Graves' disease is an autoimmune disorder where the thyroid is diffusely enlarged and overactive, producing an excessive amount of thyroid hormones. This metabolic imbalance is known as hyperthyroidism, and the enlargement of the thyroid gland caused by the Graves' disease is called goiter. The changes are caused by autoantibodies to the TSH-receptor (TSHR-Ab) that activate that TSH-receptor, thereby stimulating thyroid hormone synthesis and secretion and thyroid growth (causing a diffuse goiter). The resulting state of hyperthyroidism causes a dramatic constellation of neuropsychological and physical signs and symptoms, and has profound effects on the heart and cadiovascular system. Graves’ disease is the most common cause of severe hyperthyroidism and is accompanied by more clinical signs and symptoms and laboratory abnormalities as compared with milder forms of hyperthyroidism.
Graves' disease affects up to 2% of the female population, sometimes appears after childbirth, and has a female:male incidence of 5:1 to 10:1. It has a powerful hereditary component and frequently presents itself during early adolescence. About 20-25% of people with Graves' disease will also suffer from Graves' ophthalmopathy (a protrusion of one or both eyes), caused by inflammation of the eye muscles by attacking autoantibodies.
Diagnosis is usually made on the basis of symptoms, although thyroid hormone tests may be useful, particularly to monitor treatment. However, Graves’ thyrotoxicosis is a disease which has gradually affected the life of the patients, usually for many months, but sometimes years, prior to the diagnosis. Patients suffer from a wide range of symptoms and have major impairment in most areas of HRQL (health-related quality of life) in the untreated phase. For many patients, quality of life also stays substantially impaired for a long time during and after treatment.