Nontoxic goiter is a syndrome of thyroid enlargement without excessive thyroid hormone production. Enlargement of the thyroid gland is often due to TSH stimulation from inadequate thyroid hormone synthesis. The most common cause of nontoxic goiter worldwide is iodide deficiency, but in the United States, it is Hashimoto’s thyroiditis. Other causes include germ-line or acquired mutations in genes involved in hormone synthesis, dietary goitrogens, and neoplasms (see below).
Goiter due to iodide deficiency is best managed by prophylactic administration of iodide. The optimal daily iodide intake is 150–200 mcg. Iodized salt and iodate used as preservatives in flour and bread are excellent sources of iodine in the diet. In areas where it is difficult to introduce iodized salt or iodate preservatives, a solution of iodized poppy-seed oil has been administered intramuscularly to provide a long-term source of inorganic iodine.
Goiter due to ingestion of goitrogens in the diet is managed by elimination of the goitrogen or by adding sufficient thyroxine to shut off TSH stimulation. Similarly, in Hashimoto’s thyroiditis and dyshormonogenesis, adequate thyroxine therapy—150–200 mcg/d orally—will suppress pituitary TSH and result in slow regression of the goiter as well as correction of hypothyroidism.
Neoplasms of the thyroid gland may be benign (adenomas) or malignant. The primary diagnostic test is a fine needle aspiration biopsy and cytologic examination. Benign lesions may be monitored for growth or symptoms of local obstruction, which would mandate surgical excision. Levothyroxine therapy is not recommended for the suppression of benign nodules, especially in iodine sufficient areas. Management of thyroid carcinoma requires a total thyroidectomy, postoperative radioiodine therapy in selected instances, and lifetime replacement with levothyroxine. The evaluation for recurrence of some thyroid malignancies often involves withdrawal of thyroxine replacement for 4–6 weeks— accompanied by the development of hypothyroidism. Tumor recurrence is likely if there is a rise in serum thyroglobulin (ie, a tumor marker) or a positive 131I scan when TSH is elevated. Alternatively, administration of recombinant human TSH (Thyrogen) can produce comparable TSH elevations without discontinuing thyroxine and avoiding hypothyroidism. Recombinant human TSH is administered intramuscularly once daily for 2 days. A rise in serum thyroglobulin or a positive 131I scan will indicate a recurrence of the thyroid cancer.
Levothyroxine (T4) Generic, Levoxyl, Levo-T, Levothroid, Levolet*, Novothyrox, Synthroid, Tirosint (capsule), Unithroid
Liothyronine (T3) Generic, Cytomel, Triostat (IV)
Liotrix (a 4:1 ratio of T4: T3) Thyrolar
Radioactive iodine (131I) sodium Iodotope, Sodium Iodide I 131 Therapeutic
Methimazole Generic, Tapazole
Oral potassium iodide tablets IOSAT, Thyro-Block, Thyro-Safe
American Thyroid Association: Professional Guidelines. Available at: www.thyroid. org/professionals/ata-professional-guidelines/.
American Thyroid Association Task Force on Radiation Safety et al: Radiation safety in the treatment of patients with thyroid diseases by radioiodine 131I: Practice recommendations of the American Thyroid Association. Thyroid 2011;21:335.
Chen AY et al: American Thyroid Association Statement on Optimal Surgical Management of Goiter. Thyroid 2014;24:181.