Tryptophan Load Test Research Articles

Pyridoxine deficiency in congestive heart failure.

Summary1. Fourteen patients with congestive heart failure and 14 control patients without heart failure were studied with the tryptophan load test. 2. Urinary xanthurenic acid excretion following tryptophan load was significantly greater in the cardiac group than in controls. Mean XA excretion of the group with congestive failure was 35.6 mg/24 hours with standard deviation of 22.8. Mean excretion of the control group was 12.9 mg/24 hours with standard deviation of 5.2 mg/24 hours. 3. The heart failure group, which attained a higher level of XA excretion than the control group in the post tryptophan period, showed a greater decline in XA excretion after pyridoxine than the controls. 4. Since pyridoxine is required for orderly catabolism of tryptophan and pyridoxine corrects this metabolic aberration of tryptophan, it is not unreasonable to state that in congestive heart failure availability of Vit. B6 is limited.

INTAKE OF VITAMIN B6 AND INFANTILE CONVULSIONS: A FIRST APPROXIMATION OF REQUIREMENTS OF PYRIDOXINE IN INFANTS

Nine infants, 1 to 12 months of age, with convulsions due to inapparent cause, have remained free of seizures after a change to a diet providing an increased amount of vitamin B6, or after administration of vitamin B6 as such. Five of these infants had been receiving a proprietary milk mixture found by analysis to be low in content of vitamin B6 (0.085 mg/l), two were breastfed and two, who developed convulsions in the neonatal period, had been receiving an evaporated milk mixture. Seven of the infants became free of convulsions when given an evaporated milk mixture supplying an average of 0.26 mg of vitamin B6 daily. Four of these seven infants were studied for biochemical evidence of deficiency of vitamin B6 by the use of a tryptophan loading test. All four excreted large amounts of xanthurenic acid after receiving 0.54 gm/kg of DL-tryptophan. One to 1.4 mg of vitamin B6 daily were required to prevent the excretion of xanthurenic acid. In contrast, 10 of 11 control infants receiving 0.2 to 0.5 mg of vitamin B6 daily failed to excrete xanthurenic acid when similarly tested and two of these infants, who began to excrete xanthurenic acid after receiving for 1 month a diet low in content of vitamin B6, ceased to do so after receiving 0.3 to 0.4 mg of vitamin B6 daily. This suggests that the requirement of vitamin B6 of the seven infants who had developed the deficiency is, for some reason greater than that of the average infant. The two infants whose convulsions appeared in the neonatal period required 2 to 5 mg of vitamin B6 daily to eliminate the seizures. One of these is still dependent upon a supplement of 2 mg of vitamin B6 daily. However, these two infants, like the control infants, required only 0.3 to 0.4 mg of vitamin B6 daily to prevent excretion of xanthurenic acid after receiving a dose of tryptophan. It seems probable that these two infants have anomalous metabolism of vitamin B6 rather than simple deficiency. In view of the above observations, it is recommended that an infant's diet contain 0.2 to 0.3 mg of vitamin B6 daily. However, since there are occasional instances of anomalous requirements, it is suggested that a therapeutic trial dose of 5 to 10 mg of pyridoxine hydrochloride daily be given to any infant with convulsions resulting from inapparent cause.

Evidence for Abnormal Vitamin B6Metabolism in Pregnancy and Various Disease States

Evidence for a biochemically demonstrable disturbance in the metabolism of vitamin B6during pregnancy is based on the following observations: (1) A marked increase of xanthurenic acid excretion following a tryptophan load test. (2) An abnormal excretion pattern of tryptophan metabolites on chromatographic analysis which is strikingly similar to that described in vitamin B6-deficient rats. (3) Immediate normalization of tryptophan metabolism following the administration of relatively small amounts of pyridoxine. (4) An abnormal vitamin B6, load test indicating a significantly larger retention of the administered vitamin in comparison to non-pregnant control subjects. Some patients with hyperthyroidism, febrile diseases, and carcinoma exhibit a similar disturbance of tryptophan metabolism which responds to the administration of pyridoxine. The possible mechanism of this disturbance is discussed and certain therapeutic implications are pointed out.