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Widespread interest in 5-hydroxytryptamine (5-HTA) as a biologically active amine and the close association between this substance and malignant carcinoidosis have led to detailed studies of the 5-hydroxyindole pathway of tryptophan metabolism in man and experimental animals (1-3). Tryptophan is apparently hydroxylated to form the serotonin precursor, 5-hydroxytryptophan (5-HTP) (1, 4). In the presence of a specific, pyridoxine-dependent decarboxylase, 5-HTP is readily decarboxylated in several tissues to form 5-HTA (5). Monoamine oxidase, which is found principally in gut, lung, liver, kidney and brain, catalyzes the oxidative deamination of 5-HTA to form 5-hydroxyindoleacetic acid (5-HIAA) (6, 7). Since both 5-HTP decarboxylase and monoamine oxidase have been demonstrated in liver tissue in vitro, investigation of 5-hydroxyindole metabolism in patients with hepatic cirrhosis was undertaken. The present report summarizes studies of 5-HTA and 5-HIAA excretion in the urine following the intravenous administration of various 5-hydroxyindole compounds in human subjects with and without hepatic cirrhosis and in rats.

IN VIVO STUDIES OF 5-HYDROXYINDOLE METABOLISM IN PATIENTS WITH HEPATIC CIRRHOSIS AND IN RATS*†