Tryptophan metabolism in porphyria, schizophrenia, and a variety of neurologic and psychiatric diseases

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Abstract
The urinary excretion of 9 metabolites of L-tryptophan was determined in 18 patients with acute, chronic, or mixed hepatic porphyria, 19 patients with schizophrenia, 8 patients with a variety of psychoses, and 10 patients with a variety of neurologic diseases. Of 18 patients with porphyria, 13 showed evidence of abnormal tryptophan metabolism characterized by increased urinary excretion of kynurenine, acetylkynurenine, kynurenic acid, hydroxykynurenine, and, occasionally, xanthurenic acid or other metabolites. A similar metabolic response was found in 6 of the patients with a variety of types of psychoses. Each of the patients with neurologic conditions metabolized tryptophan in an essentially normal manner. Although the type of abnormality of the tryptophan metabolism of these patients suggests a functional pyridoxine deficiency, neither biochemical nor clinical improvement resulted from pyridoxine supplementation. Both clinical and biochemical improvement often followed treatment with chelating agents. The possibility that the clinical and biochemical manifestations of porphyria might be related to a disturbance in polyvalent cation balance was discussed.