AI Article Synopsis
- PTLD is caused by uncontrolled B-cell growth due to Epstein-Barr virus in patients with weakened immunity, especially after stem cell transplants.
- The use of anti-thymocyte globulin (ATG), particularly rabbit ATG, has been linked to an increased risk of PTLD, while equine ATG is less commonly associated.
- A case is presented involving a man who developed monoclonal plasmacytic PTLD three years after autologous HSCT, highlighting the importance of recognizing complications from immunosuppressive treatments.
Article Abstract
Post-transplant lymphoproliferative disorder (PTLD) is generally caused by an uncontrolled B-cell proliferation induced by Epstein-Barr virus (EBV) in the setting of impaired EBV-specific T-cell immunity. PTLD has been described in allogeneic hematopoietic stem cell transplant (HSCT) and rarely in autologous HSCT. Anti-thymocyte globulin (ATG) is being increasingly utilized for acute rejection in organ transplantation, severe autoimmune diseases and aplastic anemia. Mainly, the use of rabbit ATG has been associated with PTLD, which is considered to be more immunosuppressive than equine ATG. The sole administration of equine ATG has rarely been associated with PTLD. Due to the increased use of these potent and novel immunosuppressive agents, it is paramount to be aware of these complications. We present a 55-year-old man with an autologous HSCT who presented with an unusual case of monoclonal plasmacytic PTLD. His lymphoproliferative disorder occurred 3 years after his HSCT and 1 month after the use of equine ATG administered for severe aplastic anemia. We review current concepts of EBV-PTLD, including risk factors, the potential for preemptive therapy and various management strategies.
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| http://dx.doi.org/10.1007/s12032-010-9635-8 | DOI Listing |
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