Effect of sodium benzoate on blood ammonia response to oral glutamine challenge in cirrhotic patients: a note of caution.

Abstract

The administration of sodium benzoate provides an alternative pathway for the disposal of waste nitrogen and this substance has been used to treat patients with urea cycle defects and more recently cirrhotics with hepatic encephalopathy. The aim of the study was to assess the ammonia-lowering effect of benzoate in cirrhotic patients without overt hepatic encephalopathy. Glutamine challenge, a method to induce an increase of blood ammonia, was performed in six cirrhotics before and after 5 days of benzoate treatment (10 microg/day). Number Connection Test and Posner's Attention Test were also performed before and after benzoate treatment. Blood ammonia increased after the glutamine load both before (from 66 +/- 12 microg/dl to 123 +/- 34 microg/dl and 179 +/- 53 microg/dl after 30 and 60 min, respectively; ANOVA p = 0.0004) and after benzoate treatment (from 102 +/- 27 microg/dl to 185 +/- 49 microg/dl and 250 +/- 39 microg/dl after 30 and 60 min, respectively; ANOVA p = 0.00001). However, after benzoate treatment, the basal values (102 +/- 27 vs 66 +/- 12 microg/dl; p = 0.01) and peak increments of ammonia (166 +/- 56 microg/dl vs 102 +/- 40 microg/dl; p = 0.04) were significantly higher than before. The Number Connection test and the Posner's test were not altered by benzoate treatment. Benzoate increased both the basal and post-glutamine ammonia levels. These results confirm what has already been observed in experimental animals and suggest a note of caution in the use of sodium benzoate in cirrhotic patients.