Cytomegalovirus Infection and Donor/Recipient Hla Antigens: Interdependent Co-Factors in Pathogenesis of Vanishing Bileduct Syndrome After Liver Transplantation

O’Grady, Joseph P.; Sutherland, Sheena; Harvey, Felicity; Calne, R Y; Alexander, G.; Donaldson, PT; Portmann, Bernard; Williams, Roger

doi:10.1016/s0140-6736(88)92356-2

Cited by 270 publications

(90 citation statements)

References 13 publications

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“…3 An association between CMV 5 and 28 months from transplantation. In these 10 painfection and chronic liver rejection with VBDS has been sugtients, acute rejections were frequent, and nine of ten gested, 15,16 although other investigators have been unable to patients had at least one episode of rejection early after demonstrate a definite association. 17 The persistence of CMVtransplantation.…”

Section: Cal and Experimental Studies Have Shown That CMV Ismentioning

confidence: 96%

Persistent cytomegalovirus in liver allografts with chronic rejection

et al. 1997

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The etiology of chronic allograft rejection is multifactorial. 8 Cytomegalovirus (CMV) infection is one of the sugAmong the risk factors are histocompatibility, frequency of gested risk factors for chronic allograft rejection. Cliniacute rejection episodes, long ischemia time, and infections. cal and experimental studies have shown that CMV isAn association between viral infection, particularly that of somehow implicated in rejection mechanisms and in the cytomegalovirus (CMV) infection, and chronic rejection has generation of graft arteriosclerosis, characteristic of been suggested. In heart transplantation, chronic rejection chronic rejection. In liver transplantation, there is also manifests as allograft arteriosclerosis, and increased graft evidence of an association between CMV and vanishing arteriopathy has been found in recipients with previous CMV bile duct-syndrome (VBDS), which is characteristic of infection. [9][10][11] In kidney transplantation, CMV has been rechronic liver allograft rejection. In this study, the role ported to trigger rejection 12,13 by inducing major histocompatof posttransplant CMV infection and of acute rejection ibility complex antigens, especially class II molecules. 13 CMV in the patients with irreversible, histologically conis also suggested to be involved in late acute renal allograft firmed chronic liver rejection with VBDS and vasculoparejections. 14 In liver transplantation, a higher incidence of thy was analyzed. Ten of 200 (5%) consecutive liver transchronic rejection has been observed in patients with verified plants were lost due to chronic rejection, from between posttransplant CMV infection. 3 An association between CMV 5 and 28 months from transplantation. In these 10 painfection and chronic liver rejection with VBDS has been sugtients, acute rejections were frequent, and nine of ten gested, 15,16 although other investigators have been unable to patients had at least one episode of rejection early after demonstrate a definite association. 17 The persistence of CMVtransplantation. All patients (10 of 10) had a history of DNA in the hepatocytes of liver grafts in VBDS has been CMV infection usually following acute rejection. To inrecently demonstrated. 16 vestigate the role of CMV in chronic rejection, nine availIn this retrospective study, the aim was to investigate the able removed grafts were examined for the presence of role of posttransplant CMV infection in patients with chronic the CMV genome by DNA-hybridization in situ using a liver rejection and VBDS whether CMV-DNA is still found biotinylated CMV-DNA probe. Persistent CMV-DNA was in the explanted allografts and, if so, in which parenchymal found in all of those available grafts with chronic rejeccomponents of the liver. To detect the viral genome in frozen tion. CMV-DNA was strongly expressed in the remaining sections of the liver grafts, in situ hybridization and a biotinbile ducts and moderately expressed in the endothelial ylated CMV-DNA probe were used. cells of the vascular structures, the CMV positi...

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Section: Cal and Experimental Studies Have Shown That CMV Ismentioning

confidence: 96%

Persistent cytomegalovirus in liver allografts with chronic rejection

et al. 1997

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“…during blood transfusions and transplantation of li ver allografts latently infected with virus). Moreover, the pharmacologicallyinduced impairment of immunity in liver transplant recipients markedly limits the abil ity of the patients to effecti vely control "endogenously reactivated" or "allografttransmitted" CMV, leading in the shortterm to febrile and tissueinvasi ve diseases, and in the longterm to poor allograft and patient survi val [15] .…”

Section: Introductionmentioning

confidence: 99%

Current concepts on cytomegalovirus infection after liver transplantation

Lee

Razonable

2010

WJH

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Cytomegalovirus (CMV) is the most common viral pathogen that negatively impacts on the outcome of liver transplantation. CMV cause febrile illness often accompanied by bone marrow suppression, and in some cases, invades tissues including the transplanted allograft. In addition, CMV has been significantly asso ciated with an increased predisposition to allograft rejection, accelerated hepatitis C recurrence, and other opportunistic infections, as well as reduced overall pa tient and allograft survival. To negate the adverse effects of CMV on outcome, its prevention, whether through antiviral prophylaxis or preemptive therapy, is regarded as an essential component to the medical management of liver transplant patients. Two recent guidelines have suggested that antiviral prophylaxis or preemptive therapy are similarly effective in preventing CMV disease in modest-risk CMV-seropositive liver trans plant recipients, while antiviral prophylaxis is the preferred strategy over preemptive therapy for the preven tion of CMV disease in high-risk recipients [CMV-seronegative recipients of liver allografts from CMV-seropositive donors (D+/R-)]. However, antiviral prophylaxis has only delayed the onset of CMV disease in many CMV D+/R-liver transplant recipients, and at least in one study, such occurrence of late-onset primary CMV disease was significantly associated with increased mortality after liver transplantation. Therefore, optimized strategies for prevention are needed, and aggressive treatment of CMV infection and disease should be pursued. The standard treatment of CMV disease consists of intravenous ganciclovir or oral valganciclovir, and if feasible, one should also reduce the degree of immunosuppression. In one recent controlled clinical trial, val ganciclovir was found to be as effective and safe as intravenous ganciclovir for the treatment of mild to mo derate CMV disease in solid organ (including liver) tran splant recipients. In this article, the authors review the current state and the future perspectives of prevention and treatment of CMV disease after liver transplantation.

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“…The virus was demonstrated to up-regulate alloantigens and to increase the risk of acute and chronic allograft rejection [115,116] . It may be associated with vanishing bile duct syndrome and ductopenic chronic rejection and, thus, with risk of cholestatic allograft dysfunction [117,118] . Infection of endothelial vascular cells with CMV promotes the risk of hepatic artery thrombosis and subsequent liver allograft failure [119,120] .…”

Section: Cytomegalovirus Hyperimmunoglobulin After Ltmentioning

confidence: 99%