Iodine-induced hypothyroidism

Citation
K. Markou et al., Iodine-induced hypothyroidism, THYROID, 11(5), 2001, pp. 501-510
Citations number
84
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
THYROID
ISSN journal
10507256 → ACNP
Volume
11
Issue
5
Year of publication
2001
Pages
501 - 510
Database
ISI
SICI code
1050-7256(200105)11:5<501:IH>2.0.ZU;2-M
Abstract
Iodine is an essential element for thyroid hormone synthesis. The thyroid g land has the capacity and holds the machinery to handle the iodine efficien tly when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by th e thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years a fter the original description. It is proposed that iodopeptide(s) are forme d that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthe sis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff ef feet i s an effective means of rejecting the large quantities of iodide and theref ore preventing the thyroid from synthesizing large quantities of thyroid ho rmones. The acute Wolff-Chaikoff effect lasts for few a days and then, thro ugh the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T-4) and triiodothyr onine (T-3) returns. This is achieved by decreasing the intrathyroidal inor ganic iodine concentration by down regulation of the sodium iodine symporte r (NIS) and therefore permits the TPO-H2O2 system to resume normal activity . However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with a utoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euth yroid patients after a previous episode of subacute thyroiditis, and in pat ients treated with recombinant interferon-alpha who developed transient thy roid dysfunction during interferon-alpha treatment. The hypothyroidism is t ransient and thyroid function returns to normal in 2 to 3 weeks after iodid e withdrawal, but transient T-4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism.