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JAIME PARIS, WILLIAM M. McCONAHEY, CHARLES A. OWEN, LEWIS B. WOOLNER, ROBERT C. BAHN, IODIDE GOITER, The Journal of Clinical Endocrinology & Metabolism, Volume 20, Issue 1, 1 January 1960, Pages 57–67, https://doi.org/10.1210/jcem-20-1-57
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Four women and 1 man receiving protracted treatment with iodides for asthma or bronchitis and exhibiting diffuse thyroidal enlargement were studied. Needle biopsy of the thyroid gland revealed parenchymatous hypertrophy in all. The goiter and myxedema receded on discontinuance of the use of iodides or on administration of thyroid. One patient, followed for more than two years, demonstrated rapid uptake of radioactive iodine over the thyroid gland when the scrum iodide127 reached levels of 12.4 micrograms per 100 ml.; organic binding of iodine did not occur at that time, as documented by the lack of proteinbound radioiodine (PBI131) in the serum (conversion ratio), the rapid decay of radioactivity from the thyroid gland at rates parallel with the decay from the thigh, and the appearance of radioactivity in the urine. Lack of organic binding also was demonstrated by historadiologic technics. When concentrations of iodide127 had reached 0.56 microgram per 100 ml. of serum, the uptake of I131 over the thyroid gland was avid and protracted; at that time, PBI131 appeared in the serum at a rate that was faster than normal. Studies with potassium iodide showed pronounced sensitivity of the thyroid in these patients to the inhibiting effects of iodides on the organic binding of iodine, quite comparable in nature to the findings in Graves′ disease. The similarities between the clinical picture of iodide goiter and that of Hashimoto's thyroiditis are stressed.
