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Intestinal Transplantation for Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Although bacterial infections are frequently seen, especially in the early postoperative period, the real concern is for opportunistic fungal and viral infections. Previously, avoiding CMV donor/recipient mismatch was attempted, but now with better monitoring and therapy, it is no longer avoided. However, EBV has more significant issues, especially as it may be a precursor to post-transplant lymphoproliferative disorders (PTLDs), which are a type of lymphoma and are one of the most common post-transplant cancers. In the intestine, this can be a major complication. Whereas in other types of transplants where the IS can be stopped and the condition overcome, in intestinal transplants this may not be possible, as the risk of rejection is much higher, and then the treatment of rejection may make the PTLD even worse. Hence, more elaborate and heavier therapies may be required to treat the PTLD.
Central nervous system viral infections complicating immunosuppression
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Post-transplant lymphoproliferative disorders (PTLD) are a diverse group of proliferations that surface after solid or organ or HCT. The spectrum ranges from a polyclonal B cell hyperplasia to aggressive monoclonal malignancies such as primary central nervous system lymphoma (PCNSL). CNS involvement is seen in 10%–15% of PTLD patients, and the majority of these exclusively involve the CNS. Up to 70% of PTLDs are EBV positive and lack p53 and Myc expression by immunohistochemistry, features seen in de novo PCNSL in immunocompetent individuals [20]. Those PTLDs that are EBV-negative tend to occur many years after organ transplantation [21]. While CSF sampling may reveal a significant EBV viral load and confirm diagnosis, a stereotactic biopsy often is required.
Transplantation
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
PTLD is an abnormal proliferation of B lymphocytes, usually in response to Epstein–Barr virus infection. The condition presents in a variety of ways including as an infectious mononucleosis-type illness or lymphadenopathy, or with involvement of extranodal sites such as the tonsils, gastrointestinal tract, lung, liver or the transplanted organ (Figure82.13). PTLD occurs in around 1–3% of kidney and liver transplant recipients and the incidence is considerably higher in children. Those patients at most risk are those who have received aggressive immunosuppression. PTLD is a serious condition with an overall mortality rate of up to 50%. If it is identified at an early stage, reduction or cessation of immunosuppressive therapy may cause disease regression and result in a cure. Chemotherapy is often given and antiviral therapy, surgery and radiotherapy may also have a role in treating established disease. Disseminated PTLD and central nervous system (CNS) involvement have a very poor prognosis.
Who is the patient at risk for EBV reactivation and disease: expert opinion focused on post-transplant lymphoproliferative disorders following hematopoietic stem cell transplantation
Published in Expert Opinion on Biological Therapy, 2023
Agata Marjanska, Jan Styczynski
Due to the rare cases of EBV-negative PTLD observed, the etiology of this disease appears to be more complicated. The ‘hit-and-run’ hypothesis assumes that EBV mediates cellular transformation by an initial ‘hit.’ It can be determined by the viral gene expression program. After genetic mutations have been induced by the EBV in the cellular gene expression or after somatic changes have been acquired in cellular tumor-suppressor genes and oncogenes, the virus genome may not be necessary for PTLD maintenance. Then, the virus may be progressively lost from the affected cells (‘run’) after each cell cycle [63]. PTLD without EBV-DNA-emia confirmation generally arises late after HCT and it differs in pathological features and gene expression profiles from EBV-positive PTLD. This fact may suggest that EBV-negative PTLD represent a different entity or sporadic lymphoma [64].
Prior antithymocyte globulin therapy and survival in post-transplant lymphoproliferative disorders
Published in Acta Oncologica, 2021
Amelie Kinch, Eva Baecklund, Daniel Molin, Karlis Pauksens, Christer Sundström, Gunnar Tufveson, Gunilla Enblad
Transplantation of an organ from an EBV-seropositive donor to an EBV-seronegative recipient is a well-established risk factor for EBV-related PTLD [4]. EBV-positive (EBV+) PTLD is associated with early-onset, that is, development within one year post-transplant. Risk for PTLD is further associated with the immunosuppressive therapy but the contribution of each immunosuppressive agent is not clear. Use of T-cell depleting antibodies, such as antithymocyte globulin (ATG) and muromonab-CD3 (OKT-3), has been associated with the development of early-onset PTLD in particular, whereas long-term use of calcineurin inhibitors (cyclosporine and tacrolimus) has been associated with late-onset PTLD [5–10]. High rates of EBV + PTLD have been reported when belatacept was used at high dosage in EBV-seronegative kidney transplant recipients [11]. In addition to EBV and immunosuppression, the type of solid organ transplant is an important risk factor for PTLD with the highest incidence found in intestinal recipients, followed by a declining incidence in lung, heart, liver, and pancreatic recipients, and the lowest incidence found in kidney recipients [1,12].
Immunodeficiency-associated Hodgkin lymphoma
Published in Expert Review of Hematology, 2021
Antonino Carbone, Annunziata Gloghini, Diego Serraino, Michele Spina, Umberto Tirelli, Emanuela Vaccher
Long-term complications including malignancies have become a major cause of morbidity and mortality in transplant recipients as immunosuppressive therapies and patient care have improved over time [85]. Our knowledge of PTLD has improved considerably in the last decade through the application of innovative diagnostic techniques and international research collaborations. HL-like PTLD and true HL are rare PTLDs, characterized by a high mortality rate. They are two distinct entities with different immunophenotype and clinical behavior [64–67]. Histological and immunoihistochemical methods are essential tools for their diagnosis [64]. The study of EBV-latency pattern can be a supportive diagnostic tool, being latency type II pattern in HL-PTLD and latency type III pattern in HL-like PTLD [67], but it requires further evaluation in larger patient series. Because of their rarity, the full range of their clinical behavior have not been completely characterized. Further efforts to implement clinical and biological databases on these PTLD subtypes are needed to evaluate prognostic factors that may improve treatment management. To emphasize, clinical trial enrollment and multidisciplinary management should be considered for all immunosuppressed patients with HL, including transplant recipients.