Graves’ disease

Terry F. Davies*, Stig Andersen, Rauf Latif, Yuji Nagayama, Giuseppe Barbesino, Maria Brito, Anja K. Eckstein, Alex Stagnaro-Green, George J. Kahaly

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

69 Citations (Scopus)

Abstract

Graves’ disease (GD) is an autoimmune disease that primarily affects the thyroid gland. It is the most common cause of hyperthyroidism and occurs at all ages but especially in women of reproductive age. Graves’ hyperthyroidism is caused by autoantibodies to the thyroid-stimulating hormone receptor (TSHR) that act as agonists and induce excessive thyroid hormone secretion, releasing the thyroid gland from pituitary control. TSHR autoantibodies also underlie Graves’ orbitopathy (GO) and pretibial myxoedema. Additionally, the pathophysiology of GO (and likely pretibial myxoedema) involves the synergism of insulin-like growth factor 1 receptor (IGF1R) with TSHR autoantibodies, causing retro-orbital tissue expansion and inflammation. Although the aetiology of GD remains unknown, evidence indicates a strong genetic component combined with random potential environmental insults in an immunologically susceptible individual. The treatment of GD has not changed substantially for many years and remains a choice between antithyroid drugs, radioiodine or surgery. However, antithyroid drug use can cause drug-induced embryopathy in pregnancy, radioiodine therapy can exacerbate GO and surgery can result in hypoparathyroidism or laryngeal nerve damage. Therefore, future studies should focus on improved drug management, and a number of important advances are on the horizon.

Original languageEnglish
Article number52
JournalNature Reviews. Disease Primers
Volume6
Issue number1
ISSN2056-676X
DOIs
Publication statusPublished - 2 Jul 2020

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