Changes in various neurotransmitter systems, in blood brain barrier integrity and/or function, and in brain energy metabolism, may precipitate HE. Although a "specific cause" of HE (i. e. the presence of a well-defined toxin) has not been identified so far, the common denominator of all these changes is the presence of liver failure. The various hypotheses of the pathogenesis of HE are not mutually exclusive, but have to be integrated into the clinical syndrome of liver failure. It is conceivable that "specific causes" of HE do not exist at all. Brain function may be affected to a certain degree by the various consequences of liver failure (such as the accumulation of neuroactive compounds and of neurotoxins, changes in the metabolism of amino acids, decreased availability of energy fuels and circulatory changes), finally precipating the syndrome of HE.
机构:
University of Alabama at Birmingham, Department of Medicine, Birmingham, AL 35294-0005University of Alabama at Birmingham, Department of Medicine, Birmingham, AL 35294-0005
Dbouk N.
McGuire B.M.
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University of Alabama at Birmingham, Department of Medicine, Birmingham, AL 35294-0005University of Alabama at Birmingham, Department of Medicine, Birmingham, AL 35294-0005
机构:
Tulane Univ, Div Gastroenterol & Hepatol, Dept Internal Med, New Orleans, LA 70112 USATulane Univ, Div Gastroenterol & Hepatol, Dept Internal Med, New Orleans, LA 70112 USA
Parekh, Parth J.
Balart, Luis A.
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Tulane Univ, Div Gastroenterol & Hepatol, Dept Internal Med, New Orleans, LA 70112 USATulane Univ, Div Gastroenterol & Hepatol, Dept Internal Med, New Orleans, LA 70112 USA