The degradation of tryptophan in severe liver disease.

Patients with severe acute or chronic liver disease were found to have a high mean plasma free tryptophan, an abnormal urinary excretion pattern of tryptophan-kynurenine metabolites and low circulating levels of the vitamins required for tryptophan degradation, i.e. pyridoxine, thiamine and ascorbic acid. In patients with decompensated chronic liver disease (DCLD), ineffective vitamin B6(pyridoxine hydrochloride) supplementation with effective thiamine and ascorbic acid supplementation increased urinary 3-hydroxykynurenine, 3-hydroxyanthranilic acid and xanthurenic acid excretion. Effective B6(pyridoxal phosphate) supplementation did not cause a similar change. It is postulated that the combination of increased input into the pathway together with vitamin B6 deficiency may explain the abnormal tryptophan-kynurenine pathway in severe liver disease. Imbalanced or ineffective vitamin supplementation may aggravate the disturbance of tryptophan degradation.