Abstract
Tryptophan is metabolized to nicotinic acid in man through the formylkynurenine pathway. Disordered metabolism of this amino acid with the accumulation of intermediate metabolites (some of which are carcinogenic) had been encountered in patients with bilharzia. The aim of this work was to investigate the possibility that some intestinal helminths—Ascaris lumbricoides and Ancylostoma duodenale—may induce disordered tryptophan metabolism in the human host. Results revealed that infection with either A. lumbricoides (7 cases), or A. duodenale (8 cases) induced functional pyridoxine deficiency in the host. This deficiency was evidenced by the accumulation of certain metabolites along the tryptophan-nicotinic-acid pathway. The abnormal pattern encountered in these cases could be partially improved by pyridoxine supplements. Furthermore, this impairment in the reactions leading to the formation of nicotinic acid from its precursor, did not manifest itself by clinical symptoms of pellagra in the host.