Identification of an error in the tryptophan--niacin pathway in carriers of some dermatoses conditioned or aggravated by sunlight.

Abstract

The study of the tryptophan→niacin pathway showed a defect of the kynureninase activity at the level of the 3-hydroxykynurenine→3-hydroxyanthranilic acid step in a series of present acquired pellagra carriers (23) and in 5 of a series of 12 chronic erythematodes carriers. The same defect, associated with a deficit of the kynureninase activity also at the level of the kynurenine→anthranilic acid step, was observed in 52% of cases of a series of porphyria cutanea tarda carriers (23), in one case of Rothmund-Thomson syndrome and in a group of rats in which a hepatic porphyria was provoked.