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Iodine-induced thyroid dysfunction

Iodine-induced thyroid dysfunction
Author:
Martin I Surks, MD
Section Editor:
Douglas S Ross, MD
Deputy Editor:
Jean E Mulder, MD
Literature review current through: Jan 2024.
This topic last updated: May 05, 2023.

INTRODUCTION — The central role of iodide in thyroid physiology has been known for many years. The four iodine atoms of thyroxine (T4) constitute 65 percent of its weight; the three iodine atoms of triiodothyronine (T3) constitute 59 percent of its weight. Iodine is a trace element in the crust of the earth, and its distribution is quite variable. Many areas, particularly inland and mountainous regions, have minimal iodine, while others, often coastal regions, have sufficient or even excessive iodine.

Both iodine deficiency and excess can cause thyroid dysfunction. This topic will review the mechanisms by which normal subjects adapt to excess iodine and the mechanisms of iodine-induced thyroid disease. Iodine deficiency disorders and the therapeutic use of iodine in patients with hyperthyroidism are discussed separately. (See "Iodine deficiency disorders" and "Iodine in the treatment of hyperthyroidism".)

SOURCES OF IODINE — Iodide is essential for thyroid hormone synthesis. (See "Thyroid hormone synthesis and physiology".)

Iodine can be obtained by consumption of foods that contain it or to which it is added. Dietary iodine is absorbed as iodide and rapidly distributed in the extracellular fluid, which also contains iodide released from the thyroid and by extrathyroidal deiodination of the iodothyronines. Iodide leaves this pool by transport into the thyroid and excretion into the urine. The recommended minimum daily intake of iodine is 150 mcg for nonpregnant adults, 220 to 250 mcg for pregnant women, 290 mcg for lactating women, and 90 to 120 mcg/day for children aged 1 to 13 years [1,2]. The median intake in the United States is approximately 240 to 300 mcg/day [1]. In the United States, iodized salt contains 76 mcg of iodine per gram. In many countries, however, it contains less, and in some countries, iodized salt is not available. As a result, iodine deficiency is the most common cause of goiter, hypothyroidism, and mental deficiency worldwide. (See "Iodine deficiency disorders".)

Sources of excess iodine include over-the-counter and prescription medications that may be ingested or applied to the skin or vaginal mucosa, radiographic contrast agents, and dietary supplements (kelp, seaweed) (table 1). In the context of a person's usual dietary iodine intake, the amount of iodine in many of these substances is very large. As an example, a patient undergoing vascular imaging may receive several thousand mg of organic iodide. Those substances that contain organic iodide are partially deiodinated to form inorganic iodide, the form that has thyroidal actions. Some of these substances that are deiodinated to form inorganic iodine, such as amiodarone, are stored in fat and may provide excess iodide for months after the last dose is administered.

NORMAL ADAPTATION TO IODIDE INTAKE — If thyroid hormone production and secretion were solely dependent upon iodide supply, people who lived in areas of iodine deficiency would be hypothyroid, while those in areas of iodine sufficiency would be euthyroid or hyperthyroid. Instead, regulatory mechanisms maintain the euthyroid state unless the deficiency is severe or the patient has some thyroid disease.

Follicular cell autoregulation — The key factor that protects organisms against wide variations in dietary intake of iodine is autoregulation by thyroid follicular cells. Sudden exposure to excess serum iodide inhibits organification of iodide, thereby diminishing hormone biosynthesis; this phenomenon is called the Wolff-Chaikoff effect [3].

However, within two to four weeks of continued exposure to excess iodide, iodide organification and thyroid hormone biosynthesis resume in a normal fashion [4]. Studies in experimental animals suggest that this escape from the Wolff-Chaikoff effect results from decreased trapping of iodide and, therefore, restoration of the intrathyroidal iodide pool to its normal value, even though serum iodide concentrations remain elevated [5-7]. The mechanism for this escape is unknown but may relate, in part, to decreases in iodide trapping brought about by a fall in sodium/iodide symporter (NIS) activity [8,9].

Iodide effects on thyroid hormone secretion — The most rapid (hours to days) effect of pharmacologic doses of iodine is to decrease thyroglobulin proteolysis, thereby decreasing thyroid hormone secretion. The resulting slight reductions in serum T4 and T3 concentrations cause transient increases in serum concentrations of thyroid-stimulating hormone (TSH) [10-12]. This may occur after exposure to iodine-containing radiocontrast; in one study, 18 percent had transient increases in serum TSH above the normal range [13]. Older subjects may not have this increase in serum TSH in the presence of increased iodine intake [14].

