Graves' disease

Most common cause of hyperthyroidism in countries with sufficient iodine intake.

Caused by TSH receptor antibodies.

Extrathyroidal manifestations include orbitopathy, pretibial myxoedema (thyroid dermopathy), or acropachy, which do not occur with other causes of hyperthyroidism.

Diagnostic tests are suppressed serum TSH, elevated levels of circulating thyroid hormones, detectable TSH receptor antibodies, and high thyroid uptake of radioactive iodine (or technetium 99).

Treatment options are antithyroid drugs, radioactive iodine therapy, and thyroid surgery.

Untreated hyperthyroidism, particularly in older people, may result in cardiac arrhythmias, high-output cardiac failure, bone mineral loss, and, rarely, thyroid storm.

Unusual complications include vision loss secondary to orbitopathy or elephantiasis secondary to dermopathy.

Graves' disease is an autoimmune thyroid condition associated with hyperthyroidism. Associated orbitopathy occurs in around 25% of cases and is usually mild;[1]Tanda ML, Piantanida E, Liparulo L, et al. Prevalence and natural history of Graves' orbitopathy in a large series of patients with newly diagnosed graves' hyperthyroidism seen at a single center. J Clin Endocrinol Metab. 2013 Apr;98(4):1443-9. https://academic.oup.com/jcem/article/98/4/1443/2536784 http://www.ncbi.nlm.nih.gov/pubmed/23408569?tool=bestpractice.com associated dermopathy and acropachy are rare, and almost always seen with orbitopathy.[2]Smith TJ, Hegedüs L. Graves' disease. N Engl J Med. 2016 Oct 20;375(16):1552-65. http://www.ncbi.nlm.nih.gov/pubmed/27797318?tool=bestpractice.com TSH (thyroid-stimulating hormone) receptor antibodies cause the hyperthyroid syndrome.[3]Prabhakar BS, Bahn RS, Smith TJ. Current perspective on the pathogenesis of Graves' disease and ophthalmopathy. Endocrine Rev. 2003 Dec;24(6):802-35. http://www.ncbi.nlm.nih.gov/pubmed/14671007?tool=bestpractice.com The aetiology of extrathyroidal manifestations is less clear.[4]Bahn RS. Pathogenesis of Graves ophthalmopathy: the role of orbital thyroid-stimulating hormone receptor expression. Curr Opin Endocrinol Diabetes. 2003 Oct;10(5):353-6.[5]Fatourechi V. Pretibial myxedema: pathophysiology and treatment options. Am J Clin Dermatol. 2005;6(5):295-309. http://www.ncbi.nlm.nih.gov/pubmed/16252929?tool=bestpractice.com [6]Eckstein AK, Johnson KT, Thanos M, et al. Current insights into the pathogenesis of Graves' orbitopathy. Horm Metab Res. 2009 Jun;41(6):456-64. http://www.ncbi.nlm.nih.gov/pubmed/19530272?tool=bestpractice.com Diagnosis is mostly clinical and is usually confirmed by laboratory evidence of thyroid dysfunction, most commonly hyperthyroidism.[2]Smith TJ, Hegedüs L. Graves' disease. N Engl J Med. 2016 Oct 20;375(16):1552-65. http://www.ncbi.nlm.nih.gov/pubmed/27797318?tool=bestpractice.com