Patients infected with Schistosoma mansoni showed an abnormal response to a test dose of
tryptophan, with little increase in the urinary excretion of
kynurenine, hydroxykynurenine, xanthurenic and kynurenic
acids, N1-methyl
nicotinamide, methyl pyridone carboxamide,
5-hydroxytryptamine or 5-hydroxyindoleacetic
acid. In contrast to previous reports, this is different from the pattern of
tryptophan metabolism seen in
vitamin B6 deficiency. Furthermore, the patients' plasma concentrations of
pyridoxal phosphate were within the reference range, and supplementation for 5 days with 20 mg
vitamin B6/day did not affect
tryptophan metabolism. Treatment with a single dose of
Praziquantel resulted in a substantial restoration of normal
tryptophan metabolism. In mice infected with S. mansoni there was a similar impairment of
tryptophan metabolism, as shown by considerably reduced formation of 14CO2 after the administration of a tracer dose of [14C]
tryptophan. Again, the administration of
vitamin B6 supplements did not correct
tryptophan metabolism in the mice. Treatment with
Praziquantel resulted in substantial restoration of the production of 14CO2 from [14C]
tryptophan. There was no evidence of
vitamin B6 deficiency (as determined by erythrocyte
aspartate aminotransferase activation coefficient) associated with
infection in the mice, although there was a redistribution of
pyridoxal phosphate between tissues, with a reduction in the concentration of liver, spleen and kidney, and an increase in skeletal muscle.