PMID- 35282339
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220316
IS  - 2297-055X (Print)
IS  - 2297-055X (Electronic)
IS  - 2297-055X (Linking)
VI  - 9
DP  - 2022
TI  - Post-transplant Lymphoproliferative Disorder Following Cardiac Transplantation.
PG  - 787975
LID - 10.3389/fcvm.2022.787975 [doi]
LID - 787975
AB  - 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.
CI  - Copyright (c) 2022 Asleh, Alnsasra, Habermann, Briasoulis and Kushwaha.
FAU - Asleh, Rabea
AU  - Asleh R
AD  - Department of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
AD  - Heart Institute, Hadassah University Medical Center, Faculty of Medicine, Hebrew 
      University of Jerusalem, Jerusalem, Israel.
FAU - Alnsasra, Hilmi
AU  - Alnsasra H
AD  - Department of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
AD  - Soroka University Medical Center, Ben Gurion University of the Negev, Beer Sheva, 
      Israel.
FAU - Habermann, Thomas M
AU  - Habermann TM
AD  - Division of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, 
      United States.
FAU - Briasoulis, Alexandros
AU  - Briasoulis A
AD  - Division of Cardiovascular Disease, University of Iowa Hospitals and Clinics, 
      Iowa City, IA, United States.
FAU - Kushwaha, Sudhir S
AU  - Kushwaha SS
AD  - Department of Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220223
PL  - Switzerland
TA  - Front Cardiovasc Med
JT  - Frontiers in cardiovascular medicine
JID - 101653388
PMC - PMC8904724
OTO - NOTNLM
OT  - Epstein-Barr virus
OT  - PTLD
OT  - heart transplantation
OT  - immunosuppression
OT  - mTOR inhibitors
OT  - rituximab
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/03/15 06:00
MHDA- 2022/03/15 06:01
PMCR- 2022/01/01
CRDT- 2022/03/14 05:33
PHST- 2021/10/01 00:00 [received]
PHST- 2022/02/01 00:00 [accepted]
PHST- 2022/03/14 05:33 [entrez]
PHST- 2022/03/15 06:00 [pubmed]
PHST- 2022/03/15 06:01 [medline]
PHST- 2022/01/01 00:00 [pmc-release]
AID - 10.3389/fcvm.2022.787975 [doi]
PST - epublish
SO  - Front Cardiovasc Med. 2022 Feb 23;9:787975. doi: 10.3389/fcvm.2022.787975. 
      eCollection 2022.