mphoproliferative disorder included liver (n=4), lymph nodes (n=5), bo ne marrow (n=2), lungs (n=2), kidneys (n=2), brain, ovaries,: and panc reas (n=1), All lesions were classified as high-grade lymphoma, of B-c ell lineage (9 tested); Epstein-Barr virus genome was detected in 7/10 cases. Three tumours were monoclonal; four were polyclonal and three undetermined. Treatment included immunosuppression reduction, antivira l therapy with acyclovir and/or chemotherapy (CHOP or VAPEC-B). Surviv al times for those patients not treated with chemotherapy mere from 9 days to 30 months, whereas those receiving chemotherapy had remission times of 4 to 48 months. Conclusions: Longer-term remissions can be ac hieved in patients treated with systemic chemotherapy, although not wi thout morbidity. Clonality assessment is important but treatment decis ions should be based primarily on clinical features of progression, as polyclonal tumours can behave as aggressively as monoclonal tumours.