From the Guidelines
Propranolol does inhibit the peripheral conversion of T4 to T3, in addition to its beta-blocking effects, as noted in the context of treating thyrotoxicosis and hyperthyroidism. This is based on the most recent and highest quality study available, which discusses the use of beta-blockers in conditions characterized by an excess of thyroid hormones 1. The study highlights that beta-blockers, such as propranolol, may reverse some of the reduced systemic vascular resistance associated with hormonal diseases and inhibit the peripheral conversion of T4 to the more biologically active hormone, T3. Key points to consider when using propranolol in this context include:
- Its primary use is to manage symptoms like tachycardia, tremors, and anxiety by blocking beta-adrenergic receptors
- It does have an effect on the peripheral conversion of T4 to T3, which is beneficial in treating hyperthyroidism
- The typical dose of propranolol for hyperthyroid symptoms can range, but it is often used as adjunctive therapy alongside other medications that reduce thyroid hormone production or conversion. The American Association of Clinical Endocrinologists Medical Guidelines support the use of beta-blockers in conditions characterized by an excess of thyroid hormones, although they do not specifically recommend one beta-blocker over another 1.
From the FDA Drug Label
Thyrotoxicosis: Beta-adrenergic blockade may mask certain clinical signs of hyperthyroidism. Therefore, abrupt withdrawal of propranolol may be followed by an exacerbation of symptoms of hyperthyroidism, including thyroid storm. Propranolol may change thyroid-function tests, increasing T4 and reverse T3, and decreasing T3
Propranolol prevents the conversion of thyroxine (T4) to triiodothyronine (T3), as it may change thyroid-function tests, increasing T4 and reverse T3, and decreasing T3 2.
From the Research
Propranolol's Effect on Thyroxine Conversion
- Propranolol has been shown to inhibit the conversion of thyroxine (T4) to triiodothyronine (T3) in several studies 3, 4, 5, 6.
- This inhibition is thought to be due to a decrease in the production rate of T3 and a decrease in the metabolic clearance rate of reverse T3 (rT3) 6.
- The exact mechanism of this inhibition is not fully understood, but it is believed to be related to the inhibition of 5'-deiodination, an enzyme involved in the conversion of T4 to T3 3, 6.
Clinical Implications
- The inhibition of T4 to T3 conversion by propranolol can lead to a decrease in serum T3 levels and an increase in serum rT3 levels 3, 5, 6.
- This effect can be clinically significant, particularly in patients with hyperthyroidism or thyroid storm, where propranolol is often used to reduce symptoms 4, 5.
- However, the influence of beta-blockers on T4 conversion is thought to be of little importance for the clinical improvement in hyperthyroid patients, and rather it is a consequence of beta 1-adrenergic blockade interfering with the effect of T3 7.
Study Findings
- A study published in 1982 found that propranolol treatment lowered serum T3 concentration and elevated serum rT3 concentration in normal men 3.
- A study published in 2017 reported a case of propranolol-induced circulatory collapse in a patient with thyroid crisis and underlying thyrocardiac disease, highlighting the need for caution when using propranolol in these patients 4.
- A study published in 1979 found that propranolol alone decreased serum T3 and increased serum rT3 in hyperthyroid patients, and that this effect was maintained in patients receiving propranolol for more than 1 month 5.
- A study published in 1991 found that propranolol decreased plasma T3 and increased plasma rT3 in a dose-dependent manner, due to inhibition of the conversion of T4 into T3 and of rT3 into 3'-T2 6.
- A study published in 1980 found that propranolol caused a reduced heart rate, a decrease in serum T3, and an increase in serum rT3 in hyperthyroid patients, and that the plasma level of propranolol was significantly correlated with the decrease in T3 and the increase in rT3 7.