1960Experimental Biology and MedicineRequires access

Pyridoxine Deficiency in Hyperthyroidism.

Michael G. Wohl, Howard Levy, Anton Szutka, G. Maldia

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Abstract

The occurrence of pyridoxine deficiency was determined in 14 patients with hyperthyroidism and 14 control euthyroid patients by the tryptophan load test. Urinary xanthurenic acid excretion following the tryptophan load test was significantly greater in hyperthyroid patients than in controls. Mean excretion of xanthurenic acid in hyperthyroid cases was 71.9 mg/24 hr with standard deviation of 56.0. Mean xanthurenic acid excretion of control cases was 15.4 with standard deviation of 6.1. After pyridoxine administration, mean xanthurenic acid excretion was 13.2 with standard deviation of 8.7 in the hyperthyroid cases, while in the control group, xanthurenic acid excretion was 12.5 with standard deviation of 5.2. Since pyridoxine is required for orderly catabolism of tryptophan and pyridoxine corrected this metabolic aberration, it is not unreasonable to state that in hyperthyroidism, the availability of pyridoxine is limited. Until the actual significance of these findings becomes more clearly defined, it would seem reasonable to suggest that use of pyridoxine in addition to anti-thyroid medication may prove of distinct benefit in treatment of the hyperthyroid patients.

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The occurrence of pyridoxine deficiency was determined in 14 patients with hyperthyroidism and 14 control euthyroid patients by the tryptophan load test. Urinary xanthurenic acid excretion following the tryptophan load test was significantly greater in hyperthyroid patients than in controls. Mean excretion of xanthurenic acid in hyperthyroid cases was 71.9 mg/24 hr with standard deviation of 56.0. Mean xanthurenic acid excretion of control cases was 15.4 with standard deviation of 6.1. After pyridoxine administration, mean xanthurenic acid excretion was 13.2 with standard deviation of 8.7 in the hyperthyroid cases, while in the control group, xanthurenic acid excretion was 12.5 with standard deviation of 5.2. Since pyridoxine is required for orderly catabolism of tryptophan and pyridoxine corrected this metabolic aberration, it is not unreasonable to state that in hyperthyroidism, the availability of pyridoxine is limited. Until the actual significance of these findings becomes more clearly defined, it would seem reasonable to suggest that use of pyridoxine in addition to anti-thyroid medication may prove of distinct benefit in treatment of the hyperthyroid patients.

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Available abstract

The occurrence of pyridoxine deficiency was determined in 14 patients with hyperthyroidism and 14 control euthyroid patients by the tryptophan load test. Urinary xanthurenic acid excretion following the tryptophan load test was significantly greater in hyperthyroid patients than in controls. Mean excretion of xanthurenic acid in hyperthyroid cases was 71.9 mg/24 hr with standard deviation of 56.0. Mean xanthurenic acid excretion of control cases was 15.4 with standard deviation of 6.1. After pyridoxine administration, mean xanthurenic acid excretion was 13.2 with standard deviation of 8.7 in the hyperthyroid cases, while in the control group, xanthurenic acid excretion was 12.5 with standard deviation of 5.2. Since pyridoxine is required for orderly catabolism of tryptophan and pyridoxine corrected this metabolic aberration, it is not unreasonable to state that in hyperthyroidism, the availability of pyridoxine is limited. Until the actual significance of these findings becomes more clearly defined, it would seem reasonable to suggest that use of pyridoxine in addition to anti-thyroid medication may prove of distinct benefit in treatment of the hyperthyroid patients.

Key concepts: Xanthurenic acid, Pyridoxine, Excretion, Pyridoxine Deficiency, Endocrinology, Internal medicine, Euthyroid, Tryptophan

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