(131)I-Iodide is the treatment of choice in most cases of hyperthyroidism, with a standard 7,000-cGy (rad) thyroid absorbed dose generally resulting in an incidental blood absorbed dose of less than 10 cGy (rad). However, in approximately 15% of patients there is a small, rapidly secreted thyroid iodine pool (small-pool patients) and, based on theoretic calculations, an incidental blood absorbed dose of up to 150 cGy (rad) could result. In such small-pool patients, continuing antithyroid drugs (ATDs) at a reduced dosage during (131)I therapy should inhibit the formation of (131)I-labeled levothyroxine and triiodothyronine and thereby reduce the protein-bound (131)I-iodine concentration in blood and the blood absorbed dose.
Methods: To test this hypothesis, thyroid and blood time-activity data were measured and absorbed doses were calculated for an (131)I tracer administered to small-pool hyperthyroid patients (n = 9) not receiving ATDs (off ATDs) and then receiving ATDs (on ATDs).
Results: The blood absorbed dose (cGy/37 MBq [rad/mCi] administered) was reduced from 2.54 +/- 0.91 (mean +/- SD) without ATDs to 1.27 +/- 0.54 with ATDs (P < 0.0001), whereas the thyroid absorbed dose was unchanged (1,870 +/- 700 vs. 2,080 +/- 1,080). The blood absorbed dose for an administered (131)I activity required to deliver a standard prescribed absorbed dose of 7,000 cGy (rad) to the thyroid therefore was reduced by over 50% with ATDs, from 11.3 +/- 6.5 to 4.9 +/- 2.8 cGy (rad) (P < 0.001).
Conclusion: Continued administration of ATDs during (131)I therapy thus can effectively reduce extrathyroid radiation in small-pool patients without significantly reducing the target tissue (i.e., thyroid) dose.