Impact of immunosuppression on immunopathogenesis of liver damage in hepatitis C virus-infected recipients following liver transplantation

McCaughan, Geoffrey W.; Zekry, Amany

doi:10.1053/jlts.2003.50269

Cited by 40 publications

(27 citation statements)

References 44 publications

(68 reference statements)

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“…By pre-treating with thymoglobulin and minimizing immunosuppression, cellular host immunity against HCV re-infection may be improved [92] . A retrospective study on the use of thymoglobulin induction found that lower levels of Tacrolimus were achieved but HCV recurrence rates were similar between patients who had received thymoglobulin induction therapy and tacrolimus versus tacrolimus and steroids.…”

Section: Anhepatic Initiated Therapy Thymoglobulin Inductionmentioning

confidence: 99%

Strategies to reduce hepatitis C virus recurrence after liver transplantation

Ciria

Pleguezuelo²,

Khorsandi³

et al. 2013

WJH

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Hepatitis C virus (HCV) is a major health problem that leads to chronic hepatitis, cirrhosis and hepatocellular carcinoma, being the most frequent indication for liver transplantation in several countries. Unfortunately, HCV re-infects the liver graft almost invariably following reperfusion, with an accelerated history of recurrence, leading to 10%-30% of patients progressing to cirrhosis within 5 years of transplantation. In this sense, some groups have even advocated for not retransplanting this patients, as lower patient and graft outcomes have been reported. However, the management of HCV recurrence is being optimized and several strategies to reduce post-transplant recurrence could improve outcomes, decrease the rate of re-transplantation and optimize the use of available grafts. Three moments may be the focus of potential actions in order to decrease the impact of viral recurrence: the pretransplant moment, the transplant environment and the post-transplant management. In the pre-transplant setting, it is not well established if reducing the pre transplant viral load affects the risk for HCV progression after transplant. Obviously, antiviral treatment can render the patient HCV RNA negative post transplant but the long-term benefit has not yet been fully established to justify the cost and clinical risk. In the transplant moment, factors as donor age, cold ischemia time, graft steatosis and ischemia/reperfusion injury may lead to a higher and more aggressive viral recurrence. After the transplant, discussion about immunosuppression and the moment to start the treatment (prophylactic, pre-emptive or once-confirmed) together with new antiviral drugs are of interest. This review aims to help clinicians have a global overview of posttransplant HCV recurrence and strategies to reduce its impact on our patients.

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Section: Anhepatic Initiated Therapy Thymoglobulin Inductionmentioning

confidence: 99%

Strategies to reduce hepatitis C virus recurrence after liver transplantation

Ciria

Pleguezuelo²,

Khorsandi³

et al. 2013

WJH

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“…In this regard, a negative correlation between CD4 counts and HCV RNA levels [8,9,11] has been reported. In liver transplant recipients, increased HCV RNA levels are most probably due to the immunosuppressive regimen [12]. Indeed, it has been shown that HCV RNA levels are related to the levels of immunosuppression and to the severity of liver histopathology [6].…”

Section: Introductionmentioning

confidence: 99%

Polyfunctional HCV‐specific T‐cell responses are associated with effective control of HCV replication

Comte²,

et al. 2008

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HCV infection has a severe course of disease in HIV/HCV co-infection and in liver transplant recipients. However, the mechanisms involved remain unclear. Here, we evaluated functional profiles of HCV-specific T-cell responses in 86 HCV mono-infected patients, 48 HIV/HCV co-infected patients and 42 liver transplant recipients. IFN-c and IL-2 production and ability of CD4 and CD8 T cells to proliferate were assessed after stimulation with HCVderived peptides. We observed that HCV-specific T-cell responses were polyfunctional in HCV mono-infected patients, with presence of proliferating single IL-2-, dual IL-2/IFN-c and single IFN-c-producing CD4 1 and dual IL-2/IFN-c and single IFN-c-producing CD8 1 cells. In contrast, HCV-specific T-cell responses had an effector profile in HIV/HCV coinfected individuals and liver transplant recipients with absence of single IL-2-producing HCV-specific CD4 1 and dual IL-2/IFN-c-producing CD8 1 T cells. In addition, HCV-specific proliferation of CD4 1 and CD8 1 T cells was severely impaired in HIV/HCV co-infected patients and liver transplant recipients. Importantly, ''only effector'' T-cell responses were associated with significantly higher HCV viral load and more severe liver fibrosis scores.Ã These two authors contributed equally to this work. Therefore, the present results suggest that immune-based mechanisms may contribute to explain the accelerated course of HCV infection in conditions of HIV-1 co-infection and liver transplantation.

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“…In some studies, the prolonged use of maintenance corticosteroid therapy was associated with lesser severity of the hepatic disease recurrence. In this case, the method of reducing the dose was important, and gradual reductions have been associated with less aggressive forms of hepatitis C [18,19].…”

Section: Factors Associated With the Transplantmentioning

confidence: 95%