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REACTION OF THE THYROID GLAND TO INFECTIONS IN OTHER PARTS OF BODY

WARREN H. COLE, M.D.; NATHAN A. WOMACK, M.D.
JAMA. 1929;92(6):453-457. doi:10.1001/jama.1929.02700320023009.
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In previous publications we1 have called attention to the production of hyperplastic changes in the thyroid gland of animals, accompanied by loss of colloid and desquamation of the epithelium of the acini, by systemic infections and by toxemias. Although there does not appear to be any specific organism responsible for the production of these changes, the fact remains that organisms belonging to the group inhabiting the intestinal tract are more prone, in our experience, to produce these changes than others. Concomitant with these observations we noted a marked decrease in the iodine content of the gland. Sokolow,2 who reported in 1895 that pathologic changes were produced in the thyroid gland of patients with acute infectious diseases, was probably the first to record them. Roger and Garnier3 noted similar changes. Halsted4 found that infected wounds in dogs were apt to produce a hyperplasia of the thyroid.

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