Thyroid blockade in 123I-mIBG cardiac imaging: A common sense approach

Abstract

The effect of iodine excess as a suppressor of thyroxine synthesis in the thyroid was first reported more than 65 years ago. With subsequent introduction of nuclear imaging techniques using compounds labeled with radioactive iodine, it became a common clinical practice to pretreat patients to protect the thyroid gland from unnecessary radiation exposure. Large quantities of non-radioactive iodide (saturated solution of potassium iodide (SSKI) or Lugol’s solution) or other anions (usually perchlorate) that saturate the iodide transport system, if administered in advance of the radiopharmaceutical, can block entry of [95% of available radioiodine into the thyroid gland. In the case of long half-life isotopes such as iodine-131, practice guidelines often recommend use of additional doses of the thyroid blocking agent for up to 7 days after the radiopharmaceutical is administered. The biodistribution of an administered radiopharmaceutical determines to a great extent the radiation dose received by individual organs. The largest fraction of the dose to an organ usually is caused by isotope within that organ, with surrounding tissues contributing the remainder. Because of the specific iodine-concentrating capability of the thyroid, this organ is particularly susceptible to receiving increased radiation doses from radioiodine-containing preparations. However, it is important to distinguish between the radioiodine-labeled compound, which may have no special affinity for the thyroid gland, and free iodine (usually in the form of ionic iodide), which is specifically concentrated there. Thyroid blockade should be effective at reducing radiation dose from the latter while having little or no effect on the former. In practice, however, it is often difficult to characterize in vivo radioactive counts as being due to decay of bound or unbound isotope. For most radioiodinated compounds, the greatest contributor to radiation dose to the thyroid is the free iodine present in the preparation. While the US Pharmacopeia requires a minimum of 90% of radioiodine to be in the form of the labeled compound, most commercially produced radiopharmaceuticals contain at most 1-3% unbound iodine. While initial radioiodine thyroid uptake usually reflects the amount of free iodine in the administered product, over time there is a contribution from a secondary source, in vivo deiodination of the original labeled compound and its metabolites. While the iodine content of the administered product can be accurately determined from appropriate quality control tests, in vivo determination of the fate of the original radiolabeled molecules is more difficult. External measurements of activity levels in different organs are typically the most effective means to monitor radioiodine biodistribution, irrespective of the origin of the isotope. In the current issue of the Journal, Guibbini and colleagues present cardiac and thyroid uptake data from 57 clinical patients (42 cardiology, 15 neurology) who underwent cardiac I-mIBG imaging at 3 centers, 2 of which used thyroid blockade pretreatment and 1 which did not. There were differences in thyroid and cardiac uptake patterns between the cardiology and neurology patients but no difference in thyroid parameters (thyroid/mediastinum ratio and washout) between patients who did and did not receive thyroid blockade. The authors conclude that thyroid uptake on I-mIBG imaging is primarily a reflection of sympathetic neuronal activity and therefore use of thyroid blockade pretreatment to prevent uptake of free iodide may not be justified. This article raises several interesting questions. For an iodinated radiopharmaceutical for which there is See related article, doi:10.1007/s12350015-0142-3