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Article
December 18, 1943

THIAMINE DEFICIENCY IN HYPERTHYROIDISM

JAMA. 1943;123(16):1049-1050. doi:10.1001/jama.1943.02840510043011
Abstract

Experimental or spontaneous hyperthyroidism increases the rate of cell metabolism and thus leads to a higher requirement of essential factors involved in the breakdown and resynthesis of metabolites. Among these factors the important role of thiamine is well established. The phosphorylated form of thiamine, diphosphothiamine or cocarboxylase, serves as prosthetic group for the enzymes concerned with the oxidation, carboxylation, decarboxylation, dismutation and condensation of pyruvic acid. Pyruvic acid is an obligatory intermediary in the normal pathway of carbohydrate breakdown and probably in the interconversion of protein, fat and carbohydrate. Conditions that lead to increased cellular metabolism and therefore to increased requirements for essential factors tend obviously to produce a relative deficiency of thiamine.

In 1937, when methods became available for the determination of thiamine in the tissues, Drill1 confirmed this concept of thiamine deficiency. The livers and kidneys of rats receiving 100 mg. of desiccated thyroid gland daily contained

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