Radioactive Iodine
  Among different radioactive isotopes of iodine, 131I is the agent of choice in the treatment of thyroid hyperfunction[2-4]. After oral administration, radioiodine is completely absorbed, rapidly concentrated, oxidized and organified by thyroid follicular cells. The destruction of thyroid cells produced by radioiodine results from the ionizing effects of b-particles that have a path length of 1-2 mm. One microcurie of 131I retained per gram of thyroid tissue delivers approximately 70 to 90 rads. Biological effects of radioiodine include necrosis of follicular cells, shorter survival and impaired replication of nondestroyed cells, and vascular occlusion. In the long run there is atrophy and fibrosis, and a chronic inflammatory response, which ultimately may result in thyroid failure.

The goal of radioiodine therapy of hyperthyroidism is to destroy sufficient thyroid tissue to cure hyperthyroidism with one dose of 131I. Because of radiation-safety restrictions, in some centers, especially in Germany, repeated 2-3 mCi doses of radioiodine are administered. Similar to others, we calculate the dose of radioiodine on the basis of thyroid size and uptake of 131I using the following formula:

Dose (mCi)= estimated thyroid weight (g) x planned dose (µCi/g) / fraction 24-hour radioiodine uptake x 1,000)

In other centers standard fixed doses are given. It is a common experience that small glands appear to be destroyed more readily by radioiodine than larger ones, and that toxic adenoma or toxic multinodular goiter are usually more radioresistant than Graves' glands.The effect of radioiodine is relatively delayed and several months may be required for the complete control of hyperthyroidism. Thus, a course of antithyroid drugs, either before or after (or both in severe thyrotoxicosis) the administration of radioiodine is frequently used in order to avoid the inconveniences of persistent hyperthyroidism.


Possible long-term side effects

In the past, the major concerns with radioiodine therapy derived from the possible carcinogenic effects of ionizing radiation, and from the risks of congenital malformations in offspring of women treated during childbearing years. While there is no doubt that external head and neck radiation is associated with an increased rate of thyroid carcinoma, no association was found in large epidemiological studies between radioiodine administration and thyroid cancer[2]. Similarly, there is no evidence that radioiodine therapy for hyperthyroidism increases the risk of leukemia or solid tumors. A minimal increase in the risk of gastric cancer 10 years or more after treatment was found in a survey in Sweden [5], but not in an epidemiological study in the United States [6]. No association between radioiodine treatment for hyperthyroidism and congenital abnormalities in subsequent offspring has been observed[2]. A rough estimate of the dose to the ovaries is about 0.2 rad/mCi of administered 131I. Thus, the dose to ovaries for a patient receiving 10 mCi of radioiodine is similar to that from a barium enema or an intravenous pyelography [3]. It has been calculated that, if a genetic risk induced by 131I does really exist , this would be only 0.003 % per rad of parental gonadal exposure, and therefore a very small fraction of the spontaneous incidence of genetic disorders[6]. Thus, the experience accumulated in more than 50 years of radioiodine treatment for hyperthyroidism has shown that these potential risks are absent or negligible.