Graves’ disease: cause and risk factors
Since the antibodies are directed against the body’s own structures, Graves’ disease is one of the autoimmune diseases. It is also called Graves’ disease, Graves’ disease, immunogenic hyperthyroidism or immunothyroidism of the Graves’ type.
Graves’ disease preferentially affects women between the ages of 20 and 50. The disease also runs in families. This is due to certain genetic mutations that favor Graves’ disease.
Like Hashimoto’s thyroiditis, Graves’ disease may occur together with other autoimmune diseases such as Addison’s disease (hypofunction of the adrenal glands), type 1 diabetes or gluten intolerance (celiac disease, sprue).
Graves’ disease: symptoms
The three leading symptoms of Graves’ disease are:
- Enlargement of the thyroid gland (“goiter”, goiter)
- Protrusion of the eyeballs (exophthalmos)
- Palpitations (tachycardia)
In addition to the protruding eyeballs, other changes may occur in the eye area, such as swelling of the eyelids and conjunctivitis. Doctors speak of endocrine orbitopathy. Dry eyes with photophobia, increased tearing, pressure and/or foreign body sensation are also possible. In severe cases, visual deterioration and double vision may also occur.
Less frequently, Graves’ disease patients develop swelling in the lower legs (pretibial myxedema), hands and feet (acropachy).
Some of the above symptoms may also occur in other thyroid diseases. You can find out what these are on our overview page on thyroid diseases.
Graves’ disease: diagnosis
The blood test is important for the diagnosis: the doctor determines the pituitary hormone TSH (stimulates hormone production in the thyroid gland) and thyroid hormones T3 and T4.
In addition, the blood sample is tested for antibodies (autoantibodies) typical of Graves’ disease: TSH receptor antibody (TRAK, also TSH receptor autoantibodies) and thyroperoxidase antibody (TPO-Ak, anti-TPO).
Graves’ disease: Therapy
Patients with Graves’ disease initially receive so-called thyrostatic drugs, i.e. drugs to inhibit hormone production in the thyroid gland (such as thiamazole or carbimazole), for about a year. In the beginning, beta blockers are also given to relieve the symptoms of hyperthyroidism (such as palpitations). The drug of choice is propranolol, which also prevents T4 from being converted into the much more active T3.
In about half of the patients, the disease is cured after about one year of thyrostatic administration, so that no further medication is necessary.
If, on the other hand, hyperthyroidism still persists after 1 to 1.5 years of thyrostatic use or flares up again after an initial improvement (smoking increases the risk of relapse!), the thyroid function should be permanently switched off.
Before surgery, the thyroid function must be normalized with medication, because otherwise a thyrotoxic crisis (thyrotoxicosis) can occur. This life-threatening clinical picture can lead to, among other things, high fever, racing heart, vomiting and diarrhea, muscle weakness, restlessness, impaired consciousness and drowsiness, and even coma and circulatory failure, as well as a functional weakness of the adrenal glands.
Treatment for pregnant women
Treatment of eye symptoms
In Graves’ disease with endocrine orbitopathy, cortisone can be given. It helps against the protruding of the eyeballs and the severe swelling in the eye area. In mild to moderate cases, selenium is often given in addition. Dry eyes can be treated with moisturizing eye drops, ointments or gels.
In severe cases of endocrine orbitopathy, radiation or surgery is also possible.
Graves’ disease: prognosis
After one to one and a half years of treatment with thyrostatic drugs, Graves’ disease is cured in a good half of all patients. However, the disease can flare up again, usually within a year of the end of treatment. The thyroid function must then be switched off permanently.
