In the body, iodine (I) is involved primarily in the synthesis of 2 thyroid hormones, thyroxine (T4) and triiodothyronine (T3).
Iodine occurs in the environment and in the diet primarily as iodide. In adults, about 80% of the iodide absorbed is trapped by the thyroid gland. Most environmental iodine occurs in seawater as iodide; a small amount enters the atmosphere and, through rain, enters ground water and soil near the sea. Thus, people living far from the sea and at higher altitudes are at particular risk of iodine deficiency.
Fortifying table salt with iodide (typically 70 mcg/g) helps ensure adequate intake (150 mcg/day). Requirements are higher for pregnant (220 mcg/day) and lactating (290 mcg/day) women.
Iodine deficiency is rare in areas where iodized salt is used but common worldwide. Iodine deficiency develops when iodide intake is < 20 mcg/day.
In mild or moderate iodine deficiency, the thyroid gland, influenced by thyroid-stimulating hormone (TSH), hypertrophies to concentrate iodide in itself, resulting in colloid goiter. Usually, patients remain euthyroid; however, severe iodine deficiency in adults may cause hypothyroidism (endemic myxedema). It can decrease fertility and increase risk of stillbirth, spontaneous abortion, and prenatal and infant mortality.
Severe maternal iodine deficiency retards fetal growth and brain development, sometimes resulting in birth defects, and, in infants, causes cretinism, which may include intellectual disability, deaf-mutism, difficulty walking, short stature, and sometimes hypothyroidism.
Diagnosis of iodine deficiency in adults and children is usually based on thyroid function tests, examination for goiter, and imaging tests identifying abnormalities in thyroid function and structure. All neonates should be screened for hypothyroidism by measuring the TSH level.
Infants with iodine deficiency are given levothyroxine 3 mcg/kg po once/day for a week plus iodide 50 to 90 mcg po once/day for several weeks to quickly restore a euthyroid state.
Children are treated with iodide 90 to 120 mcg once/day.
Adults are given iodide 150 mcg once/day. Iodine deficiency can also be treated by giving levothyroxine.
Serum TSH levels are monitored in all patients until the levels are normal (ie, < 5 μIU/mL).
Chronic toxicity may develop when intake is > 1.1 mg/day. Most people who ingest excess amounts of iodine remain euthyroid. Some people who ingest excess amounts of iodine, particularly those who were previously deficient, develop hyperthyroidism (Jod-Basedow phenomenon). Paradoxically, excess uptake of iodine by the thyroid may inhibit thyroid hormone synthesis (called Wolff-Chaikoff effect). Thus, iodine toxicity can eventually cause iodide goiter, hypothyroidism, or myxedema.
Very large amounts of iodide may cause a brassy taste in the mouth, increased salivation, GI irritation, and acneiform skin lesions. Patients frequently exposed to large amounts of radiographic contrast dyes or the drug amiodarone need to have their thyroid function monitored.
Diagnosis of iodine toxicity is usually based on results of thyroid function testing and imaging, which are correlated with clinical data. Iodine excretion may be more specific but is not usually measured.
Treatment of iodine toxicity consists of correcting thyroid abnormalities and, if intake is excessive, dietary modification.
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