Tryptophan metabolism in hepatosplenic bilharziasis

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Abstract
Tryptophan is metabolized to nicotinic acid in man through the formylky-nurenine pathway. Disordered tryptophan metabolism with accumulation of intermediate metabolites (some of which are carcinogenic) was encountered in bilharzial cases. The aim of this work was to study the role of liver in this disordered metabolism. The abnormal pattern encountered in 6 cases of simple Schistosoma mansoni infection could be partially improved by pyridoxine supplementation, indicating that functional pyridoxine deficiency was the cause of this disordered metabolism. On the other hand, an abnormal pattern was present in 15 subjects with early and late hepatic involvement who did not respond to pyridoxine supplementation. The very low response to the tryptophan load of these subjects and the finding that no marked difference exists between the tryptophan pattern given by the 2 groups of hepatic involvement, are attributed to the inability of the liver to synthesize the enzyme proteins concerned.