Graves disease

Last updated: November 2, 2023

Summarytoggle arrow icon

Graves disease is the most common cause of hyperthyroidism and often affects women. It is an autoimmune condition that is associated with circulating TSH receptor autoantibodies leading to overstimulation of the thyroid gland with excess thyroid hormone production. The classic clinical triad of Graves disease involves a diffuse vascular goiter, ophthalmopathy, and pretibial myxedema, although not all features may be present in a patient. The clinical diagnosis of Graves disease is confirmed via assessment of TSH and T3/T4 levels as well as through detection of thyroid antibodies (TRAb, TPOAb, TgAb). In addition, a diffuse uptake of 123I may be seen on thyroid scintigraphy. Treatment includes beta blockers to quickly alleviate symptoms, antithyroid drugs to achieve euthyroid status, and radioiodine ablation or, less commonly, near-total thyroidectomy for definitive control of the disease.

Epidemiologytoggle arrow icon

  • Most common cause of hyperthyroidism in the United States
  • Incidence: ∼ 30 cases per 100,000 people per year
  • Sex: > (8:1)
  • Typical age range: 20–40 years


Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon


Pathophysiologytoggle arrow icon


Clinical featurestoggle arrow icon


Diagnosticstoggle arrow icon

The diagnosis of Graves disease is often apparent on clinical examination and is confirmed through detection of specific thyroid antibodies.


Pathologytoggle arrow icon

  • Macroscopic
    • Diffuse, uniform gland enlargement
    • Cut surfaces show beefy red appearance
  • Microscopic: histological features of an overactive gland


Treatmenttoggle arrow icon


Special patient groupstoggle arrow icon

Graves disease in children

Graves disease in the elderly

Referencestoggle arrow icon

  1. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2015
  2. Yeung S-CJ. Graves Disease. Graves Disease. New York, NY: WebMD. Updated: July 16, 2016. Accessed: February 20, 2017.
  3. Laurberg P, Andersen SL. ENDOCRINOLOGY IN PREGNANCY: Pregnancy and the incidence, diagnosing and therapy of Graves’ disease. European Journal of Endocrinology. 2016; 175 (5): p.R219-R230.doi: 10.1530/eje-16-0410 . | Open in Read by QxMD
  4. Hemminki K, Li X, Sundquist J, Sundquist K. The epidemiology of Graves' disease: evidence of a genetic and an environmental contribution. J Autoimmun. 2009; 34 (3): p.J307-713.doi: 10.1016/j.jaut.2009.11.019 . | Open in Read by QxMD
  5. Paus R. Exploring the “thyroid–skin connection”: Concepts, questions, and clinical relevance. J Invest Dermatol. 2010; 130 (1): p.7-10.doi: 10.1038/jid.2009.359 . | Open in Read by QxMD
  6. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  7. Townsend CM Jr, Beauchamp RD, Evers BM, Mattox KL. Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice. Elsevier ; 2016
  8. Williams N, O'Connell PR. Bailey & Love's Short Practice of Surgery . CRC Press ; 2008
  9. Graves disease. Updated: January 1, 2017. Accessed: January 1, 2017.
  10. Ross DS. Graves' hyperthyroidism in nonpregnant adults: Overview of treatment. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: September 22, 2016. Accessed: February 20, 2017.

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