Hyperthyroidism is a common disorder whose manifestations can range from minimal symptoms to life-threatening thyroid storm. Several of the clinical features that accompany thyrotoxicosis, including palpitations, tremor, sweating, tachycardia, and increased pulse pressure, are identical to the manifestations of hyperadrenergic states. This association led to early studies of the ability of catecholamine depletion to modify the signs and symptoms of hyperthyroidism [1, 2]. Although use of medications such as guanethidine and reserpine were found to be efficacious, numerous side effects limited their use. Over the past two decades, beta-adrenergic blocking drugs, of which propranolol is the prototype, have been employed extensively in hyperthyroidism. Their ability to improve many of the manifestations of hyperthyroidism is well documented [3–6]; however, since the precise mechanism underlying the hyperadrenergic state of thyrotoxicosis is not fully understood, the mechanisms of action for this class of drugs in this clinical setting remain unclear. This review examines the systemic effects of excess thyroid hormone, including interaction with the adrenergic nervous system, the possible mechanisms by which beta-adrenergic blocking drugs exert their action, and the clinical use of betaadrenergic blocking agents in the hyperthyroid patient.
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Ventrella et al. (1994) studied this question.