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There are no less than 22 described radioactive isotopes of iodine. Actually,
3 radioisotopes of iodine remain currently used in medicine, essentially
123I for in vivo and 125I for in vitro diagnostic procedures,
and 131I for therapeutic purposes.
131I-radioiodine is used for therapy by virtue of its large beta particulate emissions of moderate energy delivering 90% of the energy of decay within a 1-mm zone, associated with a moderate 8-day half-life. Among various effects, the radionuclide deposited in the tissues results in ionization of the thyroid cell which in turn, leads to the damage of DNA and essential proteins like enzymes. It also indirectly allows the production of many reactive free radicals or short-lived toxic compounds able to damage essential biological molecules. All these events result in a delay or inhibition of the division of the thyroid cell. Depending on the dose administered, this will allow to reach the goal of the treatment, i.e. lowering thyroid hormone production and/or achieving thyroid tissue destruction. The beta particles of 131I are essentially non-penetrating and thus act locally. An even less penetrating radionuclide as 125I has not proven itself to be more valuable than 131I, particularly with respect to the prevention of late hypothyroidism and increases the potential environmental contamination because of its long physical half-life (60 days). In the case of 131I, the whole-body radiation dose is derived from the gamma rays emitted from the accumulation of the radionuclide in the thyroid gland, the blood and the bladder. The SI unit for absorbed dose is the gray (Gy); 1 Gray = 100 rads. Dose equivalent is used to account for the variable biological consequences of radiation of different tissues. For this, the SI unit is the sievert (Sv); 1Sv = 100 rem. The amount of radioactivity is expressed in megabecquerels (MBq); 1 millicurie (mCi) equals 37 MBq. As compared to external radiotherapy, the internally administered radionuclides are less radiotoxic per gray (rad) because their irradiation is delivered slowly over time. The risk of tumour is definitely lower with 131I as compared to X-rays (4). Many people are frightened by radioactivity. It is indeed psychologically more impressive to swallow a glass of water containing radioiodine than to pass an X-ray examination. However, plain film X-ray and computed tomography often deliver a higher effective dose equivalent than many routinely used radiopharmaceuticals (5). In that respect, the long-term results of 131I treatment of hyperthyroidism are most reassuring on the basis of many hundreds of thousands patient-years' experience (6-10). Thyroid cancer and leukemia and to a lesser extent, other cancer and genetic or fetal defects do not appear to represent a significant risk consecutive to the use of radioiodine. Leukemia incidence in 131I-treated thyrotoxic patient is not greater than in those treated with antithyroid drugs and/or surgery. Exceptional cases of leukemia have been reported in patients repeatedly treated with high doses of 131I for thyroid cancer. There is no evidence of any genetic defects in the progeny of the patients treated with 131I-radioiodine either for thyroid cancer or hyperthyroidism at the time they were in a children's age (11). There is only one significant risk for radioiodine therapy of hyperthyroidism, and this is thyroid insufficiency. Except if high doses of 131I have been administered, it is almost impossible to predict when hypothyroidism will occur for a given patient. It is a general observation that except for the first year of treatment, the development of thyroid insufficiency is slowly progressive. As an average, it will concern 3-8%/year of the group of patients treated depending more particularly on the dose administered and/or on the presence of high titers of antithyroid antibodies. Thyroid insufficiency can be easily screened by a yearly blood determination of TSH. An enhanced serum TSH will indicate the beginning of thyroid failure at a time when the patient is still clinically euthyroid. This observation will be immediately followed by an appropriate thyroid substitution therapy. The delay in the appearance of hypothyroidism is statistically dose-related but individually affected by significant differences in thyroid radiosensitivity. Thus, whatever the way of calculating the therapeutic dose to be administered to a given thyrotoxic patient, most of the efforts to avoid late hypothyroidism have been practically disappointing. The therapeutic trials using the bulk of the ß-like energy of 125I absorbed within a few microns has even given worse results than with 131I (12). |
