CausesBy Mayo Clinic staff
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Graves' disease is caused by a dysfunction in the body's disease-fighting immune system.
One normal immune system response is the production of antibodies designed to target a specific virus, bacterium or other foreign substance. In Graves' disease — for reasons that aren't well understood — the body produces an antibody to a particular protein on the surface of cells in the thyroid, a hormone-producing gland in the neck.
Normally, thyroid function is regulated by a hormone released by a tiny gland at the base of the brain (pituitary gland). The antibody associated with Graves' disease — thyrotropin receptor antibody (TRAb) — can essentially mimic the action of the regulatory pituitary hormone. Therefore, TRAb overrides normal regulation of the thyroid and results in overproduction of thyroid hormones (hyperthyroidism).
Result of hyperthyroidism
Thyroid hormones affect a number of body functions, including:
- Metabolism, the processing of nutrients to create energy for cells
- Heart and nervous system function
- Body temperature
- Muscle strength
- Menstrual cycle
Consequently, the impact of Graves' disease may be widespread and result in a decline in the overall quality of life.
Cause of Graves' ophthalmopathy
The exact cause of Graves' ophthalmopathy is also not well understood. However, it appears that the same antibody that can cause thyroid dysfunction may also have an "attraction" to tissues surrounding the eyes. The antibody activity triggers inflammation and other immune system events that result in the signs and symptoms of Graves' ophthalmopathy.
Graves' ophthalmopathy often appears at the same time as hyperthyroidism or several months later. But signs and symptoms of ophthalmopathy may appear years before or after the onset of hyperthyroidism. Graves' ophthalmopathy may also appear in the absence of hyperthyroidism.
- Graves' disease. U.S. Department of Health and Human Services. http://www.endocrine.niddk.nih.gov/pubs/graves/Graves.pdf. Accessed April 19, 2011.
- Brent GA. Clinical practice: Graves' disease. The New England Journal of Medicine. 2008;358(24):2594.
- Bahn RS. Graves' ophthalmopathy. The New England Journal of Medicine. 2010;362:726.
- Bartalena L, et al. Clinical practice: Graves' ophthalmopathy. The New England Journal of Medicine 2009;360:994.
- Davies T, et al. Thyrotoxicosis. In: Kronenberg HM, et al., eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa.: Saunders Elsevier; 2008. http://www.mdconsult.com/das/book/body/191205553-3/0/1555/0.html#. Accessed April 20, 2011.
- Thyroid disorders in pregnancy. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merckmanuals.com/professional/sec18/ch261/ch261q.html. Accessed April 19, 2011.
- Stan MN, et al. Risk factors for development or deterioration of Graves' ophthalmopathy. Thyroid. 2010;20:777.
- Ross DS. Radioiodine therapy for hyperthyroidism. The New England Journal of Medicine. 2011;364:542.
- Hyperthyroidism. The Merck Manuals: The Merck Manual for Healthcare Professionals. http://www.merckmanuals.com/professional/sec12/ch152/ch152e.html. Accessed April 19, 2011.