IODINE-INDUCED HYPERTHYROIDISM — The effects of iodine administration in patients with abnormal thyroid glands differ from those in normal individuals and depend upon the underlying disease process. As an example, iodine administration may result in hyperthyroidism in patients with endemic goiter or in patients with nodular goiters containing autonomously functioning tissue. In regions of iodine deficiency, a prevalence of hyperthyroidism that varies from 1 to 20 percent has been reported after the introduction of iodine [15,16]. The higher frequency of hyperthyroidism (10 to 20 percent) occurs in individuals with nodular goiter living in areas of iodine deficiency. Thyrotoxicosis occurs because of underlying areas of autonomy within the thyroid gland. When the iodine supply increases, the autonomous areas produce thyroid hormone independent of normal regulatory mechanisms (the Jod-Basedow phenomenon) [17]. Such patients may have had subclinical hyperthyroidism before iodine repletion [16].

The lower frequency of hyperthyroidism (approximately 1 to 2 percent) noted in regions of iodine deficiency probably reflects the prevalence of undiagnosed Graves' disease in these populations. These patients are clinically euthyroid before iodine repletion because their hormone production and secretion have been limited by the limited supply of iodide. When more iodide becomes available, however, hormonogenesis and hormone secretion become excessive and clinical hyperthyroidism ensues.

Iodine-induced hyperthyroidism can rarely occur in patients without underlying thyroid disease (eg, iodine-induced thyroiditis) [18,19]. In one study, as an example, only 2 of 788 unselected patients from an iodine-deficient area developed hyperthyroidism within 12 weeks after coronary angiography [20]. Both patients had normal TSH levels at baseline and thyroid ultrasound did not show evidence of nodules. Surprisingly, 27 of the patients had subclinical hyperthyroidism before angiography, none of whom became hyperthyroid.

In North America and other iodine-replete populations, iodine-induced hyperthyroidism may occasionally occur in patients with autonomous thyroid nodules after treatment with high doses of iodine, usually in the form of drug therapy (table 1) or exposure to iodinated contrast agents during diagnostic radiography (eg, computed tomography [CT] or angiography) [16,21-24]. As an example, in a prospective study of 73 patients (mean age 65.7 years), only two developed hyperthyroidism after exposure to radiographic contrast [25]. In another study, the risk was higher in patients who had subnormal serum TSH concentrations and increased technetium thyroid uptake prior to radiographic contrast exposure [26].

Diagnosis — The diagnosis of iodine-induced hyperthyroidism should be suspected in a patient with a history of iodine exposure (eg, coronary angiography, radiographic contrast) and clinical manifestations of hyperthyroidism (eg, palpitations, tremulousness, heat intolerance), particularly in those with a thyroid nodule or nodular goiter on physical examination.

The diagnosis is confirmed with thyroid function tests (low serum TSH, high free T4 and/or T3). Iodine-induced hyperthyroidism typically begins weeks or even months after iodine administration; a single, large dose of iodine can be sufficient. (See "Overview of the clinical manifestations of hyperthyroidism in adults" and "Diagnosis of hyperthyroidism".)

Evaluation for underlying thyroid disease — Iodine-induced hyperthyroidism most often occurs in patients with underlying thyroid disease, usually nodular thyroid disease with autonomy. However, other causes of hyperthyroidism must also be considered since the hyperthyroidism may not be related to the iodine exposure. Therefore, an evaluation to determine the etiology is important. (See "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)

If the diagnosis is not apparent from physical examination (eg, multinodular gland suggests thyroid autonomy; thyroid eye disease, diffuse goiter suggests Graves' disease), diagnostic testing is indicated. Depending on available expertise and resources, testing may include measurement of TSH-receptor antibodies (TRAb), determination of radioiodine uptake, or thyroid ultrasound to assess for thyroid nodularity and thyroidal blood flow.

TRAb – If the clinical setting suggests Graves' disease, measurement of TRAb can confirm the diagnosis. However, TRAb may not be elevated in patients with mild Graves' disease. (See "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)

24-hour radioiodine uptake – The general practice of obtaining a 24-hour radioiodine uptake in a hyperthyroid patient to distinguish underlying Graves' disease or thyroid autonomy (high or normal uptake) from a destructive thyroiditis (very low uptake) may be problematic if iodine-induced hyperthyroidism is suspected (see "Diagnosis of hyperthyroidism", section on 'Radioiodine uptake'). An exogenous iodine load will dilute the administered radioiodine tracer and the uptake will be lowered depending upon the amount of the exogenous iodine load, whether the exposure is continuous (eg, amiodarone), and the interval since the iodine exposure.

