Cholestatic hepatitis leading to hepatic failure in a patient with organ-transmitted hepatitis C virus infection

Lim, Herbert L.; Lau, George; Davis, Gary L.; Dolson, David J.; Lau, Johnson Y.N.

doi:10.1016/s0016-5085(94)95829-7

Cited by 138 publications

(71 citation statements)

References 14 publications

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“…This disease has been reported to develop in HCV-positive transplant individuals or in individuals who receive HCV-positive nonliver organs (kidney, heart). [11][12][13][14] This disease is similar to fibrosing CH that develops in patients with hepatitis B after transplantation. 9 CH is characterized by a relentless progressive increase in serum bilirubin level.…”

Section: Discussionmentioning

confidence: 91%

High levels of hepatitis C virus RNA in native livers correlate with the development of cholestatic hepatitis in liver allografts and a poor outcome

et al. 2001

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A subset of hepatitis C virus (HCV)-positive liver transplant recipients develop cholestatic hepatitis (CH).We investigated the role of pretransplantation disease activity (estimated by Knodell score and HCV RNA quantitation) in the native liver explant on the development of CH and graft and patient outcome. Eight patients with CH were identified among HCV-positive liver transplants and were compared with 20 consecutive patients with recurrent HCV hepatitis of noncholestatic type in liver transplants. We evaluated all 28 explanted native livers histologically using the Knodell scoring system. HCV viral load was measured in the native explant and 5 allograft explants from the CH group using Amplicor HCV RNA Monitor test. Six of 8 patients with CH had HCV RNA levels of 5,000 copies/ g of DNA or greater in the native liver explant, whereas only 1 of the control group had viral loads greater than this level. Greater HCV RNA levels correlated with worse graft and patient survival (P < .001). The 3-year survival rate in the CH group was 18% compared with 77% in the control group (P < .001). There was no difference in the primary immunosuppressive regimens used in the 2 groups. We conclude that (1) CH has a uniformly poor prognosis, (2) type of immunosuppressive therapy appears to have little influence on the development of CH, (3) high pretransplantation HCV RNA levels in the native explant may predict the development of CH, and (4) patients with high HCV RNA levels in the explanted native liver may be appropriate candidates for antiviral therapy to prevent the development of CH. (Liver Transpl 2001;7:118-124.)

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Section: Discussionmentioning

confidence: 91%

High levels of hepatitis C virus RNA in native livers correlate with the development of cholestatic hepatitis in liver allografts and a poor outcome

et al. 2001

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“…In addition to our series, several other case reports of severe cholestatic hepatitis after receiving hearts from HCVantibody positive donors have been reported. [21][22][23][24][25] This pattern of liver injury is reminiscent of the fibrosing cholestatic hepatitis in recurrent hepatitis B virus infection 26 …”

Section: Discussionmentioning

confidence: 99%

Outcome ofDe Novohepatitis C virus infection in heart transplant recipients

et al. 1999

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The outcome of de novo hepatitis C virus (HCV) infection in heart transplant recipients of HCV-antibody positive organs is not known. The aim of the study was to determine the short-term outcome of de novo HCV infection in recipients of HCV-positive donor organs. HCV-antibody negative recipients of HCV-antibody positive hearts were identified from January 1, 1991 to February 28, 1998. Control patients matched for year of transplantation were also identified. Twenty-eight patients (22 males, mean age of 56 ؎ 11 SD) received hearts from HCV-antibody-positive donors. The control group was similar to the patients in all clinical and demographic aspects. Twenty-three patients had detectable viremia by reverse-transcription polymerase chain reaction (RT-PCR). Of these 23 patients with de novo HCV infection, 7 (30%) developed HCV-related liver disease. Three patients (13%) had chronic hepatitis and 4 patients (17%) developed severe acute cholestatic hepatitis (ACH). Mycophenolate mofetil (MMF) use (P ‫؍‬ .04) and high viral load at onset of acute liver disease (P ‫؍‬ .02) were associated with ACH. Overall survival was similar between patients with de novo HCV infection and controls (P ‫؍‬ .20). Development of ACH (P ‫؍‬ .02) and MMF use (P ‫؍‬ .0009) were associated with decreased survival in patients with de novo HCV infection. The present study showed that survival of patients with de novo HCV infection was similar to a matched control group. HCV-related severe ACH is associated with a poor short-term outcome in patients with de novo HCV infection. MMF use may be associated with a higher incidence of HCV-related severe ACH and a poor short-term outcome. (HEPATOLOGY 1999;30:1293-1298

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“…In one patient who acquired HCV during a heart transplantation and developed this pattern of liver damage, the serum HCV RNA level was shown to be very high, and a large proportion of hepatocytes were strongly positive for HCV RNA by in situ polymerase chain reaction. 16 However, only a small proportion of HCVinfected liver transplant recipients develop this pattern of liver injury, thus suggesting that other viral and/or host factors are involved in the pathogenesis of this syndrome.…”

Section: Pathogenesis Of Recurrent Hcv Infection After Liver Transplamentioning

confidence: 99%

Do viral genotypes and HLA matching influence the outcome of recurrent hepatitis C virus infection after liver transplantation?

González‐Peralta

Lau

1998

Liver Transpl

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Cholestatic hepatitis leading to hepatic failure in a patient with organ-transmitted hepatitis C virus infection

Cited by 138 publications

References 14 publications

High levels of hepatitis C virus RNA in native livers correlate with the development of cholestatic hepatitis in liver allografts and a poor outcome

High levels of hepatitis C virus RNA in native livers correlate with the development of cholestatic hepatitis in liver allografts and a poor outcome

Outcome ofDe Novohepatitis C virus infection in heart transplant recipients

Do viral genotypes and HLA matching influence the outcome of recurrent hepatitis C virus infection after liver transplantation?

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