| Literature DB >> 21857820 |
Abstract
Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic liver disease and/or portosystemic shunting of blood flow. The pathophysiology of this disease is quite complex, as it involves overproduction and reduced metabolism of various neurotoxins, particularly ammonia. Recent hypotheses implicate low-grade cerebral edema as a final common pathway for the pathophysiology of HE. Management of this condition is multifaceted and requires several steps: elimination of precipitating factors; removal of toxins, both by reducing them at their source and by augmenting scavenging pathways; modulation of resident fecal flora; proper nutritional support; and downregulation of systemic and gut-derived inflammation.Entities:
Keywords: Hepatic encephalopathy; ammonia; cerebral edema; glutaminase; urea cycle
Year: 2011 PMID: 21857820 PMCID: PMC3127024
Source DB: PubMed Journal: Gastroenterol Hepatol (N Y) ISSN: 1554-7914