Post-transplantation lymphoproliferative disorders: Current concepts and future therapeutic approaches

Table 2 Early vs late onset post-transplant lymphoproliferative disorders in adults[4]

	Early PTLD	Late onset PTLD
General characteristics	EBV positivity	Frequent EBV negative tumors
	Graft involvement	Less often graft involvement[3]
	Less often: Extranodal disease	Extra-nodal disease: Common
	Nondestructive PTLD1: Present early	High incidence of late onset Hodgkin’s lymphoma after allogeneic HSCT
	Less often: Monomorphic subtype[3]	Specific tumorigenic events: C-myc translocations
	Origin: higher % of donor-derived PTLD especially in 1st post-tx year)	Elevated LDH level
Risk factors	Same	Same
Response to therapy	Same	Same
Patient survival (at 1- and 5- yr)	65% and 46%, (In adult heart/lung tx)[1,45]	53% and 41% (In adult heart/lung tx)[1,45]
Future therapy	Proteasome inhibition (bortezomib) may be useful after allogeneic HSCT[3]
Role of immun-osuppression	Induction therapy has a role	Cumulative immunosuppression is crucial
Prevalence	Majority of PTLD cases	Less prevalent

¹Non-destructive post-transplant lymphoproliferative disorders includes plasmacytic hyperplasia post-transplant (according to the Classification of PTLD by the WHO). Tx: Transplantation; PTLD: Post-transplant lymphoproliferative disorders; EBV: Epstein-Barr virus; HSCT: Haplo-identical allogeneic hematopoietic stem-cell transplant; LDH: Lactate dehydrogenase.