Abstract
Graves’ disease (GD) is the most common cause of hyperthyroidism in the United States. GD occurs more often in women and has a population prevalence of 1–2 %. A genetic determinant to the susceptibility to GD is suspected because of familial clustering of the disease, a high sibling recurrence risk, and the familial occurrence of thyroid autoantibodies. GD is a systemic autoimmune thyroid disorder characterized by the infiltration of immune effector cells and thyroid-antigen-specific T cells into the thyroid and thyroid stimulating hormone receptor (TSHR) expressing tissues such as orbit and skin, with the production of autoantibodies to well-defined thyroidal antigens. Stimulatory autoantibodies in GD activate the TSHR leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with a diffusely enlarged, heterogeneous, hypervascular (increased Doppler flow on neck ultrasound) thyroid gland, associated orbitopathy, biochemically confirmed thyrotoxicosis, positive TSHR autoantibodies, and often a family history of autoimmune disorders. The hyperthyroidism of GD is treated by reducing thyroid hormone synthesis with the use of antithyroid drugs, or by reducing the amount of thyroid tissue with radioiodine treatment or near-total thyroidectomy.
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Kahaly, G.J. (2015). Diagnosis and Endocrine Management of Graves’ Disease. In: Douglas, R., McCoy, A., Gupta, S. (eds) Thyroid Eye Disease. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-1746-4_1
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