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The amino acid L-histidine is obtained by man primarily from dietary protein. The essential need for this amino acid, however, has not been demonstrated conclusively (1). Previous studies have indicated that the major pathways of utilization of L-histidine are by way of incorporation into body protein, excretion into the urine, and metabolism to glutamic acid. It is believed that the pertinent mammalian pathway follows the reactions outlined in Figure 1 (2-4). Prior to our initial report (5) of the compounds shown in Figure 1, histidine, a-formiminoglutamic acid (FiGlu), and glutamic acid had been definitively identified in the urine of man. Urocanic acid (UA) had been identified in the urine of small mammals (2) and tentatively identified chromatographically in the urine of man (6). Imidazolonepropionic acid has not been identified in urine as yet, although a metabolic oxidation product derived from this intermediate, hydantoin-5-propionic acid, has been identified in rat urine (7). Since our original report, characterizing the occurrence of UA in the urine of man (5), McIsaac and Page (8) have described the identification of UA in the urine of a patient with hepatic coma, and similarly UAhas been identified by Whitehead and Arnstein in a patient with kwashiorkor (9). FiGlu excretion has been studied in recent years in patients with folic acid deficiency (10-12) and treated with folic acid antagonists (13). It has been found that such patients, particularly when given loading doses of histidine, excrete increased amounts of this metabolite in the urine. Small

the journal of clinical investigation/the journal of clinical investigation

URINARY UROCANIC ACID IN MAN: THE IDENTIFICATION OF UROCANIC ACID AND THE COMPARATIVE EXCRETIONS OF UROCANIC ACID AND N-FORMIMINOGLUTAMIC ACID AFTER ORAL HISTIDINE IN PATIENTS WITH LIVER DISEASE