Goiter refers to an enlarged thyroid gland (>20–25 g), which can be diffuse or nodular. Goiter is more common in women than men. Biosynthetic defects, iodine deficiency, autoimmune disease, dietary goitrogens (cabbage, cassava root), and nodular diseases can lead to goiter. Worldwide, iodine deficiency is the most common etiology of goiter. Nontoxic MNG is common in both iodine-deficient and iodine-replete populations, with a prevalence of up to 12%. The etiology, other than iodine deficiency, is usually not known and may be multifactorial. If thyroid function is preserved, most goiters are asymptomatic. Substernal goiter may obstruct the thoracic inlet and should be evaluated with respiratory flow measurements and CT or MRI in pts with obstructive signs or symptoms (difficulty swallowing, tracheal compression, or plethora). Thyroid function tests should be performed in all pts with goiter to exclude thyrotoxicosis or hypothyroidism. Ultrasound is not generally indicated in the evaluation of diffuse goiter, unless a nodule is palpable on physical examination.

Iodine or thyroid hormone replacement induces variable regression of goiter in iodine deficiency. Thyroid hormone replacement is rarely effective for significantly shrinking a nontoxic goiter that is not due to iodine deficiency or a biosynthetic defect. Radioiodine reduces goiter size by about 50% in the majority of pts. Surgery is rarely indicated for diffuse goiter but may be required to alleviate compression in pts with nontoxic MNG.