Graves' disease affects the thyroid. It is an autoimmune disease, i.e. the gland's cells are gradually destroyed by specific antibodies in the body. As part of Graves' disease, autoantibodies bind to the TSH receptor, a hormone that stimulates the thyroid function, resulting in the increased secretion of thyroid hormones. Graves' disease is the leading cause for developing hyperthyroidism, and mainly affects young adult women.
The symptoms of Graves' disease are the following:
- the presence of a painless goiter in the lower part of the neck, accompanied by increased thyroid activity;
- the eyes give the impression of "popping out": this is called exophthalmos;
- the swelling of the eyelids is also present, called eyelid edema;
- in parallel, signs of hyperthyroidism are present, generally represented by an increased activity of many organs:
Complications are possible in the absence of care, such as cardiac arrhythmias.
The diagnosis is made after a physical examination, particularly upon palpation of the thyroid gland where the latter is found to be increased in volume without nodules. A blood test measuring TSH, the hormone that stimulates thyroid activity reflects hyperthyroidism, shows a reduction in this hormone in response to too many "real" thyroid hormones, T3 and T4 (TSH is tested, because its value is more revealing than T3 and T4). The blood will also be searched for specific antibodies of the disease, which will confirm the diagnosis. In addition, an ultrasound and thyroid scan will frequently be performed. An ophthalmologic assessment may be necessary in the case of significant ocular signs.
The various possibilities of treatment of Graves' disease are:
- the use of molecules partially blocking the formation of thyroid hormones: antithyroid drugs;
- the removal of the thyroid, called a thyroidectomy, after several months of drug treatment of hyperthyroidism;
- the use of radioactive iodine, which will destroy the overactive thyroid.