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A comprehensive study of iodine metabolism is reported in 40 cases of Hashimoto's thyroiditis. The results showed a dissociation between the mean absolute (or stable) iodine uptake by the thyroid (2.0 ;μg. per hour, which was normal) and the serum level of protein-bound iodine (2.5 μg. per 100 ml., which was significantly decreased). These findings indicate that the thyroid gland traps a normal quantity of iodine, but lacks the capacity to utilize it efficiently to form thyroid hormone. This faulty utilization of iodine is apparently a form of acquired dyshormonogenesis. Evidence of its nature is provided by the frequent discharge of iodine from the thyroid gland following administration of potassium perchlorate and by the presence of a butanol-insoluble iodinated protein in the plasma in many cases. The intrathyroidal exchangeable iodine was markedly reduced in almost all cases. This, and not the presence of the butanolinsoluble iodinated protein, explains the frequent discrepancy between the high level of PBI131 and the low level of PBI in serum. Standard radioiodine tests (thyroidal uptake and plasma activity) yield misleading results unless the foregoing abnormalities in stable iodine metabolism are taken into account.
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Buchanan et al. (1961) studied this question.
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