Iodine-induced hyperthyroidism (IIH)
Iodine-induced hyperthyroidism (IIH) is hyperthyroidism associated with increased iodine intake, or “iodine hyperthyroidism”, also known as iodinated parathyroidism or iodine-induced thyrotoxicosis (IIT). It is associated with long-term high iodine intake (or iodine-containing drugs). Patients often have defective thyroid iodine metabolism, which may be accompanied by nodules, and patients do not have proptosis. In terms of iodine intake, iodine hyperthyroidism occurs in three ways: the first is caused by one or more large doses of iodine intake; the second is by higher doses of iodine; and the third is by average doses of iodine. It is seen in iodine-deficient areas, after iodized salt is taken by patients with goiter; or after iodine is taken by patients with goiter in non-iodine-deficient areas, and after iodine is taken by patients whose original hyperthyroidism has been controlled. The clinical manifestations of iodine hyperthyroidism are similar to those of toxic diffuse goiter (Graves’ disease), but patients with iodine hyperthyroidism have an older age of onset, occurring more often in the elderly and less often in children. The male to female ratio is 1:6 to 1:10.
Causes
Iodine has a close relationship with the thyroid gland: the former is the raw material for the synthesis of thyroid hormones, and the daily iodine requirement of adults is 150 μg, and that of adolescents aged 6-12 years is 120-200 μg. Within a certain dosage range, the synthesis of thyroid hormones rises with the increase of iodine supply, but if the iodine supply is more than a certain limit (5mg/d in normal people, 2mg/d in patients with hyperthyroidism), the opposite result can occur. Results. Iodine hyperthyroidism occurs for three reasons:
1. Large doses of iodine in a short period of time
Acute suppression of thyroid hormone release, also known as the Woff-Chaikoff effect. It is a temporary protective mechanism to avoid the release and synthesis of excessive hormones; this effect is also often utilized in the treatment of hyperthyroid crisis.
2. Long-term oversupply of iodine
The Woff-Chaikoff effect gradually disappears, and the “escape phenomenon” occurs; after the escape, the synthesis and release of thyroid hormones can return to normal, or even accelerate, and sometimes iodine hyperthyroidism can occur.
3. There are two kinds of hyperthyroidism caused by iodine.
In iodine-deficient areas, endemic goiter treated with iodide accounts for the majority of iodine hyperthyroidism; ② in non-iodine-deficient areas, occasionally seen in some non-toxic multinodular goiter patients. In addition, long-term administration of iodine-containing drugs such as amiodarone is a common cause of iodine hyperthyroidism in non-iodine-deficient areas.
Symptoms.
In patients with IIH in iodine-deficient areas, most have thyroid nodules, and a few have smaller (or no) goiters. Some patients have no nodules, relatively mild disease, no thyroid gland pressure, thyroid examination can be seen nodular goiter or single nodule, usually no protruding eyes, and seldom appear in the thyroid area of vascular murmur and tremor, cardiovascular signs and symptoms are obvious, serum antithyroid antibodies are negative, the thyroid scan can be detected in the presence of the “hot zone”, its Thyroid scan can detect the presence of “hot zone”, which is characterized by decreased iodine uptake in the thyroid gland, and the 24-hour iodine uptake rate is less than 3%. Since the normal range of urinary iodine is large, the measurement of urinary iodine is not very helpful for diagnosis.
Examination
1. Laboratory tests for iodine hyperthyroidism are characterized by increased T4, although T3 is often elevated, but not as significantly as T4;
2. Thyrotropin-releasing hormone (TRH) excitability test is characterized by low or no response and extremely low iodine uptake by the thyroid gland;
3. Thyroid scans may reveal the presence of a “hot zone”.
Diagnosis
1. Medical history
A recent history of increased iodine intake, with hyperthyroidism, as well as tachycardia, sweating, weight loss, and in older patients, drowsiness and weakness.
2. Laboratory tests
Blood FT4 is elevated, and FT3 is also high, but disproportionately so; thyroid-stimulating hormone (TSH) is decreased; iodine uptake is decreased.
3. Thyroid scan
The presence of “hot spots” can be detected.
Treatment
Since iodine has the property of inducing hyperthyroidism, the amount of iodine used in the prevention and treatment of endemic goiter should be appropriate, especially in those with nodules in the thyroid gland. Iodine should be avoided in non-iodine-deficient nodular goiter, and follow-up should be paid attention to those who have been taking amiodarone for a long time. In iodine hyperthyroidism, nearly half of the patients recover spontaneously after stopping the medication, with an average time of 5.5 months. If symptoms do not resolve, antithyroid drugs may be added. Surgical removal of hyperfunctional nodules is required if necessary.