|
In the body, iodine (I) is primarily involved in the synthesis of two thyroid hormones, thyroxine and triiodothyronine. In adults, about 80% of the iodide absorbed is trapped by the thyroid gland.
Most environmental iodine occurs in seawater; 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 (100 μg/day).
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, the patient remains euthyroid; however, severe iodine deficiency in adults may cause hypothyroidism (endemic myxedema). Mild or moderate deficiency decreases IQ by about 10 to 15 points. 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 hypothyroidism (endemic cretinism) and deaf-mutism in a neurologic or myxedematous form.
Diagnosis is usually based on thyroid function test and imaging study findings identifying abnormalities in thyroid function and structure (see Thyroid Disorders: Laboratory Testing of Thyroid Function). For large populations, urinary iodine excretion may be more specific for iodine deficiency than thyroid function abnormalities, but urinary iodine excretion may be inaccurate for individuals. These levels (normally, 100 to 200 μg/L) are 50 to 99 μg/L for mild deficiency, 20 to 49 μg/L for moderate deficiency, and < 20 μg/L for severe deficiency. WHO criteria for diagnosis in school-aged children are goiter detected by palpation, increased thyroid volume (> 97th percentile) detected by ultrasonography, and decreased urinary iodine excretion. All newborns should be screened by measuring the TSH level.
Infants with iodine deficiency are given l‑thyroxine 3 μg/kg po once/day for a week plus iodide 50 μg po once/day for several weeks to quickly restore a euthyroid state. Plasma TSH levels are monitored until they are normal (ie, < 5 μIU/mL). Adults with deficiency are given iodide 150 μg once/day.
Toxicity:
Chronic toxicity develops only when intake is > 2 mg/day. Use of amiodarone can also cause toxicity.
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, iodide toxicity can eventually cause iodide goiter, hypothyroidism, or myxedema. Very large amounts of iodide may cause a brassy taste, increased salivation, GI irritation, and acneiform skin lesions.
Diagnosis is usually based on thyroid function test and imaging study findings (see Thyroid Disorders: Laboratory Testing of Thyroid Function). 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 November 2005
Content last modified November 2005
| 
