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Pathology · Neoplasia: post-transplant lymphoproliferative disorder
Sample itemA 30-year-old renal transplant recipient on tacrolimus and mycophenolate develops cervical lymphadenopathy 8 months after transplantation. Node biopsy shows a polymorphous proliferation of B cells that stain for EBV-encoded RNA. Which mechanism best explains the disorder?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Loss of T-cell control over EBV-infected B cells
Post-transplant lymphoproliferative disorder results from impaired cytotoxic T-cell surveillance during immunosuppression, which allows EBV-infected B cells to proliferate. Early lesions may regress when immunosuppression is reduced. Lesions range from polymorphous hyperplasia to monomorphic lymphoma.
Option by option
A. Donor T cells attacking recipient lymphoid tissue
Donor T cells attacking recipient tissue is graft-versus-host disease, seen mainly after marrow transplantation.
B. Loss of T-cell control over EBV-infected B cells (correct)
Correct. Failure of T-cell surveillance lets EBV-driven B-cell proliferation expand.
C. Reactivation of HHV-8 in lymph node endothelium
HHV-8 reactivation is linked to Kaposi sarcoma, and the EBV-encoded RNA here points to EBV.
D. Direct mutagenic effect of tacrolimus on B-cell DNA
Calcineurin inhibitors act by blocking T-cell signalling and are not the direct mutagen in this disorder.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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