This brief report develops the ideas of previous work underlying a possible functional disequilibrium of tryptophan metabolism in patients affected by multiple sclerosis (MS) and in animals with experimental allergic encephalomyelitis. The urinary excretion of one of the terminal metabolites of the kynurenine pathway of tryptophan, N1 methylnicotinamide, has been confronted in MS patients and in healthy volunteers in order to show a possible alteration in MS patients. The authors could not find any significant difference in N1 methylnicotinamide urinary output between controls and MS patients.
|Number of pages||4|
|Journal||Acta Vitaminologica et Enzymologica|
|Publication status||Published - 1975|
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