Hepatoblastoma in a 2-year-old child of a liver-transplanted mother

Abstract

Vol 349 • January 11, 1997 103 were HLA-typed and compared with normal organ tissue as described. Differences or a loss of HLA-allele expression in the tumour tissue could not be detected. The HLA-allele expression of hepatoblastoma tissue and normal liver tissue were identical to the child’s HLA-characteristic (HLAA1/25, B8/44) and different from those of the mother (HLA-A2/25, B51/44), and her liver graft (HLA-A2/3, B 14/35). To our knowledge this is the first case of malignancy in a child of a mother who became pregnant after solid-organ transplantation. The question arises whether hepatoblastoma occurred by chance in this child or whether there is any causal relation to the history. Several factors may be discussed. First, immunosuppressive therapy throughout fetal life may be a cause of tumour development in the child. Tumour development is reported to be increased after long-term immunosuppressive therapy in transplanted patients and it may also be increased after exposure during fetal life. Up to now no data exist on teratogenicity of ciclosporin but experience is limited. Second, could there be an unknown genetic disease of mother and child leading to cirrhosis in one and hepatoblastoma in the other? Third, could there be a relation between hepatitis B infection and tumour development? Since the child remained negative for all markers of hepatitis B infection, this seems unlikely. Whether hepatoblastoma was caused by any of these factors remains unsolved, but our case indicates that long-term follow-up programmes are necessary for all children born to transplant recipients to define their risk of later health problems and to recognise these problems early.