Abnormal Tryptophan Metabolism in Patients with Adult Celiac Disease, with Evidence for Deficiency of Vitamin B6*

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Abstract
The excretion of the metabolites of tryptophan [long dash] 5-hydroxyindoleacetic acid, indole-3-acetic acid, indican, kynurenine, xanthurenic acid, and kynurenic acid-was quantitatively determined in 10 normal subjects and in 21 patients with adult celiac disease. Five of the latter group were untreated, and 16 were studied on a gluten-free diet. The determinations were done on 3 consecutive 8-hour collections of urine for the following 24-hour periods: control, after loading with 4 g L-tryptophan, and after reloading with 4 g L-tryptophan plus 180 mg vitamin B6 intramuscularly (90 mg im on 2 consecutive days). Elevated urinary levels of 5-hydroxyindoleacetic acid, indole-3-acetic acid, and indican were found in the untreated and treated celiac patients with steatorrhea, whereas normal levels of these metabolites were obtained in the treated patients without steatorrhea. Furthermore, after loading with L-tryptophan the untreated and treated patients with steatorrhea showed a significant increase in their 5-hydroxyindoleacetic acid excretion, suggesting that this group of patients has an augmented shunt of the serotonin to 5-hydroxyindoleacetic acid pathway. Tetracycline eliminated the elevated levels of indican excretion in 2 untreated patients with celiac disease, even after the tryptophan load, suggesting that these elevated levels were due to the increased breakdown of tryptophan by gut bacteria. Patients with adult celiac disease regardless of the stage of their disease fail to metabolize an oral tryptophan load normally. This metabolic failure is characterized by significant increases in the excretion of kynurenine, xanthurenic acid, and kynurenic acid, findings seen in human subjects with a deficiency of vitamin B6. This is the first clear-cut evidence for B6 deficiency in adult celiac disease, and these results suggest that these patients should be given supplementary vitamin B6.