scholarly journals Posttransplant Lymphoproliferative Disease Presenting as an Extracranial Mass

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Reuben J. Arasaratnam ◽  
Alejandro Restrepo

Posttransplant lymphoproliferative disease is a serious complication following stem cell and solid organ transplantation. Early recognition of the disease is important in facilitating timely therapy and improving long-term outcomes. We report a renal transplant recipient presenting with an extracranial frontoparietal soft tissue mass that was subsequently diagnosed as a B-cell lymphoma. The patient was treated successfully with immunosuppression reduction, anti-CD20 monoclonal antibody therapy, and cytotoxic chemotherapy. Our case highlights the importance of recognizing soft tissue masses in the head and neck as a potential clinical manifestation of PTLD in solid organ transplant recipients.

2016 ◽  
Vol 2 (1) ◽  
pp. e48 ◽  
Author(s):  
Marieke L. Nijland ◽  
Marie José Kersten ◽  
Steven T. Pals ◽  
Frederike J. Bemelman ◽  
Ineke J.M. ten Berge

2005 ◽  
Vol 15 (2) ◽  
pp. 157-160
Author(s):  
Carol A. Lawson

Cytomegalovirus is the most common infectious complication in solid-organ transplant recipients. Despite the frequency of the problem, no commonly accepted approach to cytomegalovirus prophylaxis and treatment exists. Because cytomegalovirus may lead to the modulation of the immune system sometimes causing opportunistic superinfections, allograft injury, acute rejection, chronic rejection, and development of posttransplant lymphoproliferative disease, transplant coordinators require knowledge of the disease, diagnostic methods, and treatment and prophylaxis strategies. This case study reviews a high-risk cytomegalovirus transplant recipient after living-related kidney transplantation. In addition to a review of the pathophysiology of the disease process, patient, family, and nursing staff education, and cultural and psychosocial aspects of cytomegalovirus, prophylaxis, diagnosis, treatment strategies as well as role of the transplant coordinator, will be discussed.


2021 ◽  
Vol 8 (3) ◽  
Author(s):  
Cutini I ◽  
◽  
Peruzzi B ◽  
Caporale R ◽  
Nozzoli C ◽  
...  

Post-Transplant Lymphoproliferative Disease (PTLD) following both Solid Organ Transplantation (SOT) and Hematopoietic Stem Cell Transplantation (HSCT) is a rare life-threatening complication. The majority of PLTDs are associated to Epstein Bar Virus (EBV) [1] reactivation, usually in the early phase [2] after transplant, when the patient is severely immunocompromised and is unable to control virus replication [3]. Despite the mortality of EBV-associated PTLD has been reduced over the years, the different histological patterns of its presentation, ranging from indolent to high grade B cell lymphoma, still play a role in the outcome. Herein, we report the case of a 60-years-old man diagnosed with acute myeloid leukemia who underwent allogeneic transplantation and developed a fatal Hemophagocytic Histiocytosis (HLH) secondary to an aggressive EBV-associated PTLD, not responding to a rituximab-based treatment.


Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 972-984 ◽  
Author(s):  
SA Riddler ◽  
MC Breinig ◽  
JL McKnight

Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disease (PTLD) is an uncommon but potentially fatal complication of immunosuppression in solid-organ transplant recipients. A semiquantitative DNA polymerase chain reaction assay was developed to amplify a unique 269-bp region of the EBNA-1 gene in peripheral blood lymphocytes (PBL) using the primers described by Telenti et al (J Clin Microbiol 28:2187, 1990). Serial samples were studied from 23 transplant recipients, 12 of whom were diagnosed with PTLD. The majority of transplant recipients who were EBV seropositive at the time of transplant surgery and who did not develop PTLD (5 of 7, 71%) exhibited less than a 10-fold increase in the levels of EBV-infected PBL over the 0.1 to 5 EBV genomes/10(6) PBL observed in immunocompetent EBV seropositive controls. Transplant recipients who were seronegative at the time of transplantation and who underwent a primary EBV infection but did not develop PTLD exhibited a reduced capacity to control viremia because the levels of EBV-infected PBL were up to 400 times greater than the 1.0 to 50 EBV genomes/10(6) PBL observed in individuals undergoing acute infectious mononucleosis (Rocci et al: N Engl J Med 296:132, 1977). However, all transplant recipients who developed PTLD exhibited a marked elevation of EBV-infected PBL independent of their serologic state at the time of transplantation. Six of the 10 transplant recipients with PTLD exhibited > or = 300,000 EBV genomes/10(5) PBL, two exhibited 10,000 to 50,000 EBV-infected genomes/10(5) PBL, and one each exhibited 2,500 and 500 EBV genomes/10(5) PBL. However, the latter two samples were obtained 4 to 5 weeks after the diagnosis of PTLD and may reflect a decrease in viral load resulting from immunomodulation. Marked decreases in the levels of EBV nuclear antigen-1 (EBNA-1), EBNA-2, and EBNA-LP antibodies correlated with the increase in EBV-infected PBL. Hence, a quantitative difference in circulating EBV viral load and EBNA antibody levels is evident between transplant recipients with and without PTLD and may be useful as a noninvasive prognostic marker with which to monitor and/or predict the development of PTLD.


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
David M. Burns ◽  
Katherine Clesham ◽  
Yan A. Hodgson ◽  
Lynsey Fredrick ◽  
Joanna Haughton ◽  
...  

Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 972-984 ◽  
Author(s):  
SA Riddler ◽  
MC Breinig ◽  
JL McKnight

Abstract Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disease (PTLD) is an uncommon but potentially fatal complication of immunosuppression in solid-organ transplant recipients. A semiquantitative DNA polymerase chain reaction assay was developed to amplify a unique 269-bp region of the EBNA-1 gene in peripheral blood lymphocytes (PBL) using the primers described by Telenti et al (J Clin Microbiol 28:2187, 1990). Serial samples were studied from 23 transplant recipients, 12 of whom were diagnosed with PTLD. The majority of transplant recipients who were EBV seropositive at the time of transplant surgery and who did not develop PTLD (5 of 7, 71%) exhibited less than a 10-fold increase in the levels of EBV-infected PBL over the 0.1 to 5 EBV genomes/10(6) PBL observed in immunocompetent EBV seropositive controls. Transplant recipients who were seronegative at the time of transplantation and who underwent a primary EBV infection but did not develop PTLD exhibited a reduced capacity to control viremia because the levels of EBV-infected PBL were up to 400 times greater than the 1.0 to 50 EBV genomes/10(6) PBL observed in individuals undergoing acute infectious mononucleosis (Rocci et al: N Engl J Med 296:132, 1977). However, all transplant recipients who developed PTLD exhibited a marked elevation of EBV-infected PBL independent of their serologic state at the time of transplantation. Six of the 10 transplant recipients with PTLD exhibited > or = 300,000 EBV genomes/10(5) PBL, two exhibited 10,000 to 50,000 EBV-infected genomes/10(5) PBL, and one each exhibited 2,500 and 500 EBV genomes/10(5) PBL. However, the latter two samples were obtained 4 to 5 weeks after the diagnosis of PTLD and may reflect a decrease in viral load resulting from immunomodulation. Marked decreases in the levels of EBV nuclear antigen-1 (EBNA-1), EBNA-2, and EBNA-LP antibodies correlated with the increase in EBV-infected PBL. Hence, a quantitative difference in circulating EBV viral load and EBNA antibody levels is evident between transplant recipients with and without PTLD and may be useful as a noninvasive prognostic marker with which to monitor and/or predict the development of PTLD.


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