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Serine Metabolism After Portacaval Shunt

Frederick A. Reichle, MD; M. Prince Brigham, MD; R. Robert Tyson, MD; Rose Marie Reichle, MEd; Mercita Reilly, BA; George P. Rosemond, MD
Arch Surg. 1970;100(2):163-166. doi:10.1001/archsurg.1970.01340200051012.
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Although portacaval shunt effectively controls hemorrhage from esophageal varices by control of portal hypertension, liver function does not improve and often deteriorates after diversion of portal blood from the liver. Hepatic failure is the most common cause of the excessively high mortality following portacaval shunt. The etiology of hepatic failure and the reasons for the associated metabolic changes after portacaval shunt are not understood. It has been suggested that deterioration of liver function studies may be related to decreased total hepatic blood flow, diversion of an alleged hepatotrophic factor from the liver, or diversion of oxygen or other nutrients by the portacaval shunt. Recently, alterations in the metabolism of certain amino acids and their related enzymes and metabolites have been described in an effort to elucidate the pathogenesis of postshunt liver failure. Postshunt induction of hepatic histidase and histidine transaminase occurred selectively after portacaval shunt with no change in hepatic


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