CHANGES IN ENDOGENOUS BENZODIAZEPINE-LIKE COMPOUND LEVELS DURING THE COURSE OF FULMINANT HEPATIC-FAILURE - POTENTIAL EFFECTS OF DECREASED RENAL-FUNCTION

The pathogenetic agents which cause encephalopathy clrre to fulminant hepatic failure are still under debate. Ammonia and benzodiazepine-lik e compounds are two of the most important agents considered, so far. H erein, we report the levels of benzodiazepine-like compounds in serum and in urine and of venous ammonia measured during the course of the d isease (30 days). The patient rapidly developed stage IV encephalopath y with high levels of ammonia and with only a slight increase of benzo diazepine-like compounds. At that moment, the levels of these compound s were similar to those recorded in the blood when the patient regaine d full consciousness 28 days later During the course of the disease, t here was a 10-fold increase of benzodiazepine-like compounds at serum which was recorded in parallel with an impaired excretion due to oligu ria, This observation seems to indicate that encephalopathy may develo p in the absence of significantly increased levels of these compounds and that their episodic increase during fulminant hepatic failure may be an epiphenomenon linked with several factors such as impaired renal function.