Abstract
According to the author, the first radioactive iodine (RAI) therapy using 481 MBq (13 mCi) was given in June 2003, about a month after radioactive iodine uptake was found to be 3.1%. The second RAI therapy (481 MBq [13 mCi]) was administered in June 2005, about 3 months after RAI uptake was found to be 0.8%.
The aim of RAI therapy is to deliver sufficient absorbed radiation dose (ARD) to the thyroid cells to incapacitate their function. It is generally accepted that approximately 5000 to 10,000 Rems are necessary to achieve this goal. The ARD is affected mainly by two factors: (1) the amount of I-131 absorbed by each gram of thyroid tissue, which can be estimated by the percent uptake and scan obtained shortly before treatment, and (2) the effective half-life, a combination of the biologic half-life and physical half-life, of I-131 in the thyroid. When the latter is assumed to be 6 days, which is usually considered normal, each gram of thyroid tissue requires approximately 100 μCi of RAI-131. In clinical practice, the recommendations for the desired dose per gram of tissue range from 80 to 120 μCi (2), to as high as 200 μCi (3).
In Ohye's report, neither the percent uptake nor estimated size shortly before each treatment is known. Assuming that the iodine uptake functions as measured 1–3 months before radioiodine administration remained unchanged in this patient, we can estimate the amount of I-131 delivered to the thyroid. With the first therapy, the thyroid gland took up 403 μCi (3.1% of 13 mCi). Assuming the weight of the thyroid was twice normal or 40 g, each gram of tissue would have received 10 μCi (403 μCi divided by 40). In the second therapy, the thyroid received 104 μCi (0.8% of 13 mCi) and each gram of tissue would have received 2.6 μCi (104 μCi divided by 40). Even if the thyroid was not enlarged and weighed 20 g, the I-131 doses received would have been 20 and 5.2 μCi/g, respectively. The highest possible ARD can be estimated to be only 2000 and 520 Rems, respectively, which are insufficient doses. The actual ARD was likely even less than this since inflammation shortens the biologic half-life of iodine, and thus the effective half-life of I-131.
There is a possibility that the patient may have recovered from the episodes of thyroiditis at the time of RAI therapies and the thyroid uptake may have been higher, but this cannot be assumed without thyroid uptake measurements.
The author stated that the patient developed permanent hypothyroidism after the second RAI treatment. However, there is no convincing support for this conclusion either. The patient was continuously treated with L-thyroxine; no laboratory measurements were made in the absence of the hormone therapy.
Administering a dose of RAI-131 to a patient is not necessarily radioiodine therapy unless a sufficient ARD is delivered to the thyroid. In the case reported by the author, the permanent hypothyroidism, if it indeed occurred, may have been the consequence of repeated thyroiditis and not that of radioiodine therapies.