Morphologic and Biochemical Changes in Dogs After Portacaval Shunt Plus Bile Fistula or Ileal Bypass: Failure of Bile Fistula or Ileal Bypass to Prevent Hepatocyte Atrophy
✍ Scribed by Jon S. Thompson; Kendrick A. Porter; Nobuo Hayashida; Donald J. Mcnamara; Thomas S. Parker; William J. I. Russell; Antonio Francavilla; Thomas E. Starzl
- Book ID
- 102848286
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 800 KB
- Volume
- 3
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
External biliary fistula (BF) or ileal bypass (IB) was performed in dogs at the time of or 2 weeks after portacaval shunt (PCS). The pathologic changes in the dog livers 2 to 4 weeks later were compared to those caused by PCS alone. Histopathologic differences between PCS alone vs. PCS plus B F or IB could not be found. Thus, the experiments did not confirm recent observations by others in rats that BF prevents or reverses the hepatic injury of PCS. As estimated by plasma mevalonic acid determinations, the increase in hepatic cholesterol synthesis that is characteristic after BF or IB was suppressed in animals with PCS. BF and IB reduced but did not eliminate the postprandial elevation in serum bile acid that occurs after PCS. The findings have possible relevance in planning the treatment of patients with familial hypercholesterolemia with the combined use of PCS and IB.
Completely diverting portacaval shunt (PCS), also called Eck's fistula, has been used for its effect upon the metabolism of patients with glycogen storage disease (l), familial hypercholesterolemia (2, 3), and al-antitrypsin deficiency (4). The metabolic palliation in these diseases has been ascribed in part to the hepatocyte alterations caused by portal diversion including atrophy, deglycogentation, fat accumulation, increased mitosis, and major ultrastructural disruptions (2,(4)(5)(6)(7)(8)(9). These changes are identical in rats, dogs, and humans (5). Thus, research with any of these species should be applicable to all in spite of the fact that humans are unusually resistant to the hepatic encephalopathy that may complicate PCS. Balabaud et al. (10) and Bioulac et al. (11) have