Iodine-induced thyroid dysfunction

Abstract

Purpose of review To summarize the mechanisms of iodine-induced hypothyroidism and hyperthyroidism, identify the risk factors for thyroid dysfunction following an iodine load, and summarize the major sources of excess iodine exposure. Recent findings Excess iodine is generally well tolerated, but individuals with underlying thyroid disease or other risk factors may be susceptible to iodine-induced thyroid dysfunction following acute or chronic exposure. Sources of increased iodine exposure include the global public health efforts of iodine supplementation, the escalating use of iodinated contrast radiologic studies, amiodarone administration in vulnerable patients, excess seaweed consumption, and various miscellaneous sources. Summary Iodine-induced thyroid dysfunction may be subclinical or overt. Recognition of the association between iodine excess and iodine-induced hypothyroidism or hyperthyroidism is important in the differential diagnosis of patients who present without a known cause of thyroid dysfunction.

Hypothyroidism and the Heart

“…Early AIH may be present in 10% to 20% of patients treated with amiodarone, whereas the incidence with long-term treatment is often lower, from 5% to 10%. AIH is noted to be more frequent in iodine-sufficient areas of the world, 18 and the presence of thyroid autoantibodies is associated with an increased likelihood of developing AIH. There is also an understanding that amiodarone may hasten the pathogenesis of Hashimoto thyroiditis.…”

Iodinated contrast media exposure and incident hyperthyroidism and hypothyroidism in a community-based cohort

“…These collective data bear great clinical relevance given the known adverse effects of hyperthyroidism on multiple organ systems (i.e., bone, neuropsychiatric) 16 particularly the cardiovascular system (e.g., atrial fibrillation, high-output heart failure, angina, and possibly greater cardiovascular mortality). 17,18 Although untested, it has been suggested that prophylactic treatment with methimazole or perchlorate may be warranted in high-risk patients in advance of anticipated iodide exposure such as elective ICM-based procedures; 2,19,20 further studies are needed to evaluate the safety and effectiveness of this approach.…”

“…1,2 However, it has long been recognized that acute or chronic exposure to excess iodine from non-ICM sources (e.g., medications, disinfectants, diet) may result in thyrotoxicosis in some patients. 2,12 Iodine-induced hyperthyroidism (Jöd Basedow phenomenon) has typically been described in patients with latent nodular or diffuse goiter or Graves' disease residing in areas of iodine deficiency who remain clinically euthyroid until iodine repletion. 1,13,14 However, iodine-induced hyperthyroidism has also been observed in patients without pre-existing thyroid disease residing in iodine-replete regions.…”

“…Such phenomena have been observed in response to a variety of exposures including those that confer as little as 300 mcg of iodide. 2,3 Iodinated contrast media (ICM) exposure has risen over the past two decades in parallel with increased utilization of contrast-based computed tomography (CT) and cardiac angiography. 4 ICM represents a significant iodine load: a single dose contains 13,500 μg of free iodide, as well as 15-60 g of bound iodine that may be liberated to free iodide following administration.…”

“…1,2 However, in some patients exposure to supraphysiologic levels inhibits thyroid hormone synthesis, resulting in hypothyroidism. Conversely, in other patients high iodide levels provide excess substrate for unregulated thyroid hormone formation, resulting in hyperthyroidism (Jöd Basedow phenomenon).…”