Iodine-Induced Hypothyroidism

Abstract

Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H202 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 autoimmune 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 euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-alpha who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 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.

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels

“…Vitale et al (30) and our previous experimental studies revealed that high iodine intake damages endogenous thyroid peroxidase and induces apoptosis in these cells through a mechanism that involves the generation of free radicals (30)(31)(32), but whether the iodine-induced apoptosis contributes to chronic iodine-induced hypothyroidism is unknown. It has been reported that iodine-induced hypothyroidism usually resolves quickly after iodine withdrawal, but if the administration of iodide continues, overt or subclinical hypothyroidism will persist (33). Even though the symptoms of subclinical hypothyroidism are less, complications can be severe.…”

The Danish investigation on iodine intake and thyroid disease, DanThyr: status and perspectives

“…The mechanism behind an iodine-induced increase in the incidence of hypothyroidism is unknown, but several mechanisms could be involved. Iodine has been associated with thyroid autoimmunity (43), and it has a number of autoregulatory inhibitory effects on thyroid hormone production and secretion (44). Moreover, excess iodine may lead to apoptosis of thyroid follicular cells as studied in in vitro systems (45).…”

Excess dietary iodine intake in long-term African refugees

“…The effect of the consumption of additional iodine is also dependent on the initial status of the population. In populations that are mildly deficient or replete, increases in dietary iodine may induce hypothyroidism, while in populations that were previously severely deficient, increased dietary iodine is associated with hyperthyroidism 4,5 . Iodine-induced hyperthyroidism (IIH) is a serious condition that may in extreme cases lead to death, usually from heart-associated causes 6 .…”