Orthotopic liver transplantation, Epstein-Barr virus, cyclosporine, and lymphoproliferative disease: A growing concern

Malatack, J. Jeffrey; Gartner, J. Carlton; Urbach, Andrew H.; Zitelli, Basil J.

doi:10.1016/s0022-3476(05)80024-1

Cited by 144 publications

(67 citation statements)

References 19 publications

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“…42 The actuarial 1-year incidence of PTLD is approximately 2%, although the incidence is up to 10 times greater in children aged younger than 5 years (more likely to be EBV seronegative) compared with adults (usually EBV seropositive). 43,44 Of note to this discussion are recent reports of an increased incidence of PTLD in patients with hepatitis C virus coinfection, not only in liver transplant recipients, but in heart transplant recipients, as well 45,46 The pathophysiological course of PTLD is not completely understood. 41 The majority of PTLDs are of B cell origin (Ͼ90%), whereas the remainder is of T cell origin, and only rarely of null cell, i.e., without identifiable T-or B-cell markers.…”

Section: Discussionmentioning

confidence: 99%

De novo malignancies after liver transplantation: A major cause of late death

Fung

Jain

Kwak

et al. 2001

Liver Transplantation

181

145

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Section: Discussionmentioning

confidence: 99%

De novo malignancies after liver transplantation: A major cause of late death

Fung

Jain

Kwak

et al. 2001

Liver Transplantation

181

145

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“…Early depletion approaches, such as polyclonal antibodies and OKT3, have been linked with the risk of developing posttransplantation lymphoproliferative disease (PTLD) when combined with maintenance immunosuppressants (Penn 1990;Malatack et al 1991;MeierKriesche et al 2002;Cherikh et al 2003). In an exemplary analysis of 157 consecutive cardiac transplant recipients, a ninefold higher incidence of PTLD was observed in OKT-3 treated cardiac allograft patients.…”

Section: Malignant Complicationsmentioning

confidence: 99%

Lymphodepletional Strategies in Transplantation

Page

Kwun

et al. 2013

Cold Spring Harbor Perspectives in Medicine

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Because lymphocytes were shown to mediate transplant rejection, their depletion has been studied as a mechanism of preventing rejection and perhaps inducing immunologic tolerance. Agents that profoundly deplete lymphocytes have included monoclonal antibodies, cytotoxic drugs, and radiation. We have studied several such agents but focused on antibodies that deplete not only peripheral blood lymphocytes, but also lymph node lymphocytes. Depletion of lymph node T lymphocytes appears to permit peripheral tolerance at least for T cells in animal models. Nevertheless, B-cell responses may be resistant to such approaches, and T memory cells are likewise relatively resistant to depleting antibodies. We review the experimental and clinical approaches to depletion strategies and outline some of the pitfalls of depletion, such as limitations of currently available agents, duration of tolerance, infection, and malignancy. It is notable that most tolerogenic strategies that have been attempted experimentally and clinically include depleting agents even when they are not named as the underlying strategy. Thus, there is an implicitly acknowledged role for reducing the precursor frequency of donor antigen-specific lymphocytes when approaching the daunting goal of transplant tolerance.

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“…27,28 The risk for lymphoproliferative disease is particularly high (4% to 10%) after liver transplantation in children. 29,30 Although our patient may be at increased risk for the development of EBV-related lymphoproliferative disease, there is no data available to quantitate this risk because this is the first report of OLT for primary EBV-related fulminant hepatic failure. Recently, the use of serum quantitative EBV DNA by PCR has been proposed as a useful tool for the monitoring of patients for lymphoproliferative disease after transplantation.…”

Section: Liver Transplantation For Fulminant Ebv Hepatitismentioning

confidence: 96%

Fulminant epstein-barr viral hepatitis: Orthotopic liver transplantation and review of the literature

et al. 1998

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Acute hepatic failure caused by primary EpsteinBarr virus (EBV) infection has been reported in the literature in 16 cases, with an overall mortality of 87%. We report a case of fulminant hepatic failure in an immunocompetent young girl caused by primary EBV infection that was treated by orthotopic liver transplantation. After transplantation she has been treated with low-dose immunosuppression, a pooled gammaglobulin preparation containing anti-EBV antibodies, and anti-viral therapy. The patient is presently doing well 2 years after transplantation without evidence of clinical EBV infection, primary immunodeficiency, or lymphoproliferative disease.

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Orthotopic liver transplantation, Epstein-Barr virus, cyclosporine, and lymphoproliferative disease: A growing concern

Cited by 144 publications

References 19 publications

De novo malignancies after liver transplantation: A major cause of late death

De novo malignancies after liver transplantation: A major cause of late death

Lymphodepletional Strategies in Transplantation

Fulminant epstein-barr viral hepatitis: Orthotopic liver transplantation and review of the literature

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