Is Hyperammonemia Really the True Cause of Altered Neuropsychology, Brain MR Spectroscopy and Magnetization Transfer After an Oral Amino Acid Load in Cirrhosis? To the Editor:

We read the very interesting article by Balata et al.1 showing that an oral load of an amino acid mixture mimicking hemoglobin increased plasma ammonia and brain glutamate/glutamine levels and changed psy-chometric performance of cirrhotic patients. The amino acid load was also followed by a reduction in myoinositol and magnetization transfer ratio (MTR), suggesting the occurrence of increased brain water, and support-ing the brain swelling hypothesis of hepatic encephalopathy (HE).2 However, could the changes described be unequivocally attributed to ammonia? Together with ammonia, the amino acid load induced an in-crease of a number of amino acids including phenylalanine, tyrosine, and tryptophan, all formerly involved in the pathogenesis of HE. Moreover, the time course of ammonia elevation and psychometric and brain mod-ifications are not coincident: the peak of ammonia occurring earlier than the reduction in myoinositol and MTR. Finally, in cirrhotic patients the effects of acute ammonia elevation on the psychometric performance ar