Potential conflict of interest: Nothing to report.
Liver Failure/Cirrhosis/Portal Hypertension
Persistent abnormal liver fibrosis after weaning off parenteral nutrition in pediatric intestinal failure
Article first published online: 17 JUN 2013
Copyright © 2013 American Association for the Study of Liver Diseases
Volume 58, Issue 2, pages 729–738, August 2013
How to Cite
Mutanen, A., Lohi, J., Heikkilä, P., Koivusalo, A. I., Rintala, R. J. and Pakarinen, M. P. (2013), Persistent abnormal liver fibrosis after weaning off parenteral nutrition in pediatric intestinal failure. Hepatology, 58: 729–738. doi: 10.1002/hep.26360
This work was supported by grants from the Mary and Georg C. Ehnroth Foundation, the Finnish Medical Association, the Sigrid Juselius Foundation, and the Finnish Pediatric Research Foundation.
- Issue published online: 29 JUL 2013
- Article first published online: 17 JUN 2013
- Accepted manuscript online: 4 MAR 2013 12:24PM EST
- Manuscript Accepted: 20 FEB 2013
- Manuscript Revised: 3 FEB 2013
- Manuscript Received: 28 NOV 2012
The aim of this study was to evaluate the long-term effects of pediatric intestinal failure (IF) on liver histology. Altogether, 38 IF patients (median age: 7.2 years; range, 0.2-27) underwent liver biopsy, gastroscopy, abdominal ultrasound, and laboratory tests. Sixteen patients were on parenteral nutrition (PN) after 74 PN months (range, 2.5-204). Twenty-two had weaned off PN 8.8 years (range, 0.3-27) earlier, after 35 PN months (range, 0.7-250). Fifteen transplant donor livers served as controls. Abnormal liver histology was found in 94% of patients on PN and 77% of patients weaned off PN (P = 0.370). During PN, liver histology weighted with cholestasis (38% of patients on PN versus 0% of patients weaned off PN; P = 0.003) and portal inflammation (38% versus 9%; P = 0.050) were found. Fibrosis (88% versus 64%; P = 0.143; Metavir stage: 1.6 [range, 0-4] versus 1.1 [range, 0-2]; P = 0.089) and steatosis (50% versus 45%; P = 1.000) were equally common during and after weaning off PN. Plasma alanine aminotransferase (78 U/L [range, 19-204] versus 34 [range, 9-129]; P = 0.009) and conjugated bilirubin (43 μmol/L [range, 1-215] versus 4 [range, 1-23]; P = 0.037) were significantly higher during than after weaning off PN. Esophageal varices were encountered in 1 patient after weaning off PN. Metavir stage was associated with small bowel length (r = −0.486; P = 0.002) and number of septic episodes (r = 0.480; P = 0.002). In a multivariate analysis, age-adjusted small bowel length (ß = −0.533; P = 0.001), portal inflammation (ß = 0.291; P = 0.030), and absence of an ileocecal valve (ß = 0.267; P = 0.048) were predictive for fibrosis stage. Conclusion: Despite resolution of cholestasis and portal inflammation, significant liver fibrosis and steatosis persist after weaning off PN. Extensive small intestinal resection was the major predictor for liver fibrosis stage. (Hepatology 2013;58:729–738)