الفهرس 
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Abstract
Hepatic encephalopathy (N.E.) is a reversible neuropsychiatric syndrome which can accompany advanced liver disease, of all types and/or extensive portal systemic shunting. It is a feature of the natural history of the disease that most patients with liver cirrhosis will develop hepatic encephalopathy and coma at some stage (Silk, 1986).
Hepatic failure is asociatod with a characLe ristic plasma amino acids pattern: high levels of aromatic amino acids (AAA) and reduced branched chain amino acids (BCAA) (Iber et al., 1957).
As aromatic amino acids and branched chain amino acids are transported into brain through a common carrier system in the blood brain barrier (BEB) (Oldendorf et al., 1976), brain uptake of aromatic amino acids may be favoured by the reduction in the plasma values of branched chain amino acids.
Accuninial-jon of aromatic amino acids in Llie brain lead to a• change in synthesis of neurotrans— mutters, resulting in a depletion of putative neuro— transmitters such as norepinephrine and dopamine, and increased synthesis of false or weak transmitters such as octopamine and phenylethylamine (Fischer et al., 1971), such disturbance in neurotransmitter synthesis is thought to be responsible for neurological disorders seen in patients with chronic liver disease.
Trials were done to normalize plasma amino acids through infusion of formulated amino acids mixture, maintenance of nutrition and positive nitrogen balance.
However, the effect of other measures of treatment of hepatic encephalopathy on the amino acids levels was not thought of ‘
Furthermore, the correlation of the changes in amino acid levels with the changes in mental function and outcome after treatment of H.E. is not well known.
Studies on cerebrospinal fluid amino acid levels before and after treatment and any value of their estimation in guiding therapy are lacking except for the diagnostic value of glutamine (Duffy, 1982).
Mannitol was mediated for the treatment of cerebral oedema of fulminant hepatic failure (Canalese et al., 1982). However, it is not known whether it can offer any additional benefit to standard treatment of acute exacerbations of chronic thE.