Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis

Davies, Susan; Portmann, Bernard; O’Grady, John; Aldis, Peter; Chaggar, Kanchan; Alexander, Graeme; Williams, Roger

doi:10.1002/hep.1840130122

Cited by 449 publications

(218 citation statements)

References 17 publications

(7 reference statements)

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“…In contrast to the rather frequent occurrence of FCH in HBV-infected liver allografts, [1][2][3][4] in our series of HCV-infected renal transplant recipients, it was found in only 5% of the patients. The interval from transplantation to appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months.…”

Section: Discussioncontrasting

confidence: 94%

“…Copyright 1999 by the American Association for the Study of Liver Diseases F ibrosing cholestatic hepatitis (FCH) was introduced as a complication of hepatitis B recurrence in liver allografts, usually developing 2 to 10 months after transplantation and leading within weeks or a few months to end-stage liver failure. [1][2][3][4] It has been closely associated with immunosuppression within the setting of liver transplantation, whereas a direct cytopathic effect of massively accumulated hepatitis B virus (HBV) antigens has been implicated in its pathogenesis. FCH has been reported sporadically in other immunocompromised patients infected with HBV, including renal graft recipients, [5][6][7][8][9][10] as well as a few transplant patients with hepatitis C virus (HCV) infection, in particular in 4 liver transplant recipients, 11 1 heart transplant recipient, 12 and recently in 1 renal transplant recipient.…”

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confidence: 99%

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Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

et al. 1999

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Fibrosing cholestatic hepatitis (FCH) has been described as a specific manifestation of hepatitis B virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been reported in other immunocompromised groups infected with HBV and in a few transplant recipients with hepatitis C virus (HCV) infection. We present the occurrence of FCH in 4 HCV-infected renal transplant recipients within a series of 73 renal transplant recipients with HCV infection followed up closely serologically and with consecutive liver biopsies. All 4 patients received the triple-immunosuppressive regimen (azathioprine, cyclosporine A, methylprednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months. The biochemical profile was analogous to a progressive cholestatic syndrome in 3 patients, whereas the fourth patient had only slightly increased alanine aminotransferase and ␥-glutamyl transferase (␥GT) levels. Liver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an early stage. All patients were anti-HCV negative at the time of transplantation, whereas 2 patients, 1 with incomplete and 1with complete histological FCH features, seroconverted after 3 and 31 months, respectively. The patients were HCV RNA positive at the time of the first liver biopsy and showed high serum HCV RNA levels (14 to 58 ؋ 10 6 Eq/mL, branched DNA). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis, immunosuppression was drastically reduced. Two patients died of sepsis and liver failure 16 and 18 months posttransplantation, whereas the seroconverted patients showed marked improvement of their liver disease, which was histologically verified in 1 patient. In conclusion, FCH can occur in HCV-infected renal transplant recipients. It seems to develop as a complication of a recent HCV infection during the period of maximal immunosuppression and is associated with high HCV viremia levels. There are indications that drastic reduction of immunosuppression may have a beneficial effect on the outcome of the disease.

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Section: Discussioncontrasting

confidence: 94%

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confidence: 99%

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

et al. 1999

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“…12,13 A similar pattern has been described in a proportion of patients with severe recurrent HBV infection after transplantation, a syndrome known as fibrosing cholestatic hepatitis, whose pathogenesis is believed to be related to very high levels of HBV in the liver graft. 14,15 Detailed studies of HCV antigens and genome expression in this group of patients with recurrent cholestatic hepatitis have not been reported. 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.…”

Section: Pathogenesis Of Recurrent Hcv Infection After Liver Transplamentioning

confidence: 96%

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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“…Despite high levels of HBV viremia, we have not found any case of fibrotic cholestatic hepatitis. 28 Preliminary experience with lamivudine in transplant recipients with recurrent hepatitis has been encouraging. 29,30 Therapy frequently has been associated with loss of HBV DNA by standard hybridization, and histological improvement has also been reported after 6 months of treatment.…”

Section: Discussionmentioning

confidence: 99%

Severe clinical course of de novo hepatitis B infection after liver transplantation

et al. 1999

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The aim of this study is to determine the origin, clinical outcome, allograft histological characteristics, and virological outcome of de novo hepatitis B virus (HBV) infection after orthotopic liver transplantation (OLT). We studied 136 hepatitis B surface antigen (HBsAg)-negative liver transplant recipients. HBV DNA was detected by dot-blot hybridization and polymerase chain reaction (PCR). The S gene was sequenced. Hepatitis C virus (HCV) RNA was assessed by PCR. The long-term clinical and histological outcome was determined. Six of 136 HBsAg-negative patients (4.4%) became HBsAg positive after transplantation. The source of HBV infection was reactivation of latent HBV infection in 2 patients and was not identified in 4 patients. Two donors had isolated core antibody. Two of these 6 patients developed acute liver failure related to hepatitis B. The 4 other patients had severe chronic hepatitis related to hepatitis B. All patients had high-level HBV replication. No significant mutations in the S gene were found. These data suggest that de novo hepatitis B infection is not a mild disease and might represent a significant cause of graft dysfunction. This is the first report of fulminant hepatitis caused by de novo hepatitis B infection after OLT.

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Hepatic histological findings after transplantation for chronic hepatitis B virus infection, including a unique pattern of fibrosing cholestatic hepatitis

Cited by 449 publications

References 17 publications

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

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

Severe clinical course of de novo hepatitis B infection after liver transplantation

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