In previous publications,1 we have called attention to the hyperplasia, desquamation and loss of colloid that occur in the thyroid gland during the course of systemic infections and toxemias. This triad of changes in the thyroid gland seems clearly to be due to a demand for excessive function of the thyroid cells as a result of chemical or physiologic stimulation. It is secondary rather than primary, since the cellular changes obtained were brought about without any possibility of a direct local action of the bacteria on the thyroid cells. This explanation also adequately accounts for the loss of colloid and iodine in the gland. If it is assumed that the process is best explained on a chemical basis, one's attention is offhand directed toward the by-products of protein catabolism, since so many of them are known to be toxic, and because many of the bacterial toxins themselves are proteins.
COLE WH, WOMACK NA, ELLETT WH. THE PRODUCTION OF HYPERPLASIA OF THE THYROID GLAND BY CHEMICAL MEANS: WITH SPECIAL REFERENCE TO PURINE BASES AND THEIR DERIVATIVES. Arch Surg. 1931;22(6):926–935. doi:10.1001/archsurg.1931.01160060054003
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