Graves' Disease.

Graves’ disease was first recognized in the 19th century as a syndrome comprising an enlarged and overactive thyroid gland, an accelerated heart rate, and ocular abnormalities (Fig. 1). Critical for our current understanding of this disease was the discovery of its autoimmune basis, which results from complex interactions between genetic and environmental factors.1,2 Graves’ disease has adverse effects on quality of life,3 as a consequence of somatic4 and psychiatric5 symptoms and an inability to work,6 and is associated with an increased risk of death.7 Activating thyrotropin-receptor antibodies induce thyroid hormone overproduction. Many characteristic signs and symptoms of Graves’ disease result from elevated thyroid hormone levels. Debate persists concerning the diagnosis of hyperthyroidism and adequate clinical care of affected patients.8,9 Thyroid-associated ophthalmopathy (Fig. 1B), the most common and serious extrathyroidal manifestation, results from underlying autoimmunity, but insights into its pathogenesis and care remain elusive.