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 underlying 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 and, in iodine-deficient countries, ingestion of foods that contain substances that inhibit thyroid hormone synthesis (goitrogens, eg, cassava, broccoli, cauliflower, cabbage). Other causes include the use of drugs that can decrease the synthesis of thyroid hormone (eg, amiodaroneSome Trade Names
CORDARONE
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or other iodine-containing compounds, lithiumSome Trade Names
ESKALITH
LITHOBID
LITHONATE
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).

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.

Symptoms and Signs

The patient may have a history of low iodine intake or overingestion of food goitrogens, but these phenomena are rare in North America. In the early stages, the goiter is typically soft, symmetric, and smooth. Later, multiple nodules and cysts may develop.

Diagnosis

• Thyroidal radioactive iodine uptake
• Thyroid scan
• Thyroxine (T₄), triiodothyronine (T₃), and TSH levels

In the early stages, thyroidal radioactive iodine uptake may be normal or high with normal thyroid scans. Thyroid function tests are usually normal. Thyroid antibodies are measured to rule out Hashimoto's 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.

Treatment

• Depends on cause

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 μg/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.

Key Points

• 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.

Last full review/revision May 2012 by Jerome M. Hershman, MD

Content last modified May 2012