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

Citation
Jk. Delladetsima et al., Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection, LIVER TR S, 5(4), 1999, pp. 294-300
Citations number
22
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
LIVER TRANSPLANTATION AND SURGERY
ISSN journal
10743022 → ACNP
Volume
5
Issue
4
Year of publication
1999
Pages
294 - 300
Database
ISI
SICI code
1074-3022(199907)5:4<294:FCHIRT>2.0.ZU;2-S
Abstract
patitis B virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been rep orted in other immunocompromised groups infected with HBV and in a few tran splant recipients with hepatitis C virus (HCV) infection. We present the oc currence of FCH in 4 NOV-infected renal transplant recipients within a seri es 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, methyl prednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 month s. The biochemical profile was analogous to a progressive cholestatic syndr ome in 3 patients, whereas the fourth patient had only slightly increased a lanine aminotransferase and gamma-glutamyl transferase (gamma GT) levels, L iver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an earl y stage; All patients were anti-NOV negative at the time of transplantation , whereas 2 patients, 1 with incomplete and 1 with complete histological FC H features, seroconverted after 3 and 31 months, respectively. The patients were HCV RNA positive at the time of the first liver biopsy and showed hig h serum HCV RNA levels (14 to 58 x 10(6) Eq/mL, branched DNA). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis; im munosuppression was drastically reduced. Two patients died of sepsis and li ver: failure 16 and 18 months posttransplantation, whereas the seroconverte d patients showed marked improvement of their liver disease, which was hist ologically verified in 1 patient. In conclusion, FCH can occur in HCV-infec ted 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 drasti c reduction of immunosuppression may have a beneficial effect on the outcom e of the disease. Copyright (C) 1999 by the American Association for the St udy of Liver Diseases.