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Effects of thyroid dysfunction on propranolol kinetics

J G Riddell, J D Neill, J G Kelly

    Clinical Pharmacology and Therapeutics
    |November 1, 1980
    PubMed
    Summary
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    Thyroid status affects propranolol pharmacokinetics. Hyperthyroidism increased propranolol clearance, while hypothyroidism prolonged its half-life, potentially requiring dosage adjustments for effective beta-adrenoceptor blockade.

    Area of Science:

    • Pharmacology
    • Endocrinology
    • Clinical Pharmacy

    Background:

    • Thyroid hormones significantly influence drug metabolism and disposition.
    • Propranolol, a beta-adrenergic receptor antagonist, is commonly used but its pharmacokinetics can be altered by thyroid dysfunction.

    Purpose of the Study:

    • To investigate the impact of hyperthyroidism and hypothyroidism on the pharmacokinetic parameters of propranolol.
    • To determine if thyroid status influences propranolol's elimination half-life, clearance, and volume of distribution.

    Main Methods:

    • A pharmacokinetic study involving six hyperthyroid and six hypothyroid patients.
    • Patients received single oral and intravenous doses of propranolol during both diseased and euthyroid states.
    • Key pharmacokinetic parameters including elimination half-life (t 1/2), oral clearance, systemic clearance, and apparent volume of distribution were measured.

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    Main Results:

    • In hyperthyroid patients, systemic clearance of propranolol was significantly higher compared to the euthyroid state.
    • Hypothyroidism prolonged the elimination half-life of oral propranolol compared to the euthyroid state.
    • No significant changes in oral propranolol half-life, oral clearance, intravenous half-life, or volume of distribution were observed when hyperthyroid patients became euthyroid.

    Conclusions:

    • Thyroid dysfunction alters propranolol pharmacokinetics, specifically affecting its clearance and elimination half-life.
    • Hyperthyroidism increases propranolol systemic clearance, suggesting a need for potentially higher doses to achieve adequate beta-adrenoceptor blockade.
    • Hypothyroidism prolongs propranolol's elimination half-life, indicating a potential for increased drug accumulation or effects.