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 deficiency. Fortifying table salt with iodide (typically 70 μg/g) helps ensure adequate intake (150 μg/day). Requirements are higher for pregnant (220 μg/day) and lactating (290 μg/day) women.

Iodine Deficiency

Deficiency is rare in areas where iodized salt is used but common worldwide. Iodine deficiency develops when iodide intake is < 20 μg/day. In mild or moderate 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 mental retardation, deaf-mutism, difficulty walking, short stature, and sometimes hypothyroidism.

Diagnosis

• Assessment of thyroid structure and function

Diagnosis in adults and children is usually based on thyroid function, examination for goiter, and imaging tests identifying abnormalities in thyroid function and structure (see Thyroid Disorders: Laboratory Testing of Thyroid Function). All neonates should be screened by measuring the TSH level.

Treatment

• Iodide with or without levothyroxineSome Trade Names
  LEVOXYL
  SYNTHROID
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Infants with iodine deficiency are given l-thyroxine 3 μg/kg po once/day for a week plus iodide 50 to 90 μg po once/day for several weeks to quickly restore a euthyroid state. Children are treated with iodide 90 to 120 μg once/day. Adults are given iodide 150 μg once/day. Iodine deficiency can also be treated by giving levothyroxineSome Trade Names
LEVOXYL
SYNTHROID
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. Serum TSH levels are monitored in all patients until the levels are normal (ie, < 5 μIU/mL).

Iodine Toxicity

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 exposed to frequent large amounts of radiographic contrast dyes or the drug amiodaroneSome Trade Names
CORDARONE
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also need to have their thyroid function monitored.

Diagnosis is usually based on thyroid function and imaging test findings (see Thyroid Disorders: Laboratory Testing of Thyroid Function), which are correlated with clinical data. Iodine excretion may be more specific but is not usually measured. Treatment consists of correcting thyroid abnormalities and, if intake is excessive, dietary modification.

Last full review/revision August 2008 by Larry E. Johnson, MD, PhD

Content last modified February 2012