Usually a single iodine load (eg, radiocontrast for a CT scan) may transiently reduce the radioiodine uptake in patients with Graves' disease or toxic nodular goiter to less than 10 percent for up to two to four weeks but rarely reduces the uptake to less than 1 percent as occurs in patients with painless thyroiditis. A continuous iodine load, however, may reduce the uptake to less than 1 percent. Thus, the distinction between Graves' disease or toxic nodular goiter and painless thyroiditis may be very difficult or impossible in the setting of continuous iodine exposure.

If a 24-hour radioiodine uptake is obtained and is unexpectedly low in a patient with presumed Graves' disease or autonomous thyroid nodular disease and the history of iodine exposure is uncertain, a 24-hour urinary iodine level (or a spot urine iodine and creatinine to estimate the 24-hour urinary iodine concentration) can be obtained to assess the degree of iodine exposure. When urinary iodine levels are above 1000 mcg/day, iodine-induced thyroid dysfunction is likely, and the results of the radioiodine uptake should be interpreted accordingly [27].

Thyroid ultrasound – The use of thyroid ultrasound to assess nodularity and thyroidal blood flow may be particularly useful in hyperthyroid patients with a history of high iodine exposures. Low vascularity suggests a destructive thyroiditis, while increased vascularity suggests Graves' disease or a toxic nodular goiter. While autonomous and toxic nodules may have increased vascularity, many nonfunctioning nodules (including cancers) may also have increased vascularity. Thus, the lack of vascularity on ultrasound may be used to support a diagnosis of a destructive thyroiditis, but the presence of increased focal vascularity over a nodule does not necessarily identify that specific nodule as being a toxic adenoma. Therefore, in a hyperthyroid patient with a vascular nodular thyroid and a limited iodine exposure, it is still optimal to obtain a thyroid scan to ascertain the functionality of the nodule(s). The results may be equivocal, and a repeat scan two to four weeks after an iodine load may be diagnostic. However, if the patient was started on methimazole, the scan will only be informative if obtained when the TSH is still suppressed. The methimazole is held for two to three days before obtaining the scan.

Management — Iodine-induced hyperthyroidism is usually self-limited (lasting 1 to 18 months) if the source of iodine is discontinued. The appropriate initial therapy for patients with iodine-induced hyperthyroidism is [28]:

Discontinuation of iodine.

Avoidance of further exposure.

Administration of a beta-adrenergic antagonist drug (assuming there are no contraindications to its use) to minimize the manifestations of hyperthyroidism. We typically use atenolol in an initial dose of 25 to 50 mg/day. However, all beta-adrenergic blocking drugs effectively diminish hyperthyroid symptoms. (See "Beta blockers in the treatment of hyperthyroidism".)

Thyroid tests (TSH, free T4, total T3) should be measured initially at four- to six-week intervals and then less frequently (TSH and free T4 every three months) depending upon the results of prior testing. Beta blockers can be tapered and discontinued after thyroid tests return to normal.

Administration of a thionamide may speed recovery [27,29]. When hyperthyroid symptoms are severe or prolonged (>1 month), or the patient is older and has underlying heart disease, we add methimazole (starting dose 10 to 20 mg once daily) because of its long duration of action, allowing for once-daily dosing, more rapid efficacy, and lower incidence of side effects. Propylthiouracil should be used instead of methimazole in pregnant women during their first trimester. Thyroid function should be assessed after four weeks by measurement of serum TSH, free T4, and T3. The dose of methimazole is then tapered with the goal of maintaining a euthyroid state. Thereafter, thyroid function tests (TSH, free T4) should be measured every three months. Many patients with underlying autonomous nodular thyroid disease are able to taper and discontinue methimazole within 6 to 12 months. (See "Treatment of toxic adenoma and toxic multinodular goiter", section on 'Choice of therapy' and "Thionamides in the treatment of Graves' disease" and "Thionamides: Side effects and toxicities".)

