Simple Nontoxic Goiter
(See also Overview of Thyroid Function.)
Simple nontoxic goiter, which may be diffuse or nodular, is noncancerous hypertrophy of the thyroid without hyperthyroidism, hypothyroidism, or inflammation. Except in severe iodine deficiency, thyroid function is normal and patients are asymptomatic except for an obviously enlarged, nontender thyroid. Diagnosis is clinical and with determination of normal thyroid function. Treatment is directed at the cause, but partial surgical removal may be required for very large goiters.
Simple nontoxic goiter, the most common type of thyroid enlargement, is frequently noted at puberty, during pregnancy, and at menopause. The cause at these times is usually unclear. Known causes include
Intrinsic thyroid hormone production defects
Ingestion of foods that contain substances that inhibit thyroid hormone synthesis (goitrogens, eg, cassava, broccoli, cauliflower, cabbage), as may occur in countries in which iodine deficiency is common
Drugs that can decrease the synthesis of thyroid hormone (eg, amiodarone or other iodine-containing compounds, lithium)
Iodine deficiency is rare in North America but remains the most common cause of goiter worldwide (termed endemic goiter). Compensatory small elevations in thyroid-stimulating hormone (TSH) occur, preventing hypothyroidism, but the TSH stimulation results in goiter formation. Recurrent cycles of stimulation and involution may result in nontoxic nodular goiters. However, the true etiology of most nontoxic goiters in iodine-sufficient areas is unknown.
In the early stages, thyroidal radioactive iodine uptake may be normal or high with normal thyroid scans. Thyroid function test results are usually normal. Thyroid antibodies are measured to rule out Hashimoto thyroiditis.
In endemic goiter, serum TSH may be slightly elevated, and serum T4 may be low-normal or slightly low, but serum T3 is usually normal or slightly elevated.
Thyroid ultrasonography is done to determine whether there are nodules that are suggestive of cancer.
In iodine-deficient areas, iodine supplementation of salt; oral or IM administration of iodized oil yearly; and iodination of water, crops, or animal fodder eliminates iodine-deficiency goiter. Goitrogens being ingested should be stopped.
In other instances, suppression of the hypothalamic-pituitary axis with thyroid hormone blocks TSH production (and hence stimulation of the thyroid). Full TSH-suppressive doses of l-thyroxine (100 to 150 mcg/day po depending on the serum TSH) are useful in younger patients.
l-Thyroxine is contraindicated in older patients with nontoxic nodular goiter, because these goiters rarely shrink and may harbor areas of autonomy so that l-thyroxine therapy can result in hyperthyroidism.
Large goiters occasionally require surgery or 131I to shrink the gland enough to prevent interference with respiration or swallowing or to correct cosmetic problems.
Thyroid function is usually normal.
When the cause is iodine deficiency, iodine supplementation is effective treatment.
Blocking TSH production by giving l-thyroxine is useful in younger patients to halt stimulation of the thyroid and shrink the goiter.
Surgery or 131I may be needed for large goiters.