The changing face of post-transplant lymphoproliferative disease in the era of molecular EBV monitoring
Version of Record online: 7 JAN 2010
© 2010 John Wiley & Sons A/S
Volume 14, Issue 4, pages 504–511, June 2010
How to Cite
Kerkar, N., Morotti, R. A., Madan, R. P., Shneider, B., Herold, B. C., Dugan, C., Miloh, T., Karabicak, I., Strauchen, J. A. and Emre, S. (2010), The changing face of post-transplant lymphoproliferative disease in the era of molecular EBV monitoring. Pediatric Transplantation, 14: 504–511. doi: 10.1111/j.1399-3046.2009.01258.x
- Issue online: 9 MAY 2010
- Version of Record online: 7 JAN 2010
- Accepted for publication 16 September 2009
- liver transplantation;
- Epstein–Barr virus;
- lymphoproliferative disease;
Kerkar N, Morotti RA, Madan RP, Shneider B, Herold BC, Dugan C, Miloh T, Karabicak I, Strauchen JA, Emre S. The changing face of post-transplant lymphoproliferative disease in the era of molecular EBV monitoring. Pediatr Transplantation 2010: 14:504–511. © 2010 John Wiley & Sons A/S.
Abstract: Pediatric PTLD is often associated with primary EBV infection and immunosuppression. The aim was to retrospectively review the spectrum of histologically documented PTLD for two time intervals differentiated by changes in use of molecular EBV monitoring. Eleven of 146 patients (7.5%) in 2001–2005 (Era A) and 10 of 92 (10.9%) in 1993–1997 (Era B) were diagnosed with PTLD. The median age at liver transplantation (0.8 and 0.9 yr, respectively) and the median duration between liver transplant and diagnosis of PTLD (0.6 and 0.7 yr, respectively) were similar in both eras. However, patients in Era A presented with significantly less advanced histological disease compared to patients in Era B (p = 0.03). Specifically, nine patients (82%) in Era A had Pl hyperplasia/polymorphic PTLD, whereas in Era B, six had advanced histological disease (five monomorphic and one unclassified). Three transplant recipients in Era B died secondary to PTLD, whereas there were no PTLD-related deaths in Era A (p = 0.03). Heightened awareness of risk for PTLD, alterations in baseline immunosuppression regimens, implementation of molecular EBV monitoring, pre-emptive reduction in immunosuppression and improved therapeutic options may have all contributed to a milder PTLD phenotype and improved clinical outcomes.