Post-transplant Lymphoproliferative Disorder Following Cardiac Transplantation

Post-transplant lymphoproliferative disorder (PTLD) is a spectrum of lymphoid conditions frequently associated with the Epstein Barr Virus (EBV) and the use of potent immunosuppressive drugs after solid organ transplantation. PTLD remains a major cause of long-term morbidity and mortality following...

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Published inFrontiers in cardiovascular medicine Vol. 9; p. 787975
Main Authors Asleh, Rabea, Alnsasra, Hilmi, Habermann, Thomas M, Briasoulis, Alexandros, Kushwaha, Sudhir S
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 23.02.2022
Subjects
Cardiovascular Medicine
Epstein-Barr virus
heart transplantation
immunosuppression
mTOR inhibitors
PTLD
rituximab
mTOR inhibitors
PTLD
immunosuppression
Epstein-Barr virus
heart transplantation
rituximab
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Summary:Post-transplant lymphoproliferative disorder (PTLD) is a spectrum of lymphoid conditions frequently associated with the Epstein Barr Virus (EBV) and the use of potent immunosuppressive drugs after solid organ transplantation. PTLD remains a major cause of long-term morbidity and mortality following heart transplantation (HT). Epstein-Barr virus (EBV) is a key pathogenic driver in many PTLD cases. In the majority of PTLD cases, the proliferating immune cell is the B-cell, and the impaired T-cell immune surveillance against infected B cells in immunosuppressed transplant patients plays a key role in the pathogenesis of EBV-positive PTLD. Preventive screening strategies have been attempted for PTLD including limiting patient exposure to aggressive immunosuppressive regimens by tailoring or minimizing immunosuppression while preserving graft function, anti-viral prophylaxis, routine EBV monitoring, and avoidance of EBV seromismatch. Our group has also demonstrated that conversion from calcineurin inhibitor to the mammalian target of rapamycin (mTOR) inhibitor, sirolimus, as a primary immunosuppression was associated with a decreased risk of PTLD following HT. The main therapeutic measures consist of immunosuppression reduction, treatment with rituximab and use of immunochemotherapy regimens. The purpose of this article is to review the potential mechanisms underlying PTLD pathogenesis, discuss recent advances, and review potential therapeutic targets to decrease the burden of PTLD after HT.
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Edited by: Gaurang Vaidya, University of Kentucky, United States
This article was submitted to Heart Failure and Transplantation, a section of the journal Frontiers in Cardiovascular Medicine
Reviewed by: Zeinab Afify, The University of Utah, United States; Birte Wistinghausen, Children's National Hospital, United States
ISSN:2297-055X
2297-055X
DOI:10.3389/fcvm.2022.787975