Seroconversion after the addition of famciclovir therapy in a child with hepatitis B virus infection after liver transplantation who developed lamivudine resistance.

There is very little information about hepatitis B virus (HBV) infection in children after liver transplantation. This is the first report of the addition of famciclovir in a child who developed lamivudine resistance.A 5-year-old boy who was serum HBsAg-negative and was not vaccinated against HBV underwent living-related liver transplantation for fulminant hepatitis A. The donor was his mother, who was serum HBcAb-positive. No immunoprophylaxis was administered. HBV infection developed after 18 months and was treated with 3 mg/kg daily of lamivudine. Serum alanine aminotransferase normalized and HBV DNA load decreased significantly. Sixteen months later, lamivudine resistance developed; a mutation (M552I) was confirmed by sequencing through the YMDD locus of the HBV polymerase gene. The addition of 750 mg daily of famciclovir led to seroconversion and the disappearance of serum HBV DNA. Lamivudine in combination with famciclovir might be a therapeutic option for HBV reinfection after liver transplantation, also in children. Suppression of viral replication to undetectable values is possible even in the lamivudine-resistant mutant.

Chronic hepatitis C in Israeli children.

Natural history, epidemiology, and histopathological features of chronic hepatis C (CHC) are well established in adults. Data on histopathological findings of CHC in children are still limited and controversial. We aimed to evaluate the histopathological features of CHC in children in Israel. We reviewed, retrospectively, 20 liver specimens from 20 children with CHC for inflammation and fibrosis, hepatocyte necrosis, fatty changes, cholestasis, bile duct damage, sinusoidal lymphocytosis, and glycogen storage. The most common histological feature was portal inflammation (95%) and lobular inflammation (70%). Sinusoidal lymphocytosis was present in 85% and glycogen storage vacuoles in 40%. Most of the children (80%) had no fibrosis, 15% had mild fibrosis and 5% moderate fibrosis. Advanced fibrosis or cirrhosis was not found. No correlation was found between the age at biopsy and any of the histological parameters. Our study shows that children with CHC have a different phenotype of liver disease with slowly progressive natural history irrespective of duration of the disease.