Hyperthyroidism vs. thyrotoxicosis, new developments in the therapy of Gravesʼ disease

This article aims to review the clinical differentiation of hyperthyroidism from other forms of thyrotoxicosis as well as new therapeutic strategies for Graves’ disease. The term thyrotoxicosis describes any state characterized by excess thyroid hormones. On the contrary, hyperthyroidism per se only refers to disorders caused by an excessive secretion of hormones by the thyroid itself, even though the terms are clinically often used interchangeably. Differentiation of hyperthyroidism from other forms of thyrotoxicosis is of clinical importance, since they usually require different therapeutic measures. In most cases, this can be achieved by measuring TSH-receptor antibodies or radionuclide imaging. In certain circumstances, however, these studies may yield inconclusive results or cannot be performed at all (e.g., thyroid scintigraphy in pregnant patients). Thus, calculation of the fT3/fT4 ratio and measurement of blood flow in the thyroid arteries can be helpful to differentiate different etiologies of thyrotoxicosis in certain patient groups. The therapeutic strategy in Graves’ disease has remained substantially unchanged for the last 70 years, consisting of antithyroid drug treatment or definitive therapy, that is, radioactive iodine therapy or thyroidectomy. Since these therapies are associated with adverse consequences like relapse of the disease or permanent hypothyroidism, new treatment alternatives are needed. Thus, therapies modulating B‑cell function are currently under investigation in Graves’ disease. Other therapeutic alternatives that aim to affect TSH-receptor signaling are also in development.