Mitochondrial pathways of cell death are stimulated in human hepatic mitochondria exposed to GCDC consistent with the role of mitochondrial dysfunction in the pathogenesis of cholestatic liver injury. These results parallel those reported in rodents, supporting the extrapolation of mechanistic studies of bile acid toxicity from rodent to humans.
These data indicate that persistent leaking necessitating surgical closure of a gastrocutaneous fistula does not occur in children with a PEG tube removed within 11 months of insertion. In contrast, 23% of children with a PEG tube removed 11 or more months after insertion require surgery. In patients identified as candidates for tube removal, this time frame may be important in clinical decision making.
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