Increase in thyroid hormones as a result of the thyroid gland becoming overactive. It is more common in women over the age of 20.
The cause is autoimmune, meaning that the person's immune system produces antibodies that attack the body's own tissues. The antibodies damage the cells and make them less able to function. In this disease, the antibodies cause the thyroid gland to produce and secrete too much thyroid hormone into the bloodstream.
The most common symptoms are goitre (swelling of the thyroid), bulging eyes (exophthalmos) and localised swelling (myxoedema). It can be characterised by tremors, tachycardia, nervousness, insomnia, excessive sweating and weight loss.
It is diagnosed clinically by interview and physical examination. A blood test is also required to confirm an excess of thyroid hormones. An imaging test may be needed to complete the examination of the gland.
Basic treatment consists of reducing thyroid activity through medication, radioactive iodine and/or surgery. Beta-blockers speed up the improvement of symptoms.
- Terry F Davies. Pathogenesis and clinical features of Graves' ophthalmopathy (orbitopathy). UpToDate. Dec 18, 2015.
- Terry F Davies. Pathogenesis of Graves' disease. UpToDate. Nov 19, 2015.
- Davies TF, Ando T, Lin RY, et al. Thyrotropin receptor-associated diseases: from adenomata to Graves disease. J Clin Invest 2005; 115:1972.
- Menconi F, Hasham A, Tomer Y. Environmental triggers of thyroiditis: hepatitis C and interferon-α. J Endocrinol Invest 2011; 34:78.
- Stan MN, Bahn RS. Risk factors for development or deterioration of Graves' ophthalmopathy. Thyroid 2010; 20:777.
- Jameson JL, Mandel SJ, Weetman AP. Trastornos de la glándula tiroides. Harrison. Principios de Medicina Interna. Volumen 2. 19º Edición: 2293-2298.
