Graves’ disease is the second important autoimmune thyroid disease in addition to Hashimoto’s thyroiditis. In both cases, specific antibodies trigger autoimmune inflammatory processes. These lead in the case of Graves’ disease to an overactive thyroid (hyperthyroidism). In addition, Graves’ disease can affect the eyes, lower legs, hands and feet. Read all important information about Graves’ disease here.
Graves’ disease: cause
Graves’ disease prefers to meet women between the ages of 20 and 50 years. The disease is also referred to as Basedow’s disease, Graves ‘disease, immunogenic hyperthyroidism or Graves’ type immune thyroid disease.
In Graves’ disease, the body produces certain antibodies (antibodies) that increase thyroid hormone production – hyperthyroidism develops. A large proportion of patients additionally develop inflammatory disease of the eye sockets (endocrine orbitopathy). Moreover, Graves’ disease may also affect the connective tissue of lower legs, hands and feet.
Graves’ disease occurs frequently in the family. In such families, cases of Hashimoto’s thyroiditis are also often observed, which is why certain genetic changes are suspected as the cause of disease development. Whether and when the Basedow disease breaks out, however, can not be predicted. Sometimes the outbreak follows a viral infection or severe mental stress. In other cases, out of complete well-being, patients suffer from Graves’ disease.
Like Hashimoto’s thyroiditis, Graves’ disease often coexists with other autoimmune diseases such as Addison’s disease (adrenal adrenal gland), type 1 diabetes or gluten intolerance (celiac disease, native sprue).
Graves’ disease: symptoms
The three guiding symptoms of Graves’ disease are:
- Enlargement of the thyroid gland (“goiter”, goiter)
- Emergence of eyeballs (exophthalmos)
- Palpitations (tachycardia)
These three symptoms together are also called “Merseburger Trias”.
In addition to the protruding eyeballs, there may be further changes in the eye area such as eyelash swelling and conjunctivitis. Physicians then speak of endocrine orbitopathy. Even dry eyes with photophobia, increased tears, pressure and / or foreign body sensation are possible. In severe cases, vision deterioration and double vision may also occur.
Other symptoms of thyroid hyperfunction in Graves’ disease include weight loss, sleep disturbances, hypersensitivity, sweating, high blood pressure, hair loss, frequent bowel movements, menstrual cycle and female infertility, muscle weakness, inner restlessness, irritability, anxiety and lack of concentration.
Rarely, Graves’ disease patients develop swelling in the lower leg area (pratibial myxedema), hands and feet (acropachy).
Graves’ disease: diagnosis
The doctor first conducts a detailed conversation with the patient to collect the medical history (anamnesis). This is followed by a physical examination with blood pressure measurement and examination of the eyes, lower legs and hands.
Also important for the diagnosis is a blood test: the blood levels of the thyroid hormones T3 and T4 as well as the pituitary hormone TSH (stimulates the hormone production in the thyroid gland) are measured. In addition, the blood sample is examined for antibodies typical for Graves’ disease.
As part of the Graves disease diagnosis, the thyroid gland is also examined ultrasonically.
Graves’ disease: therapy
Patients with Graves’ disease initially receive so-called antithyroid drugs for about one year, ie drugs that inhibit hormone production in the thyroid gland (such as thiamazole or carbimazole). In the beginning, beta-blockers are added to alleviate hyperthyroidism symptoms (such as palpitations).
In about half of the patients, the disease heals after about one year of thyreostatic use, so that no further medication is necessary.
However, if thyroid hyperfunction persists after 1 to 1,5 years of antithyroid therapy, or flares again after an initial recovery, the thyroid gland function should be switched off permanently. This is done either by radioiodine therapy or by surgical removal of the thyroid (the whole organ or parts of it). Patients must then take the missing thyroid hormone in tablet form for life. However, this is associated with fewer complications and side effects than would be the case with a long-term or permanent use of antithyroid drugs.
Before surgery, thyroid function must be normalized by medication, otherwise thyrotoxic crisis (thyrotoxicosis) can occur. Among other things, this life-threatening clinical picture can lead to high fever, palpitations, vomiting and diarrhea, muscle weakness, restlessness, drowsiness of consciousness and dizziness, as well as coma and circulatory failure, as well as dysfunction of the adrenal glands.
Treatment of ocular symptoms
In Graves’ disease with endocrine orbitopathy, cortisone may be given. It helps against the appearance of the eyeballs and the strong puffiness in the eye area. Selenium is often given in mild to moderate cases. Dry eyes can be treated with moisturizing eye drops, ointments or gels.
Graves’ disease: prognosis
In about 50 percent of patients, Graves’ disease heals on its own. Nevertheless, timely treatment with antithyroid drugs is necessary. Even after successful therapy, the disease can flare up again. The thyroid function must then be turned off definitively.
A dreaded complication of hyperthyroidism due to Graves’ disease or another disease is the thyrotoxic crisis. The mortality here is 20 to 30 percent.