Iodine Deficiency Disorders and Their Elimination by Elizabeth N. Pearce

Author:Elizabeth N. Pearce
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

Thyroidal Response to Iodine Excess

The normal physiologic adaptation to excess iodine exposure is known as the acute Wolff-Chaikoff effect. From experiments during the 1940s, it was recognized that rats exposed to high amounts of iodide through the peritoneum have a reduction in thyroid hormone synthesis that persists for approximately 24 h [5] and thus a corresponding decreased risk for the development of iodine-induced thyrotoxicosis. Although the exact mechanism for this decrease in thyroid hormone production (the acute Wolff-Chaikoff effect) is not completely understood, it has been postulated that several compounds, including intrathyroidal iodolactones, iodoaldehydes, and/or iodolipids, on thyroid peroxidase activity, are formed and work to inhibit thyroid hormone synthesis in the thyroid follicular cell [6]. Furthermore, there may also be a reduction of deiodinase activity within the thyroid, as a result of the excess iodine exposure, which contributes toward decreased thyroid hormone production.

The physiologic phenomena of the acute Wolff-Chaikoff effect and decreased thyroid hormone production are transient in most individuals, as escape from the acute Wolff-Chaikoff effect occurs and normal thyroid hormone production resumes within a few days [7]. The mechanism for the escape was elucidated in 1999, when Eng and colleagues reported that there is a marked decrease in expression of the sodium-iodide symporter (NIS) present on the basolateral membrane of thyroid follicular cells 24 h after the excess iodine exposure occurs [8]. NIS is a 13-transmembrane glycoprotein which mediates the active transport of iodine from the circulation into the thyroid [9], and decreased thyroidal NIS expression thus results in lower intrathyroidal iodine concentrations. The reduction in intrathyroidal iodine stores results in decreased formation of the iodinated inhibitory substances on thyroid hormone synthesis, thereby enabling the resumption of normal thyroid hormone production.

However, there are certain instances in which the acute Wolff-Chaikoff effect or escape from the effect do not occur, resulting in iodine-induced thyrotoxicosis or iodine-induced hypothyroidism, respectively. Predisposing factors include those which result in dysregulation of the thyroid follicular cell. Thus, individuals with a history of Hashimoto’s thyroiditis, Graves’ disease (even if treated), postpartum thyroiditis, subacute thyroiditis, partial thyroidectomy, or use of lithium (which traps iodine in the thyroid gland), may be particularly susceptible. The developing fetus or neonate (in whom thyroid development is still occurring) is also particularly vulnerable. In these instances, the iodine-induced thyroid dysfunction may be transient or permanent.

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