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Article
February 1958

Thyroid Function and the Metabolism of Iodine in Patients with Subacute Thyroiditis

Author Affiliations

Boston

From the Department of Biophysics, Army Medical Service Graduate School, Walter Reed Army Medical Center, Washington, D. C.; the Thorndike Memorial Laboratory and Second and Fourth (Harvard) Medical Services, Boston City Hospital; the Department of Medicine, Harvard Medical School, Boston, and the Howard Hughes Medical Institute. Formerly Captain (MC), U. S. Army; at present, Investigator, Howard Hughes Medical Institute (Drs. Ingbar and Freinkel).

AMA Arch Intern Med. 1958;101(2):339-346. doi:10.1001/archinte.1958.00260140171026
Abstract

Recent advances have provided a great variety of techniques designed to assess the normal and disordered physiology of the thyroid gland. By and large, these procedures supplement rather than replace one another, and, when employed together, they make possible an integrated analysis of diverse aspects of thyroidal function and the metabolism of iodine. Thus, it is possible to assess the avidity of the thyroid gland for iodine, the quantity of thyroid hormone produced, its rate of release from the gland, the rate of peripheral degradation of hormone, and the concentration and chemical nature of hormonal iodine in the blood.1,2

Subacute, giant cell, or de Quervain's thyroiditis is a disease which is puzzling both in its etiology and in its pathologic physiology. In this disease, commonly employed measures of thyroidal function frequently display a seemingly paradoxical divergence from normality. For example, although the thyroidal uptake of radioiodine is characteristically diminished,

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