The sodium iodide symporter (NIS) is responsible for the specificity of RAI for thyroid tissue. This transmembrane protein transports iodide against an electrochemical gradient via a sodium-dependent active transport mechanism by which two sodium ions are transported along with one iodide ion (4). Synthesis of this protein is regulated by activation at the thyrotropin receptor (5). Following the characterization of the NIS gene in 1996, much research has been directed toward understanding the role of the NIS in autoimmune and malignant thyroid disease.
The NIS protein is most abundantly expressed in thyroid tissue, although it is also present in glandular and mucosal tissue, choroid plexus, ciliary body of the eye, and placenta. Normal NIS protein expression is limited to the basolateral membrane in a small percentage of thyroid follicular cells at any one time (6). However, in autoimmune thyroid disease, thyrotropin receptor-mediated activation by stimulating auto-antibodies increases the NIS protein expression to the point that it is expressed on both basolateral and apical surfaces in the majority of thyroid follicular cells. Synthetic mechanisms responsible for iodine organification and incorporation into colloid matrix are also increased, leading to enhanced thyroid hormone turnover, resulting in the manifestations of hyperthyroidism.
Radiotherapy of thyroid disease using iodine-131 relies on the emission of high-energy beta particles to cause damage to thyroid gland tissue. Iodine-131 has a physical half-life of 8.1 days, a principal gamma-ray energy of 364 keV, and beta-particle emission with an average energy of 0.192 MeV. With a tissue range of 0.8 mm, beta-particle emission is responsible for the majority of local therapeutic effect. The ensuing inflammation caused by radiation is followed by fibrosis, resulting in the reduction of the synthetic capacity of the thyroid gland. For this type of therapy to be effective, thyroid tissues must accumulate and retain iodine-131 long enough for adequate amounts of radiation to be delivered. With increased iodine turnover in hyperthyroid disease states, such as GD, the effective biological half-life is shortened to an estimated four to six days. It is important to keep in mind that although hyperthyroidism related to GD may be eliminated by RAI, the underlying autoimmune disease may persist indefinitely, and that continued follow-up is necessary to monitor associated autoimmune syndromes, such as ophthalmopathy.
Was this article helpful?