Hyperthyroidism, Thyroid Storm, and Graves Disease Medication
- Author: Erik D Schraga, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
The goals of medical therapy are blockade of peripheral effects, inhibition of hormone synthesis, blockade of hormone release, and prevention of peripheral conversion of T4 to T3. Restoration of a clinical euthyroid state may take up to 8 weeks.
Blocking agents such as beta-blockers reduce sympathetic hyperactivity and decrease peripheral conversion of T4 to T3.
Guanethidine and reserpine have been used to provide sympathetic blockade and may be effective agents if beta-blockers are contraindicated or not tolerated.
Iodides and lithium work to block release of preformed thyroid hormone.
Thionamides prevent synthesis of new thyroid hormone.
Inhibitors of hormone synthesis
Thionamides (eg, propylthiouracil, methimazole) prevent hormone synthesis by inhibiting both the organification of iodine to tyrosine residues and the coupling of iodotyrosines. The drug must be given orally or via a nasogastric tube. PTU has the added benefit of inhibiting peripheral conversion of T4 to T3.
DOC; effects may be seen soon after drug is started, but therapy may need to be continued for 4-12 wk. Laboratory monitoring of T4 and T3 levels may be required to adjust therapy. Although classified as pregnancy category D, recommended as DOC for women who are pregnant or breastfeeding.
An effective inhibitor of thyroid synthesis; however, it does not inhibit peripheral conversion of thyroid hormone
Blockade of hormone release
Iodides and lithium are used effectively to block the release of thyroid hormone. Effects are exerted directly on the thyroid gland. Lithium is used only as a secondary agent due to difficulty in titrating to an effective dose and its narrow therapeutic window. These agents should be administered at least 1 hour after PTU is given to ensure the advance blockade of thyroid hormone formation; otherwise, administering iodides could worsen symptoms. Iodide preparations are known to cause serum sickness–type reactions. Iodides should not be used for long-term therapy in thyrotoxicosis. Preparations include saturated solution of potassium iodide (SSKI), iopanoic acid, and Lugol iodine.
Absorption from GI tract is rapid and complete. Iodine equilibrates in extracellular fluids and is concentrated specifically by thyroid gland. For treatment of thyrotoxicosis, parenteral iodine may be used.
Inhibits thyroid hormone secretion. Solution contains 50 mg of iodide per drop and may be mixed with juice or water.
Inhibits thyroid hormone secretion. Contains 8 mg of iodide per drop. May be mixed with juice or water for intake.
Beta-blockade is mainstay of symptomatic therapy; antiadrenergic effects block effects of excess thyroid hormone. Beta-blockade also plays a role in the prevention of peripheral conversion of T4 to T3. Propranolol is the best studied in this class, but other beta-blockers have similar effects in hyperthyroidism.
Effects are relatively dramatic, and results may be seen within 10 minutes after administration.
Use of beta-blockers improves heart failure that is due to thyrotoxic tachycardia or thyrotoxic myocardial depression but may worsen heart failure that is due to other causes. When in doubt, therapy may be begun with a short-acting titratable agent, such as esmolol.
Reserpine and guanethidine are effective autonomic blockers that may be used if beta-blockers are contraindicated.
DOC; can control cardiac and psychomotor manifestations within minutes.
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