Goiter can be use to describe any non-neoplastic enlargement of the thyroid. Pathologists generally limit the term to thyroid enlargement not due to neoplasm, inflammation or defined autoimmune syndromes. To a pathologist, goiter implies a compensatory hypertrophy and hyperplasia of follicular epithelium resulting from an inability of the gland to produce sufficient thyroid hormone. To a clinician it may simply mean an enlarged thyroid gland.
Goiters are usually classified as endemic or sporadic. Endemic goiters are found in iodine deficient regions. At one time they were common in the Ohio River valley but now that iodine is routinely added to salt, endemic goiters are uncommon.
The most common type is sporadic goiter. Sporadic goiters show a marked female predominance (8:1) and have a peak incidence during puberty and early adulthood. The etiology is not known but biochemical defects in thyroid hormone production and autoantibodies to TSH receptors that stimulate thyroid growth but not function are known to cause some cases.
Goiters can be classified as simple (diffuse nontoxic) or as multinodular.
Simple goiters are usually associated with normal thyroid hormone levels, however, hypothyroidism is not uncommon. The distinction between sporadic goiter and goitrous hypothyroidism is determined by the ability of the thyroid to maintain normal T4 and T3 levels in the serum. Most diffuse goiters become multinodular with time.
Multinodular goiters can be euthyroid but often cause hyperthyroidism (a.k.a. toxic goiter). Chronic over stimulation of the gland may lead to autonomous hormone production and loss of feedback inhibition.
Microscopic examination of a simple goiter reveals small follicles lined by cuboidal to columnar cells. Multinodular goiters have very large follicles containing abundant colloid in addition to small follicles. Follicles may become so large that they form colloid cysts. Fibrosis, hemorrhage and cyst formation are common in the multinodular form. Gross and microscopic appearance are not reliable for determining the functional status of the thyroid.
Simple goiters may not require treatment except for thyroid hormone replacement if there is associated hypothyroidism. Multinodular goiters may need to be ablated surgically or with radioactive iodine. The differentiation of diffuse and multinodular goiter is usually evident on physical examination, however, transitional states are not uncommon.