Epstein–Barr virus‐associated risk factors for post‐transplant lymphoproliferative disease in pediatric liver transplant recipients

• Published in: Pediatric transplantation Vol. 26; no. 6; pp. e14292 - n/a
• Main Authors: Quintero Bernabeu, Jesus, Juamperez, Javier, Mercadal‐Hally, Maria, Larrarte King, Mauricio, Gallego Melcon, Soledad, Gros Subias, Luis, Sábado Álvarez, Constantino, Soler‐Palacin, Pere, Melendo Pérez, Susana, Esperalba, Juliana, Navarro Jiménez, Alexandra, Garrido Pontnou, Marta, Camacho Soriano, Jessica, Hidalgo Llompart, Ernest, Bilbao Aguirre, Itxarone, Charco Torra, Ramón
• Format: Journal Article
• Language: English
• Published: Denmark Wiley Subscription Services, Inc 01-09-2022
• Subjects: Epstein-Barr virus; Epstein–Barr virus infection; Hodgkin's lymphoma; Hyperplasia; Immunoproliferative diseases; Immunotherapy; Liver diseases; Liver transplantation; Liver transplants; Lymphocytes; Monoclonal antibodies; Patients; PCR; pediatric liver transplantation; Pediatrics; Posttransplant lymphoproliferative disorders; post‐transplant lymphoproliferative; Risk factors; rituximab; Targeted cancer therapy; Transplants & implants; Epstein-Barr virus infection; pediatric liver transplantation; PCR; post-transplant lymphoproliferative; rituximab
• ISSN: 1397-3142; 1399-3046
• DOI: 10.1111/petr.14292

Background
Post‐transplant lymphoproliferative disorder (PTLD) are the most common de novo malignancies after liver transplantation (LT) in children. The aim of our study was to assess the role of pre‐LT EBV status and post‐LT EBV viral load as risk factors for developing PTLD in a cohort of pediatric LT recipients.
Methods
Data of all children who underwent LT between January 2002 and December 2019 were collected. Two cohorts were built EBV pre‐LT primary infected cohort and EBV post‐LT primary infected cohort. Moreover, using the maximal EBV viral load, a ROC curve was constructed to find a cutoff point for the diagnosis of PTLD.
Results
Among the 251 patients included in the study, fifteen PTLD episodes in 14 LT recipients were detected (2 plasmacytic hyperplasia, 10 polymorphic PTLD, 2 monomorphic PTLD, and 1 Classical‐Hodgkin's lymphoma). Patients of the EBV post‐LT primary infected cohort were 17.1 times more likely to develop a PTLD than patients of the EBV pre‐LT primary infected cohort (2.2–133.5). The EBV viral load value to predict PTLD was set at 211 000 UI/mL (93.3% sensitivity and 77.1% specificity; AUC 93.8%; IC 0.89–0.98). In EBV post‐LT primary infected cohort, patients with a viral load above 211 000 were 30 times more likely to develop PTLD than patients with a viral load below this value (OR 29.8; 3.7–241.1; p < 0.001).
Conclusions
The combination of pretransplant EBV serological status with EBV post‐transplant viral load could be a powerful tool to stratify the risk of PTLD in pediatric LT patients.