Iodine Deficiency

At a Glance

Iodine is an essential element needed for the production of thyroid hormone. It is a component of thyroxine (T4 with four iodine molecules) and triiodothyronine (T3 with three iodine mol). Iodine is not produced by the body, so it must be part of the diet. It is found in various foods, including dairy products, seafood, meat, some breads, eggs, and iodized salt, and is found naturally in soil and seawater. Inadequate intake of iodine leads to inadequate thyroid hormone production, resulting in goiter (enlargement of the thyroid), hypothyroidism, and pregnancy-related problems.

Goiter is thse most obvious manifestation of iodine deficiency. The primary activity of the thyroid gland is to concentrate iodine absorbed in the gastrointestinal tract and circulating in blood to make thyroid hormone. Low iodine intake leads to reduced T4 and T3 production and, thus, hypothyroidism. There is then an increase in thyrotropin (TSH) secretion in an attempt to restore T4 and T3 levels to normal. TSH also stimulates thyroid growth, resulting in the goiter. In areas of iodine deficiency, children generally have diffuse goiters, whereas adults who have experienced long periods of iodine deficiency have nodular goiters.

Although it is uncommon in the United States for adults to have hypothyroidism due to low iodine intake, iodine deficiency is the most common cause of hypothyroidism worldwide. Iodine deficiency is on the rise in the United States. In the United States iodine deficiency occurred at a rate of 2.6% between 1971-1994 and a rate of 11.8% from 1988 to 1999. Iodine deficient patients have the usual clinical manifestation of hypothyroidism, including fatigue, weight gain, and depression, as well as a goiter.

Other symptoms of hypothyroidism include brittle fingernails; coarsening and thinning of hair; puffy eyes; pale, dry skin; weakness; and constipation. Symptoms expressing themselves later in the course of the disease are hoarseness; menstrual disorders; puffy hands, face, and feet; thickening of the skin; thinning of eyebrows; increased cholesterol levels; muscle and/or joint aches and stiffness; slowed speech; and decreased hearing.

Thyroid hormone is essential during pregnancy for the normal maturation of the fetal central nervous system; therefore, iodine deficiency is especially important in pregnant women. Severe iodine deficiency in pregnant women has been associated with miscarriages, stillbirth, preterm delivery, and congenital abnormalities.

Hypothyroidism during critical periods of fetal development can lead to mental retardation and problems with growth, hearing, and speech. Mental retardation in the most severe form is known as cretinism, which is a syndrome characterized by permanent brain damage, mental retardation, deaf mutism, spasticity, and short stature. Although cretinism is not common, all fetuses and infants in regions of iodine deficiency are at risk for some degree of mental retardation. Even mild iodine deficiency during pregnancy can lead to low intelligence in children.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

Iodine deficiency is not diagnosed specifically in individuals, but rather across populations. To assess iodine nutrition across populations, measurements of urinary iodine, thyroid size, serum TSH, and thyroglobulin levels are used. The urinary iodine concentration indicates current iodine nutrition, whereas thyroid size and serum thyroglobulin concentration reflect iodine nutrition over a period of months or years.

Urinary iodine excretion (UI) is an excellent indicator of recent iodine intake, because more than 90% of ingested iodine eventually appears in the urine. Since iodine deficiency is diagnosed across populations, UI can be measured as random samples from a group and expressed as the median. The median UI in random samples correlates well with 24-hour urine collections, which may be impractical to obtain in large populations. A median UI less than 20 mcg/L is indicative of severe iodine deficiency. Moderate deficiency is indicated with a median UI of 20-49 mcg/L and mild deficiency with a median UI of 50-99 mcg/L.

Thyroid size is a sensitive marker for iodine deficiency, because goiter is the most obvious manifestation. Goiter can be measured through neck inspection and palpation or with ultrasonography. The World Health Organization (WHO) recommends the total goiter rate be used to define severity of iodine deficiency in populations using the following criteria

• less than 5% iodine sufficiency

• 5-19.9% mild deficiency

• 20-29.9% moderate deficiency

• more than 30% severe deficiency

Serum TSH can be used as a sensitive indicator of iodine nutrition in the newborn (not in children and adults). Iodine deficiency in the population is determined when there is an increase in transient newborn hypothyroidism as indicated when more than 3% of newborn TSH concentrations are greater than 5 mIU/L in blood spots collected 3-4 days after birth. TSH screening in newborns is used in many countries to detect congenital hypothyroidism due to iodine deficiency, which is the most common preventable cause of mental retardation in the world.

Serum thyroglobulin concentration (Tg) is elevated more often than serum TSH in infants and children. It is a sensitive measure of thyroid activity but is a nonspecific test, as any type of thyroid stimulation or injury can raise Tg levels. Increased Tg levels greater than 40 mcg/L correlate well with iodine deficiency.

Taking too much iodine, whether through medications (such as amiodarone, radiology procedures, or dietary excess), can cause or worsen hyperthyroidism and counterintuitively hypothyroidism. Also, people who move from iodine deficient regions of the world to iodine sufficient areas may develop thyroid problems. These patients usually develop iodine induced hyperthyroidism.(Table 1).