Clinical thyroid dysfunction produced by chronic iodide uptake in euthyroid individuals is rare but well established. The abnormalities so produced include goiter,1,2 goiter with myxedema,1-12 and, more rarely, myxedema without goiter formation.3,4,13 Although many studies have been performed to determine the mechanisms by which iodides produce their effects upon the thyroid gland and upon the thyroid-pituitary axis, the precise loci of this halide's action remain imperfectly understood. The various hypotheses proposed on the subject have been recently reviewed.3,9
Three main types of radioiodine uptake abnormalities have been noted in patients on iodide medication. The best known is transient depression of the 24-hour I131 uptake. In those patients who developed clinical evidence of thyroid dysfunction, two other less well-recognized patterns were described.4,7,9-12 One was an abnormally high 24-hour radioiodine uptake occurring 1 to 12 days following discontinuance of iodides. The other was a high two-hour uptake with subsequent rapid fall indicating
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