Intestinal failure associated liver disease in a short bowel syndrome pediatric cohort: Incidence and prognosis

2014 ◽  
Vol 46 ◽  
pp. e81
Author(s):  
Antonella Diamanti ◽  
Teresa Capriati ◽  
Vincenzo Di Ciommo Laurora ◽  
Lidia Monti ◽  
Giuliano Torre ◽  
...  
Keyword(s):  
Liver Disease ◽  
Short Bowel Syndrome ◽  
Intestinal Failure ◽  
Short Bowel

scholarly journals What is the optimal lipid emulsion for preventing intestinal failure-associated liver disease following parenteral feeding in a rat model of short-bowel syndrome?

2021 ◽  
Author(s):  
Seiro Machigashira ◽  
Tatsuru Kaji ◽  
Shun Onishi ◽  
Keisuke Yano ◽  
Toshio Harumatsu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fish Oil ◽  
Hepatic Steatosis ◽  
Short Bowel Syndrome ◽  
Rat Model ◽  
Lipid Emulsion ◽  
Intestinal Failure ◽  
Small Bowel Resection ◽  
Sprague Dawley ◽  
Short Bowel

Abstract Purpose Composite lipid emulsion (CLE) has been used for intestinal failure-associated liver disease (IFALD) to compensate for the disadvantages of soybean oil lipid emulsion (SOLE) or fish oil lipid emulsion (FOLE). However, the influence of its administration is unclear. We evaluated the effects of these emulsions on IFALD using a rat model of the short-bowel syndrome. Methods We performed jugular vein catheterization and 90% small bowel resection in Sprague–Dawley rats and divided them into four groups: control (C group), regular chow with intravenous administration of saline; and total parenteral nutrition co-infused with SOLE (SOLE group), CLE (CLE group) or FOLE (FOLE group). Results Histologically, obvious hepatic steatosis was observed in the SOLE and CLE groups but not the FOLE group. The liver injury grade of the steatosis and ballooning in the FOLE group was significantly better than in the SOLE group (p < 0.05). The TNF-α levels in the liver in the FOLE group were significantly lower than in the SOLE group (p < 0.05). Essential fatty acid deficiency (EFAD) was not observed in any group. Conclusion Fish oil lipid emulsion attenuated hepatic steatosis without EFAD, while CLE induced moderate hepatic steatosis. The administration of CLE requires careful observation to prevent PN-induced hepatic steatosis.

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