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.

Liver transplantation (LT) for alcoholic cirrhosis remains controversial. This controversy surrounding LT in alcoholics focuses on the risk of alcohol recidivism and on potential noncompliance with the immunosuppressive regimen, both of which result in graft failure. Our study examined alcohol recidivism after LT by measuring alcohol in urine and its repercussion on the allograft. Forty-four consecutive alcoholic patients and a comparison group of 17 patients receiving LT were included in this study and followed up for a mean of 39.5 +/- 19.6 months. Seven percent (3 of 44) of patients with alcoholic liver disease and 0% of patients in the comparison group admitted to having used alcohol after LT. Alcohol in urine, however, was detected in 18% (8 of 44) of the alcoholic group; therefore the true recidivism rate was higher than the rate admitted. All patients in both groups were compliant with the medications, because the cyclosporine levels were within the therapeutic range in all. On histologic examination the only alcohol-induced lesion found in three of the eight recidivistic patients was steatosis. Therefore, although alcoholic recidivism occurs, it does not seem to affect compliance to treatment profoundly or to compromise graft function. Therefore, LT seems justified for end-stage alcoholic cirrhosis.

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