PATHOLOGICAL CHANGES AFTER LIVING DONOR LIVER
TRANSPLANTATION IN PEDIATRIC AGE GROUP
M. S. El Monayeri1,2 , MD, M. A. Kotb2,3, MD, N. A. Hegazy1, MD, A. F. Hamza1,2, MD,
M. S. El Meteini1,2, MD
Ain Shams Center of Organ Transplantation1, Wadi El Neel Hospital2 and
Department of Pediatrics, Cairo University3, Cairo, Egypt
Introduction: The long term histological outcome after pediatric liver transplantation is not
yet fully understood. Histological abnormalities are commonly present; with many known to
be found in some children who appear clinically well with good graft function.
Objectives: The purpose of this study was to define histopathological changes during longterm follow-up in the liver allograft of children who had undergone living donor liver
transplantation
Methods: Forty infants and children (20 males and 20 females) had Living donor liver
transplantation at Wadi El Neel hospital between October 2001 and March 2010. Their age
ranged between 8 months and 16 years. Thirty two of the transplanted cases, who survived
more than one year, were included in the analysis. Sixty six protocol and clinically indicated
liver biopsy specimens were reviewed, with at least 1 year follow-up; biopsy findings were
correlated with clinical, biochemical and serological findings.
Results: Normal or near normal histology was reported in 11 (34.4%) cases. Chronic
hepatitis was diagnosed in 7 (21.8%) cases (mild in 5 cases and moderate in 2 cases),
serological findings were normal, however, patients responded to treatment with increase
immunosuppressant and addition of steroids. Late cellular rejection was reported in 4
(12.5%) cases, ductopenic rejection in 5 cases (15.6%), biliary/vascular complications in 4
(12.5%) cases and recurrent disease ( HCV) in 1 (3.1%) case. Among cases with abnormal
biopsy findings (21 cases,) serum transaminases were normal in 5 cases (23.8%) and the
biopsies showed late cellular rejection, chronic hepatitis, ductopenic rejection and periportal
fibrosis; follow-up showed progression of disease process. Graft fibrosis was detected as an
isolated finding or associated with other pathological changes. The incidence of graft fibrosis
increased with time (18.75%, 25.32% and 43.7% at 1,3 and 5 years respectively(
Conclusion: Children are more liable to develop late cellular rejection and idiopathic chronic
hepatitis, but they are much less likely to suffer problems with disease recurrence. The
cause of chronic hepatitis in transplanted allografts is uncertain and may be immune
mediated, representing a hepatitic form of chronic rejection. Transplanted livers of
immunosuppressed children who are clinically healthy and have normal transaminase levels
may show histological changes necessitating change of therapeutic strategies