Pyridoxine Deficiency in Hyperthyroidism.

Abstract

Fourteen patients with clinical and laboratory signs of hyperthyroidism and 14 nonhyperthyroid patients were studied. The increased excretion of xanthurenic acid (XA) after tryptophan load and its correction by pyridoxine served as an index of relative pyridoxine deficiency. The hyperthyroid group and the control group was comparable with respect to both mean and standard deviation in pre-tryptophan level of XA excretion with means of 7.3 and 5.1 mg/24 hr., respectively. Following tryptophan load, the mean increase for the hyperthyroid group was singificantly greater than that for the control group (probability of "T" less than 0.01) so that the former reached a significantly higher mean level of excretion (71.9 vs. only 15.4 mg/24 hr.). After pyridoxine, the hyperthyroid group showed a greater decline in Xa excretion than the controls. The biochemical response to the administration of pyridoxine with improvement in the derangement of tryptophan metabolism would tend to indicate that the nutritional status of hyperthyroid patients with respect to vitamin B6 is subnormal. Until the actual signuicance of these findings become more clearly defined, it would seem reasonable to suggest that the use of pyridoxine in addition to antithyroid medication, may prove of distinct benefit in the treatment of the hyperthyroid patient.