Annual Meeting of the European Society of Pediatric Gastroenterology and Nutrition
Aim: To identify pretransplant factors which are influencing survival after orthotopic liver transplantation (OLT) a Cox proportional hazards regression model was applied to 63 children transplanted at Medical School Hannover during the period of 1978 to 1994. Patients and methods: Fiftysix of the patients were suffering from biliary atersia, three from nonsyndromatic biliary hypoplasia and 4 from Alagille syndrome. The median age at first OLT was 3.05 years (range 0.57 - 18.29). A total of 77 OLT were performed. In 29 occasions a reduced size OLT was done. The response variable in the Cox model was survival, as covariates 15 pretransplant variables were entered i.e. age, sex, laparotomy prior to OLT, height, weight, standard deviation scores (SDS) for height and weight, data of first OLT, serum alanin aminotransferase, asparagin aminotransferase, albumin, total bilirubin, cholinesterase activity, glomerular filtration rate and prothrombin time. Results: Significant independent predictors of survival after OLT were pre transplantation SDS for height (p < 0.002), bilirubin (p < 0.03) and albumin (p < 0.04). In a subsequent discriminant analysis cut off points for these variables could be identified i.e. SDS for height < -1.8, bilirubin > 360 μmol/l, and albumin < 36 g/l. The parameter with the highest predictive value was used to split up the patients into a group with urgent indication for OLT (SDS for height < -1.8, n = 43) and an elective indication group (SDS for height ≥ -1.8, n = 20). Comparing the posttransplantation survival in these groups there was a statistically significant difference at 1 year (60.5% vs. 85%) and 5 years (47.8% vs. 85%) after OLT (p < 0.006, log rank test). Conclusion: The mortality after OLT is high if liver function prior to OLT is very poor. Optimal nutritional support before transplantation is mandatory to improve the growth and clinical status of the children. The OLT should be done before the deteriorating liver function leads to stagnation in growth development in children with biliary atresia or hypoplasia.