ABSTRACT
Deoxypyridoxine has been used many times in man, its use has generally been restricted to tests of its antitumor activity or to induction of a B6 deficiency. The most serious consequence of deoxypyridoxine is convulsions which were noted by Gellhorn and Jones who were the first to report using deoxypyridoxine in humans. Yamada and Tsuji studied the transport of vitamin B6 in human erythrocytes. Gailani et al. noted occasional changes in blood urea nitrogen and serum protein in patients receiving a B6-deficient diet supplemented in some cases with deoxypyridoxine. Increased excretion of xanthurenic acid following a tryptophan load is the most well-documented metabolic effect of deoxypyridoxine in humans. Mueller and Iacono reported that serum aspartate aminotransferase activity decreased in thirteen chronically ill patients treated with a normal diet plus 300 or 400 mg deoxypyridoxine per day. Vilter et al. failed to find any alteration in blood glucose to oral or intravenous glucose tolerance tests as a result of deoxypyridoxine treatment.
