At our institution, approximately 70 patients are treated with I-131 therapy at a standard dose of 3.70 GBq each year, and from the beginning of quantitative measurements in 2017 to the completion of this report in mid-2025, we have encountered only three patients with laryngeal edema. The occurrence of laryngeal edema following radioactive iodine therapy is rare, with only a small number of cases documented. However, Kinuya et al. reported that three (2.9%) of 102 patients who underwent I-131 therapy for thyroid cancer developed laryngeal edema, suggesting that the incidence of laryngeal edema might be higher than previously thought [5]. Particularly in Japan, when doses of 1.11 GBq or more are administered, patients must be hospitalized in treatment rooms, requiring isolation for a certain period. If laryngeal edema occurs during this isolation period, it could lead to significant confusion regarding the treatment site.

Bal et al. reported that 15 (16.1%) of 93 patients who received 0.55–2.22 GBq of I-131 after undergoing a hemithyroidectomy for thyroid cancer developed laryngeal edema [6]. Among them, three patients were treated with prednisolone; the remaining patients were managed with analgesics alone. Bal et al. noted that they considered radiation-induced thyroiditis to be the cause of laryngeal edema in each case, but their report does not mention differences in quantitative values of the thyroid bed between the cases with and without edema.

Kinuya et al. suggested that the mechanism of laryngeal edema caused by RAI remains largely unclear but the edema is often improved with antiallergic medications and hydrocortisone, leading them to speculate that some form of allergic reaction might be involved [7]. Similarly, Goolden et al. suggested that an allergic reaction to degenerated thyroid tissue might be a potential mechanism for dyspnea occurring within 48 h after I-131 administration [2].

Although our present sample size is limited to the cases of three patients with laryngeal edema, all three patients demonstrated significantly higher quantitative values in the thyroid bed compared to 14 patients without edema. This suggests that high I-131 uptake in the thyroid bed might be a contributing factor to the development of laryngeal edema.

Although not directly related to the study’s primary aim, we note that external radiation exposure at a distance of 1 m from the patients was measured 48 h after I-131 administration as part of routine discharge criteria in Japan (< 30 μSv/h). However, no consistent relationship between this measurement and the occurrence of laryngeal edema was observed in the present cases.

Landström et al. suggested, based on their own cases and a review of 4studies, that residual thyroid tissue and high doses of I-131 might contribute to the development of laryngeal edema [8]. However, they also did not mention differences in the quantitative values of the thyroid bed uptake between cases with and without edema. In contrast, our study provides novel findings by quantitatively demonstrating that the radiation dose to the thyroid bed in cases with laryngeal edema was significantly higher compared to cases without edema.

One limitation of this study is the small sample size (n = 3). A further accumulation of cases is necessary to validate these findings.