After resolution of the acute episode of iodine-induced hyperthyroidism, treatment of the underlying thyroid disease should be addressed. For patients with underlying Graves' disease, treatment options include continuing methimazole, radioiodine ablation, or surgery (see "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment"). Patients with underlying autonomous adenoma or multinodular goiter who return to euthyroidism after discontinuation of iodine do not necessarily require definitive treatment. However, these patients are at risk for recurrent hyperthyroidism if given iodine again. For this reason, many clinicians prefer to treat with surgery or radioiodine, particularly if they develop persistent subclinical hyperthyroidism (low serum TSH but normal free T4 and T3). The management of patients with subclinical hyperthyroidism is reviewed in detail separately. (See "Subclinical hyperthyroidism in nonpregnant adults", section on 'Endogenous subclinical hyperthyroidism'.)

Radioiodine treatment for an underlying adenoma or multinodular goiter with autonomy may not be possible for several weeks to months after iodine exposure, since the exogenous iodine will limit entry of radioiodine into the thyroid gland. Urinary iodine can be measured to assess the clearance of the iodine load. Once the iodine load has cleared, treatment with radioiodine can proceed. In a previously iodine-exposed patient, a radioiodine uptake should be obtained to calculate the radioiodine treatment dose rather than using fixed-dose radioiodine treatment. (See "Treatment of toxic adenoma and toxic multinodular goiter" and "Radioiodine in the treatment of hyperthyroidism", section on 'Dosing of radioiodine'.)

Prevention in older adults — We do not generally suggest preventive therapy. However, older patients with known multinodular goiter and/or subclinical hyperthyroidism should be told of the risk for iodine-induced hyperthyroidism, and alternatives to CT scanning with contrast should be considered when appropriate (eg, noncontrast CT, magnetic resonance imaging [MRI]).

Iodine-induced hyperthyroidism is particularly important in geriatric patients for several reasons; the prevalence of thyroid nodular disease is higher than in younger patients, the hyperthyroidism may be more difficult to detect clinically, and older adults more often have underlying heart disease [17]. These points are well illustrated by a retrospective study of 60 hospitalized older patients (average age 80 years) with hyperthyroidism [30]. The diagnosis of hyperthyroidism was not initially suspected in 62 percent, and many were diagnosed only upon routine screening of thyroid function. Apathetic hyperthyroidism (lack of typical symptoms and signs of hypermetabolism) was present in 15 percent of patients. Contrast radiography with iodide-containing material had been performed in the six months before diagnosis in 23 percent. (See "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Geriatric hyperthyroidism'.)

In high-risk patients (older, history of multinodular goiter with autonomy), treatment with a thionamide or perchlorate prior to the administration of an iodine load (eg, coronary arteriography) may blunt or prevent the induction of hyperthyroidism [31,32]. However, there are insufficient randomized trial data to support the use of thionamides or perchlorate (not available in United States) for the prevention of iodine-induced hyperthyroidism. In addition, even in high-risk patients, the occurrence of iodine-induced hyperthyroidism is not common, the hyperthyroidism is usually transient, and beta-adrenergic drugs and/or methimazole can be administered if hyperthyroidism develops.

Routine measurement of thyroid function tests (TSH, and if low, free T4 and T3) in older patients after exposure to iodinated radiographic contrast agents is favored by some experts, particularly since the symptoms of hyperthyroidism in older adults may be atypical [30]. We do not suggest routine measurement of thyroid function tests in all older patients. However, in older patients with known nodular goiter and borderline low or subnormal TSH concentrations, we suggest measurement of thyroid function tests three to four weeks after exposure to radiographic contrast agents to assess for iodine-induced hyperthyroidism.

IODIDE-INDUCED HYPOTHYROIDISM — Iodine administration may induce or exacerbate hypothyroidism in patients with underlying autoimmune thyroiditis. Patients at risk for iodine-induced hypothyroidism include those with chronic autoimmune thyroiditis (Hashimoto's thyroiditis), with Graves' hyperthyroidism previously treated either with radioiodine or subtotal thyroidectomy, and those with painless, postpartum, or subacute granulomatous thyroiditis [12,21,33-35]. Such patients appear to be unusually sensitive to the inhibitory effects of iodide upon its own organification, in part due to a sustained activity of the sodium/iodide symporter (NIS) [21]. This sustained activity of the NIS results in a prolonged inhibition of thyroid hormone synthesis and an increase in TSH. Thus, hypothyroidism occurs in these patients because of failure to escape from the acute Wolff-Chaikoff effect. (See 'Follicular cell autoregulation' above.)

