Macroscopic and microscopic imaging of stable iodine (127I) in the thyroid.

Abstract

The purpose of this review is to describe the two imaging methods which allow direct estimation of stable iodine (127I) within thyroid gland either in vivo by X-ray fluorescence or in vitro by secondary ion mass spectrometry (SISM) microscopy. X-ray fluorescence of thyroid is mainly used for the estimation of thyroid iodine content (TIC) in human pathophysiology. Although its measurement has little revelance for routine explorations of thyroid function, this is a valuable method for understanding complex pathophysiological conditions such as hyperthyroidism without radioactive uptake, the fate of irradiated glands or the thyroid adaptation to iodine overload. On the other hand, SIMS microscopy which combines the phenomena of secondary ion emission and mass spectrometry, makes possible the quantitative mapping of 127I on tissue section. This technique is able to characterize the functional activity of thyroid tissue without prior administration of radioiodine by measuring 127I concentration within the thyroid follicles. Furthermore, SIMS microscopy can be used to determine the extent to which exogeneous iodine affects the regulation of iodine within the thyroid follicles. Both methods were used to evaluate the quantitative changes in thyroid 127I induced by amiodarone overload. TIC measurements shows that hyperthyroidism occurred only in patients who increased their iodine stores, while the patients who developed hypothyroidism had low iodine stores. These data demonstrate that the mechanisms by which subjects who become hypothyroid under amiodarone iodine overload differ from those of subjects who remain euthyroid or become hyperthyroid: iodine organification is blocked in hypothyroid patients and increased in the euthyroid and hyperthyroid patients. The SIMS microscopy data obtained in mice demonstrated that the thyroid response to amiodarone is related to dietary iodine intake leading to an increase in iodine stores in iodine deficient mice and a decrease in iodine supplemented mice. These results could explain that hyperthyroidism with high thyroid iodine content occurred in areas with low thyroid iodine intake and hypothyroidism with low thyroid iodine content in areas with a supplemented iodine diet.