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WITH SPECIAL REFERENCE TO PURINE BASES AND THEIR DERIVATIVES

W. H. COLE, M.D.; N. A. WOMACK, M.D.; W. H. ELLETT, M.D.

Arch Surg. 1931;22(6):926-935.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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. . . . [Full Text PDF of this Article]

Author Affiliations
ST. LOUIS

From the Department of Surgery, Washington University School of Medicine.

Footnotes
Submitted for publication, Aug. 1, 1930.

Read at the Annual Meeting of the American Association for the Study of Goitre, Seattle, July, 1930.

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