Iodide-associated hypothyroidism has also been reported after hemithyroidectomy for thyroid nodules [35]. The cause of the iodide-induced hypothyroidism in patients after hemithyroidectomy for nodular disease is not known. In addition, several nonthyroidal diseases also appear to place patients at increased risk for developing iodide-induced hypothyroidism. These include cystic fibrosis and thalassemia major in conjunction with repeated blood transfusions [36,37]. Iodine-induced hypothyroidism may rarely occur in individuals with normal underlying thyroid glands [38].

Iodide readily crosses the placenta, and the fetal thyroid appears particularly sensitive to its inhibitory effects [39]. Thus, maternal exposure to iodide during pregnancy may result in fetal goiter and hypothyroidism. Exposures as minor as vaginal application of povidone-iodine during delivery or topical use of disinfectant in newborns can lead to increased serum TSH concentrations [40-43] and transient neonatal hypothyroidism [44,45]. (See "Clinical features and detection of congenital hypothyroidism".)

Dietary iodine supplementation may increase the prevalence of hypothyroidism and Hashimoto's thyroiditis in the supplemented population [46,47]. Some patients take iodine supplements with the mistaken idea that more iodine is beneficial to thyroid function when, in fact, the opposite may be true.

Diagnosis and management — The clinical manifestations of iodine-induced hypothyroidism are similar to those seen in patients with other causes of hypothyroidism (see "Clinical manifestations of hypothyroidism"). The history may uncover past treatment of hyperthyroidism with radioiodine or thyroidectomy or a past history of postpartum thyroiditis. A history of iodine ingestion or administration should be elicited. Physical examination may reveal thyroid enlargement. The diagnosis of iodine-induced hypothyroidism is primarily based upon a history of iodine ingestion and laboratory testing (a high serum TSH concentration and a low serum free T4 concentration). (See "Diagnosis of and screening for hypothyroidism in nonpregnant adults", section on 'Diagnosis'.)

Iodine-induced hypothyroidism typically resolves spontaneously and rapidly (within one to two weeks) after withdrawal of iodine [38,48,49]. Most patients do not require thyroid hormone replacement. The time to recovery may be prolonged (eight weeks or longer) in patients exposed to iodide-containing substances that are not rapidly eliminated from the body. In such cases, or in cases where the source of iodine cannot be withdrawn (eg, amiodarone), thyroid function can be easily normalized by replacement with T4 (levothyroxine) while exposure to the iodine source continues. (See "Treatment of primary hypothyroidism in adults" and "Amiodarone and thyroid dysfunction", section on 'Hypothyroidism'.)

Because of the underlying thyroid disease, patients who develop transient iodine-induced hypothyroidism are at risk for permanent hypothyroidism in the future [38].

AMIODARONE — Both hypothyroidism and hyperthyroidism are complications of amiodarone therapy. The clinical effects of amiodarone on thyroid function in a given individual are dependent upon the underlying status of that individual's thyroid gland. The diagnosis and treatment of amiodarone-induced thyroid dysfunction are reviewed in detail separately. (See "Amiodarone and thyroid dysfunction".)

SUMMARY AND RECOMMENDATIONS

Sources of iodine – Iodine is essential for normal thyroid function, and it can be obtained by consumption of foods that contain it or to which it is added. The recommended minimum daily intake of iodine is 150 mcg for nonpregnant adults, 220 to 250 mcg for pregnant women, 290 mcg for lactating women, and 90 to 120 mcg/day for children aged 1 to 13. (See 'Sources of iodine' above.)

Normal adaptation to iodide intake – Regulatory mechanisms in the thyroid gland maintain the euthyroid state in the face of wide variation in dietary intake of iodine, unless iodine deficiency is severe or the patient has thyroid disease. (See 'Normal adaptation to iodide intake' above.)

Iodine-induced hyperthyroidism – The effects of iodine administration in patients with abnormal thyroid glands differ from those with normal thyroid glands and depend upon the underlying thyroid disease. Iodine administration may result in hyperthyroidism in patients with endemic goiter or in patients with nodular goiters containing autonomously functioning tissue. (See 'Iodine-induced hyperthyroidism' above.)

Clinical manifestations and diagnosis – The diagnosis of iodine-induced hyperthyroidism should be suspected in a patient with a history of iodine exposure (eg, coronary angiography, radiographic contrast) and clinical manifestations of hyperthyroidism (eg, palpitations, tremulousness, heat intolerance), particularly in those with a thyroid nodule or nodular goiter on physical examination. The diagnosis is confirmed with thyroid function tests (low serum thyroid-stimulating hormone [TSH], high free thyroxine [T4] and/or triiodothyronine [T3]). Iodine-induced hyperthyroidism typically begins weeks or even months after iodine administration. (See 'Diagnosis' above.)

