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Beta blockers in the treatment of hyperthyroidism

Douglas S Ross, MD
Section Editor
David S Cooper, MD
Deputy Editor
Jean E Mulder, MD


Beta blockers ameliorate the symptoms of hyperthyroidism that are caused by increased beta-adrenergic tone. These include palpitations, tachycardia, tremulousness, anxiety, and heat intolerance. Thus, a beta blocker should be started (assuming there are no contraindications to its use) in most patients as soon as the diagnosis of hyperthyroidism is made, even before determining the cause of the hyperthyroidism. They should be continued until resolution of hyperthyroidism.

The clinical use and efficacy of beta blockers in the treatment of hyperthyroidism will be reviewed here. The clinical manifestations, diagnosis, and treatment of hyperthyroidism are reviewed separately. (See "Overview of the clinical manifestations of hyperthyroidism in adults" and "Diagnosis of hyperthyroidism" and "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment" and "Surgical management of hyperthyroidism" and "Thyroid storm".)


In many tissues, hyperthyroidism is associated with an increased number of beta-adrenergic receptors [1]. The ensuing increase in beta-adrenergic activity is responsible for many of the symptoms associated with this disorder. It also explains the ability of beta blockers to ameliorate rapidly many of the symptoms, including palpitations, tachycardia, tremulousness, anxiety, and heat intolerance [2]. In a small, randomized trial, patients receiving beta blockers with methimazole, compared with patients receiving methimazole alone, had a lower heart rate and improvement in fatigability, shortness of breath, and physical functioning after four weeks of therapy [3].

Propranolol in high doses (above 160 mg/day) also slowly decreases serum triiodothyronine (T3) concentrations by as much as 30 percent [4], via inhibition of the 5'-monodeiodinase that converts thyroxine (T4) to T3. Propranolol is highly lipid soluble, allowing it to become sufficiently concentrated in tissues to inhibit monodeiodinase activity. This effect of propranolol is slow, occurring over 7 to 10 days, and contributes little to the therapeutic effects of the drug. Atenolol, alprenolol, and metoprolol similarly cause minimal reductions in serum T3 concentrations, whereas sotalol and nadolol do not [5].

Despite this theoretical advantage of propranolol and related drugs, the small effect and slow onset severely limit their usefulness for reducing serum T3 concentrations. If deiodinase inhibition is considered important in a patient with severe hyperthyroidism (eg, thyroid storm or impending thyroid storm), it is best achieved by the addition of an iodinated radiocontrast agent to the medical regimen (these agents are currently not available in the United States), or the use of propylthiouracil (PTU). (See "Iodinated radiocontrast agents in the treatment of hyperthyroidism" and "Thyroid storm".)

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Literature review current through: Nov 2017. | This topic last updated: Nov 24, 2017.
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