Tryptophan metabolism in alcoholic pellagra patients: measurements of urinary metabolites and histochemical studies of related muscle enzymes.

Biochemical and enzymatic aspects of tryptophan-niacin metabolism were studied in 15 adult alcoholic pellagra patients and in 14 controls. In addition to the clinical signs of niacin deficiency, most of the pellagra patients had other signs of malnutrition. Plasma tryptophan in pellagra patients was 2.07 +/- 1.27 mumol/dl, and in the controls 4.84 +/- 2.21 mumol/dl (p less than 0.001). The erythrocyte glutamic oxaloacetic transaminase index was 1.94 +/- 0.77 in the pellagra patients and 1.58 +/- 0.73 in the controls. The urinary levels of 3-hydroxyanthranilic acid were 34.49 +/- 21.47 mumol/g of creatinine in the pellagra patients and 14.51 +/- 8.02 mumol/g creatinine in the controls (p less than 0.02). The urinary levels of N'methylinicotinamide were 2.13 +/- 1.18 mg/g creatinine in the pellagra patients and 4.76 +/- 1.94 mg/g creatinine in the controls (p less than 0.01). The excretion of N'-methyl-2-pyridone-5-carboxamide (2-pyridone) was 2.94 +/- 2.37 mg/g creatinine in the pellagra patients and 10.19 +/- 7.49 mg/g creatinine in the controls (p less than 0.01). The histoenzymological activity of 3-hydroxyanthranilate oxidase in the deltoid muscle was higher in the pellagra patients than in the controls, whereas alpha-glycerophosphate dehydrogenase activity was higher in the controls. These results suggest that for alcoholic pellagra patients the tryptophan-niacin pathway is inhibited after the 3-hydroxyanthranilate oxidase step.