ESSENTIALS OF DIAGNOSIS
Common in regions with low-iodine diets.
High rate of congenital hypothyroidism and cretinism.
Goiters may become multinodular and enlarge.
Most adults with endemic goiter are euthyroid; however, some are hypothyroid or hyperthyroid.
The daily minimum dietary requirement for iodine is 150 mcg/day in nonpregnant adults and 250 mcg/day for pregnant or lactating women. Mild-to-moderate and sometimes severe iodine deficiency exists in 30 countries. An estimated 1.9 billion people have insufficient iodine intake. Severe iodine deficiency increases the risk of miscarriage and stillbirth. Cretinism occurs in about 0.5% of live births in iodine-deficient areas. Moderate iodine deficiency during gestation and infancy can cause manifestations of hypothyroidism, deafness, short stature, and lowers a child’s intelligence quotient by 10–15 points. Even mild-to-moderate iodine deficiency appears to impair a child’s perceptual reasoning and global cognitive index.
Although iodine deficiency is the most common cause of endemic goiter, there are other natural goitrogens, including certain foods (eg, sorghum, millet, maize, cassava), mineral deficiencies (selenium, iron, zinc), and water pollutants, which can themselves cause goiter or aggravate a goiter proclivity caused by iodine deficiency. In iodine-deficient patients, smoking can induce goiter growth. Pregnancy aggravates iodine deficiency and can increase the size of thyroid nodules and cause new nodules. Some individuals are particularly susceptible to goiter owing to congenital partial defects in thyroid enzyme activity.
Endemic goiters may become multinodular and very large. Growth often occurs during pregnancy and may cause compressive symptoms.
Substernal goiters are usually asymptomatic but can cause tracheal compression, respiratory distress and failure, dysphagia, superior vena cava syndrome, gastrointestinal bleeding from esophageal varices, palsies of the phrenic or recurrent laryngeal nerves, or Horner syndrome. Cerebral ischemia and stroke can result from arterial compression or thyrocervical steal syndrome. Substernal goiters can rarely cause pleural or pericardial effusions. The incidence of significant malignancy is less than 1%.
Some patients with endemic goiter may become hypothyroid. Others may become thyrotoxic as the goiter grows and becomes more autonomous, especially if iodine is added to the diet.
The serum T4 and TSH are generally normal. TSH falls in the presence of hyperthyroidism if a multinodular goiter has become autonomous in the presence of sufficient amounts of iodine for thyroid hormone synthesis. TSH rises with hypothyroidism. Thyroid RAI uptake is usually elevated, but it may be normal if iodine intake has improved. Serum levels of antithyroid antibodies are usually either undetectable or in low titers. Serum thyroglobulin is often elevated above 13 mcg/L. Urine iodine concentrations are low.
Endemic goiter must be distinguished from all other forms of nodular goiter that may coexist in an endemic region.