OVERVIEW
Iodine-induced hyperthyroidism is hyperthyroidism associated with increased iodine intake, referred to as iodine-induced hyperthyroidism or iodine-induced thyrotoxicosis. In terms of the amount of iodine ingested, there are 3 types of iodine hyperthyroidism: iodine-induced hyperthyroidism is divided into two types, type 1 is iodine agent as the raw material for synthesizing thyroid hormones, the patient is in a state of subclinical hyperthyroidism, and too much iodine agent leads to the patient’s manifestation of clinical hyperthyroidism. type 2 is mainly caused by amiodarone, which is the toxic effect of amiodarone on the thyroid gland, causing destructive hyperthyroidism.
Etiology
Iodine is the raw material for the synthesis of thyroid hormones, and the daily iodine requirement of adults is 100-200µg, and 150-250µg/day for pregnant and lactating women. Short-term large doses of iodine supply, can make the release of thyroid hormones by acute inhibition, this inhibition effect is also known as the Woff-Chaikoff effect, clinical use of this effect to treat hyperthyroidism crisis, the Wolff-Chaikoff effect in about 14 days will gradually disappear, there is the so-called “escape phenomenon”, after the escape of thyroid hormones, the so-called “escape phenomenon”, after the release of thyroid hormones. The Wolff-Chaikoff effect gradually disappears in about 14 days, resulting in the so-called “escape phenomenon”, after which the synthesis and release of thyroid hormones return to normal.
There are two types of iodine-induced hyperthyroidism:
1.1 Iodine-induced hyperthyroidism
Mainly occurs in iodine-deficient areas, epidemiological blood data found in iodine-deficient areas after supplementation of iodine, the incidence of hyperthyroidism increased significantly, these patients in the supplementation of iodine itself in the state of subclinical hyperthyroidism, supplementation of iodine enough, the patient manifested clinical hyperthyroidism, this iodine-induced hyperthyroidism in the supplementation of iodine after 4-6 years, the incidence of hyperthyroidism returned to the normal level. This iodine-induced hyperthyroidism is also seen in patients with autonomous adenomas of the thyroid function (Plummer’s disease) and some elderly patients with subclinical hyperthyroidism. It accounts for the majority of iodine-induced hyperthyroidism.
2. Iodine-induced hyperthyroidism mainly caused by amiodarone.
The dose of amiodarone for the treatment of cardiac rhythm disorders is 200mg/day, which contains 75mg of iodine, and about 6mg of free iodine enters the bloodstream after deiodination. This iodine dose is 40 times the plain recommended amount of 150 micrograms/day. The half-life is up to 20-100 days. The pharmacologic effects of amiodarone on the thyroid are complex, and several mechanisms include: ① Reducing deiodination of thyroid hormones and inhibiting the conversion of T4 to T3, resulting in elevated T4 and normal T3. (ii) Reduction of T3 and nuclear receptor binding, causing a temporary elevation of TSH after amiodarone treatment. ③ Cytotoxic effect, inducing destructive thyroiditis.
Symptoms
The clinical manifestations of iodine-induced hyperthyroidism are similar to those of Graves’ disease, except that the former is older and occurs more often in the elderly and less often in children (it has been reported that none of the 50,000 cases of iodine-treated children developed IIH), and the male-to-female ratio of 1:6 to 1:10 is similar to that of Graves’ disease (in patients with IIH in iodine-deficient areas, the majority of them have nodules of the thyroid gland, and 15% to 30% of them have a smaller or absent goiter, some patients have no nodules), the condition is relatively mild, there is no pressure pain in the thyroid gland, thyroid examination reveals nodular goiter or single nodule, there is usually no protruding eyes, and there is rarely vascular murmur and tremor in the thyroid area, cardiovascular signs and symptoms are obvious, and the serum antithyroid antibody is negative.
Laboratory tests for iodine hyperthyroidism
Laboratory examination of iodine-induced hyperthyroidism is characterized by increased T4, although T3 is also often elevated, but not as significant as T4; TSH is low, TRAb is negative, and there is low or no response to TRH excitation test.
In type 1 iodine-induced hyperthyroidism (Plummer’s disease), thyroid scanning reveals the presence of “functionally autonomous thermal nodules”, with complete suppression of iodine uptake by the surrounding thyroid tissue. Ultrasound shows increased thyroid blood flow. Measurement of urinary iodine is of little diagnostic help because of the wide range of normal values for urinary iodine.
In type 2 iodine-induced hyperthyroidism, laboratory tests reveal an increase in interleukin-6, an increase in thyroid hormones, a decrease in TSH, but a low iodine uptake by the thyroid gland, with hormonal and iodine uptake anomalies characteristic of disruptive hyperthyroidism, and a low blood flow on ultrasound examination of the thyroid gland.
Diagnosis
1. Recent history of increased iodine intake and clinical manifestations of hyperthyroidism: tachycardia, sweating, fatigue, weight loss, etc.
2. Laboratory tests show elevated blood FT4 and also elevated FT3, but out of proportion to elevated T4; decreased TSH; decreased iodine uptake (type 2 iodine-induced hyperthyroidism).
3. Thyroid scanning may reveal the presence of “hot spots” (only in patients with “thyroid functionally autonomous hot nodules”).
4. Other causes of hyperthyroidism should be excluded.
Treatment
Iodine-induced hyperthyroidism is relatively self-sustaining, treatment must stop supplementation of additional iodine agents, due to the increase in thyroid iodine storage and plasma iodine, hyperthyroidism often lasts for weeks to months, stop additional iodine agents, hyperthyroidism can be naturally relieved, the mild cases can be used with β-blocking drugs alone, the severe cases can be applied to short-term antithyroid medication, surgical procedures are generally not necessary, due to the low iodine uptake of the thyroid gland, it is not advisable to perform Due to low iodine uptake by the thyroid gland, radioactive iodine therapy, amiodarone-induced hyperthyroidism can be combined with antithyroid medication (tapazole or propylthiouracil) and potassium perchlorate 1 g. The effect can be seen in 3 weeks, and the treatment lasts for 2 months, and the weekly test of thyroid function can be initiated, because potassium perchlorate has the side effect of inhibiting bone marrow, and the blood routine can be examined every 2 weeks, and bone marrow examination can be performed when necessary, and the treatment lasts for 8 weeks, and the treatment can be discontinued if the T4 decreases to the normal range. If the T4 drops to the normal range, stop potassium perchlorate and reduce the dose of antithyroid drugs. If T4 remains elevated after 2 to 4 weeks of treatment, prednisone needs to be increased to 40-60 mg/d. Surgery may also be considered in individual cases of unsatisfactory hyperthyroidism control.
Because iodine has the property of inducing hyperthyroidism, therefore, in the prevention and treatment of endemic goiter, the dosage of iodine should be appropriate, especially for those with nodules in the thyroid gland, the use of iodine should be avoided for those with non-iodine-deficient nodular goiter, and attention should be paid to the follow-up of those who have been taking amiodarone for a long time. Nearly half of the patients with iodine-induced hyperthyroidism can recover spontaneously after stopping the drug, with an average time of about 5.5 months.
Prevention
Iodine-induced hyperthyroidism mostly occurs in patients with thyroid abnormalities, so patients with thyroid diseases (including goiter, hyperthyroidism, chronic thyroiditis, etc.) need to avoid some high iodine foods and medications (such as kelp, seaweed, iodine contrast medium and amiodarone, etc.). If high iodine foods or medications are needed for treatment or other reasons, thyroid function tests should be done during and after the treatment in order to find out the problem at an early stage and deal with it at an early stage. and early treatment.