期刊
JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
卷 47, 期 1, 页码 41-50出版社
WILEY
DOI: 10.1002/jpen.2416
关键词
hepatic steatosis; intestinal failure-associated liver disease; liver fibrosis; parenteral nutrition; pediatric intestinal failure
High doses of parenteral glucose, amino acids, and energy are associated with steatosis in infants with short bowel syndrome (SBS).
Background: Steatosis is a common feature of intestinal failure-associated liver disease (IFALD) in adult and older pediatric patients receiving long-term parenteral nutrition (PN). There are limited clinical data concerning steatosis in infants with short bowel syndrome (SBS). We investigated early histopathological steatosis and its association to PN. Methods: In this retrospective study, 31 patients with SBS had a diagnostic liver biopsy taken at the median age of 5 (IQR 3-8) months. Follow-up biopsy was available for 24 patients at the median age of 29 (IQR 14-52) months. We evaluated the biopsies for steatosis and other histopathological signs of IFALD and compared results with patient characteristics, PN composition, and liver biochemistry. Results: Diagnostic biopsies revealed steatosis in 8 (26%) patients. At the age of 3 months, patients with steatosis had received higher amounts of parenteral glucose: median 15.1 (IQR 12.4-17.2) vs 12.3 (8.7-14.4) g/kg/d (P = 0.04), amino acids: 2.9 (2.5-3.4) vs 2.2 (1.6-2.7) g/kg/d (P = 0.03), and energy: 87 (80-98) vs 73 (54-79) kcal/kg/d (P = 0.01) than those without steatosis. We detected no significant differences in parenteral lipid intake between the groups. Steatosis also associated with increased serum bile acid (P = 0.02), alanine aminotransferase (P = 0.0002), and aspartate aminotransferase (P = 0.001) levels. Conclusions: In this cohort, high parenteral glucose, amino acid, and energy provision associated with liver steatosis in infants with SBS. We recommend monitoring of bile acid and transaminase levels while aiming for PN with balanced macronutrient supply according to current recommendations to protect the liver from steatosis.
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