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Cerebrospinal fluid content of diazepam binding inhibitor in chronic hepatic encephalopathy
Author(s) -
Rothstein Jeffrey D.,
McKhann Guy,
Guarneri Patrizia,
Barbaccia Maria Luisa,
Guidotti Alessandro,
Costa Erminio
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410260109
Subject(s) - hepatic encephalopathy , cerebrospinal fluid , medicine , neurochemical , endocrinology , encephalopathy , gabaa receptor , diazepam , glutamine , benzodiazepine , chemistry , pharmacology , receptor , amino acid , cirrhosis , biochemistry
The neuropeptide diazepam binding inhibitor (DBI) is an endogeneous allosteric modulator of gamma‐aminobutyric acid (GABA) receptors at the benzodiazepine recognition site. Recent theories on the neurochemical cause for hepatic encephalopathy have implicated activation of inhibitory neurotransmitter GABA systems. In 20 patients with hepatic disease, blood and cerebrospinal fluid (CSF) levels of ammonia and amino acids were measured. As in previous studies there was a selective elevation of CSF amino acids as well as a correlation between CSF glutamine levels and encephalopathy. CSF DBI levels were maximally elevated 5‐fold in patients with hepatic encephalopathy, but they were normal in those patients with liver disease not associated with changes in mental status and in patients with nonhepatic encephalopathy. Levels of DBI correlated with the clinical staging of hepatic encephalopathy. These data suggest that DBI may participate in the modulation of cerebral function in hepatic encephalopathy.