Tryptophan and hepatic coma.
To clarify the involvement of tryptophan in the pathogenesis of hepatic coma, plasma and cerebrospinal fluid (CSF) tryptophan was studied in three patient groups (hepatic coma, stable cirrhosis, and control). An assessment of free fatty acids, some of the amino acids reported to compete with tryptophan for brain uptake, and albumin was also made. The data demonstrated that, whereas the elevated CSF tryptophan levels in cirrhotic patients compared to controls may have been attributable to decreased plasma branched chain amino acids, the elevated CSF tryptophan levels in hepatic coma compared to stable cirrhotic patients were probably attributable to increased plasma free tryptophan concentrations. Associated with the elevated plasma free tryptophan in coma patients was an increase in plasma free fatty acids and a marked decrease in serum albumin levels. Of all the amino acids investigated in the CSF, only tryptophan was significantly increased in patients in hepatic coma compared to cirrhotic patients not in coma.
D000596:Amino Acids / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006501:Hepatic Encephalopathy / Q000150:complications / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D014364:Tryptophan / Q000097:blood / Q000134:cerebrospinal fluid / Q000378:metabolism*
D000596:Amino Acids; D005230:Fatty Acids, Nonesterified; D012709:Serum Albumin; D014364:Tryptophan