Hyperthyroidism Medication

Drug therapy includes medications that reduce the symptoms of thyrotoxicosis and decrease the synthesis and release of thyroid hormone. In the United States, the most common definitive therapy for hyperthyroidism is ablation of the hyperactive thyroid with an oral dose of¹³¹ I.

Sometimes, the patient is treated with antithyroid medication to return thyroid hormone levels to normal. When that is accomplished, some patients (eg, those with a toxic multinodular goiter or toxic adenoma) are treated immediately with radioactive iodine, while patients with autoimmune Graves disease may be treated for 12-18 months with antithyroid medications because of the possibility that the patient will go into remission.^[11] Nevertheless, the most common treatment for these patients in the United States is to receive¹³¹ I as their first and only medication.

Patients with other forms of hyperthyroidism, including toxic multinodular goiter and toxic adenoma, continue indefinitely to be thyrotoxic, and remissions with antithyroid medications are not expected.

Class Summary

These agents inhibit T₄ and T₃ synthesis.

Propylthiouracil

Propylthiouracil is a derivative of thiourea that inhibits organification of iodine by the thyroid gland. It blocks oxidation of iodine in the thyroid gland, thereby inhibiting thyroid hormone synthesis; the drug inhibits T4-to-T3 conversion (an advantage over other agents).

Propylthiouracil is available as a 50-mg tablet. It is readily absorbed and has a serum half-life of 1-2 hours. It is highly protein bound in the serum. The drug's duration of action is longer than its half-life, and propylthiouracil should be dosed every 6-8 hours (although it can be administered twice daily).

If patient compliance is an issue, methimazole is better choice because of daily dosing.

Thyroid hormone levels (TSH, T4, FTI or FT4, and T3) should be reassessed in 4 weeks and increased if thyroid hormone levels have not significantly fallen or decreased if thyroid hormone levels have fallen by 50% or more (even if still thyrotoxic). Usually, after thyroid function improves, the dose should be gradually decreased to 50-150 mg/d in divided doses (or the patient will become hypothyroid).

Methimazole (Tapazole)

Methimazole inhibits thyroid hormone by blocking oxidation of iodine in the thyroid gland. However, it is not known to inhibit peripheral conversion of thyroid hormone. The drug is available as 5-mg or 10-mg tablets. It is readily absorbed and has a serum half-life of 6-8 hours. Methimazole is less protein bound than propylthiouracil and generally is not used in pregnancy because of increased placental transfer and risk of a rare fetal condition (cutis aplasia). It has higher transfer rate into the milk of lactating women.

Methimazole's duration of action is longer than its half-life, and the drug should be dosed every 12-24 hours. Studies have shown that rectal suppositories or retention enemas can be used at the same dose as orally administered methimazole for patients who cannot take oral medications. Usually, after thyroid function improves, the dose must be decreased, or patient will become hypothyroid.

Class Summary

These reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Usually, propranolol is recommended because of central nervous system (CNS) penetration, but some patients prefer longer-acting beta blockers. Patients note an immediate improvement in tachycardia, anxiety, heat intolerance, and tremor. Calcium channel blockers for tachycardia sometimes are used when beta blockers are contraindicated or not tolerated.

Propranolol (Inderal, InnoPran XL)

This is the drug of choice in treating cardiac arrhythmias resulting from hyperthyroidism. It controls cardiac and psychomotor manifestations within minutes.

Atenolol (Tenormin)

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types.

Class Summary

High intrathyroidal iodine levels in Graves thyrotoxicosis lead to an inhibition of iodine transport and thyroid hormone synthesis (Wolff-Chaikoff effect) and block the release of T₄ and T₃ from the thyroid. Excess iodide with toxic multinodular goiter or toxic adenoma may result in exacerbation of thyrotoxicosis. Administration of pharmacologic doses of iodide prevents radioactive iodine therapy for many weeks. Many patients unexpectedly escape from the inhibitory effects of iodide. Therefore, it is not used in long-term maintenance therapy of Graves thyrotoxicosis.

Iopanoic acid (Telepaque)

This is an oral contrast agent for the rapid and significant inhibition of peripheral T4-to-T3 conversion. Inorganic iodide released also blocks the release of thyroid hormones. Iopanoic acid quickly reduces levels of the biologically active form of thyroid hormone, T3, and decreases symptoms accordingly. This drug has been discontinued in the United States.

Potassium iodide (Lugol solution, SSKI)

Potassium iodide inhibits thyroid hormone secretion. Lugol solution contains 8 mg of iodide per drop; SSKI contains approximately 35-50 mg of iodide per drop. Iodide therapy is reserved for the treatment of thyroid storm or is used for 10-14 days prior to surgical procedure, including thyroidectomy. Potassium iodide can be used in Graves thyrotoxicosis, but it exacerbates thyrotoxicosis from toxic multinodular goiter and toxic adenoma.

Sodium iodide 131I (Iodotope, Hicon)

This is the most common treatment for hyperthyroidism in adults in the United States. The agent is quickly absorbed and taken up by the thyroid. No other tissue or organ in the body is capable of retaining radioactive iodine; therefore, few adverse effects develop.