Evaluation for underlying thyroid disease – Iodine-induced hyperthyroidism typically occurs in patients with underlying thyroid disease, usually nodular thyroid disease with autonomy. However, other causes of hyperthyroidism must also be considered since the hyperthyroidism may not be related to the iodine exposure. If the underlying thyroid disease is not apparent from physical examination (multinodular gland suggests thyroid autonomy; thyroid eye disease, diffuse goiter suggests Graves' disease), diagnostic testing may include measurement of TSH-receptor antibodies (TRAb), 24-hour radioiodine uptake, thyroid ultrasound (to assess for nodularity and thyroidal blood flow), or 24-hour urinary iodine level. (See 'Evaluation for underlying thyroid disease' above.)

Although a 24-hour thyroid radioiodine uptake and scan are frequently performed to distinguish underlying Graves' disease or thyroid autonomy (high uptake) from thyroiditis (low uptake), a radioiodine uptake test performed immediately after an iodine load must be interpreted with regard to the iodine load. An exogenous iodine load will dilute the administered radioiodine tracer, and the radioiodine uptake will be lowered depending upon the amount of the exogenous iodine load, whether the exposure is continuous (eg, amiodarone), and the interval since the iodine exposure. In this setting, a 24-hour urinary iodine level (or a spot urine iodine and creatinine to estimate the 24-hour urinary iodine concentration) can be obtained to assess the degree of iodine exposure. When urinary iodine levels are above 1000 mcg/day, iodine-induced thyroid dysfunction is likely and the results of the radioiodine uptake should be interpreted accordingly. (See 'Evaluation for underlying thyroid disease' above and "Diagnosis of hyperthyroidism", section on 'Determining the etiology'.)

Management – Iodine-induced hyperthyroidism is self-limiting (lasting 1 to 18 months) if the source of iodine is discontinued. The appropriate therapy for patients with iodine-induced hyperthyroidism is discontinuation of iodine, avoidance of further exposure, and the administration of a beta-adrenergic antagonist drug (assuming there are no contraindications to its use) to minimize the manifestations of hyperthyroidism. For patients with nodular thyroid disease who have severe or prolonged (>1 month) hyperthyroid symptoms and in older patients with underlying heart disease, we suggest starting a thionamide (methimazole) to achieve euthyroidism quickly (Grade 2C). After resolution of the acute episode of iodine-induced hyperthyroidism, treatment of the underlying thyroid disease should be addressed. (See 'Management' above.)

Prevention in older adults – Iodine-induced hyperthyroidism is particularly important in older patients for several reasons; the prevalence of thyroid nodular disease is higher than in younger patients, the hyperthyroidism may be more difficult to detect clinically, and older adults more often have underlying heart disease. For high-risk, older patients (nodular goiter and borderline low or subnormal TSH concentrations), we suggest not administering routine preventive therapy with thionamides prior to radiographic contrast administration (Grade 2C). However, in older patients at high risk for iodine-induced hyperthyroidism, we measure thyroid function tests (TSH, free T4, and T3) three to four weeks after exposure to radiographic contrast agents to assess for iodine-induced hyperthyroidism. (See 'Prevention in older adults' above.)

Iodine-induced hypothyroidism – Iodine administration may induce or exacerbate hypothyroidism in patients with underlying autoimmune thyroiditis.

Clinical manifestations and diagnosis – The clinical manifestations of iodine-induced hypothyroidism are similar to those seen in patients with other causes of hypothyroidism. The diagnosis of iodine-induced hypothyroidism is primarily based upon laboratory testing (a high serum TSH concentration and a low serum free T4 concentration). (See 'Iodide-induced hypothyroidism' above.)

Management – Iodine-induced hypothyroidism typically resolves spontaneously and rapidly (within one to two weeks) after withdrawal of iodine. Most patients do not require thyroid hormone replacement. The time to recovery may be prolonged (eight weeks or longer) in patients exposed to iodides that are not rapidly eliminated from the body. In such cases, thyroid function can be easily normalized by replacement with T4 (levothyroxine) until the iodine is eliminated. (See 'Diagnosis and management' above.)

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Topic 7844 Version 12.0

References

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