From the Guidelines
Propranolol does inhibit the peripheral conversion of T4 to T3, a more biologically active hormone, in addition to its beta-blocking effects. Propranolol is a non-selective beta-blocker that primarily works by blocking beta-adrenergic receptors in the heart and other tissues, reducing the effects of adrenaline and noradrenaline. While propranolol is sometimes used in the management of hyperthyroidism, its role in inhibiting the peripheral conversion of thyroid hormones is an important aspect of its therapeutic effect in this context, as noted in a 2022 study published in Hypertension 1. This is different from medications like propylthiouracil (PTU) or methimazole, which actually inhibit thyroid hormone synthesis. Propranolol is typically dosed at 10-40 mg three to four times daily when used for hyperthyroidism symptoms, with the dose adjusted based on heart rate response and symptom control. Some key points to consider when using propranolol in this context include:
- Its ability to reverse some of the reduced systemic vascular resistance associated with hormonal disease
- Its use in patients with thyrotoxicosis (thyroid storm) or symptomatic hyperthyroidism, thyroiditis, and Graves’ disease
- The importance of individualized treatment, as discussed in the 2022 study 1, to ensure optimal management of high blood pressure and other comorbidities.
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 inhibits the conversion of T4 to T3, as it may increase T4 and reverse T3, and decrease T3. 2
From the Research
Propranolol's Effect on Thyroid Hormone Conversion
- Propranolol has been shown to decrease the conversion of T4 to T3, a process known as 5'-deiodination, in a dose-dependent manner 3.
- This decrease in T4 to T3 conversion leads to a decrease in plasma T3 levels and an increase in plasma reverse T3 (rT3) levels 4, 3, 5, 6.
- The exact mechanism of propranolol's effect on thyroid hormone conversion is not fully understood, but it is thought to be related to an unidentified metabolite of propranolol rather than the drug itself or its major metabolite, 4-hydroxypropranolol 3.
- The D-isomer of propranolol, which has no beta-blocking action, has been shown to be responsible for the decrease in T4 to T3 conversion, rather than the L-isomer, which has beta-blocking action 7.
Clinical Implications
- The decrease in T4 to T3 conversion and subsequent decrease in plasma T3 levels may contribute to some of the metabolic responses to beta-blockers in hyperthyroid patients 3, 6.
- However, the clinical improvement in hyperthyroid patients treated with propranolol is thought to be primarily due to beta-adrenergic receptor blockade, rather than the effects on thyroid hormone conversion 4, 6.
- Individualized dosage of propranolol may be necessary to achieve optimal treatment of hyperthyroidism, as some patients may not respond to standard doses 6.