Some Factors Influencing Urinary Excretion of 3-Hydroxyanthranilic Acid

Excretion of a metabolite of tryptophan, 3-hydroxyanthranilic acid (3HAA), was studied in rabbits under varying conditions (immunization with gram negative bacteria, starvation, tryptophan loading, injection of 3HAA, sodium salicylate or cortisone). Starvation for 3 days resulted in a significant decrease in excretion of 3HAA, and injection of 500 mg of tryptophan (I.V.) was followed by an approximate doubling of 3HAA excretion. Immunization and injection with either salicylate or 3HAA (1000 fig) were not accompanied by significant changes in excretion of the metabolite. Administration of hydrocortisone, an agent known to increase liver tryptophan pyrrolase in other species, resulted in the maximal output of 3HAA observed. By inference, it is suggested that the higher excretion of 3HAA and other metabolites of tryptophan observed in some patients with rheumatoid arthritis may result from the preferential shunting of tryptophan metabolism into the kynurenine pathway. Although the basis for such a shunt in rheumatoid subjects is not known, it is unlikely that adrenocortical steroids are responsible.