Graves’ disease is an autoimmune disease of the thyroid gland. It leads to an overactive thyroid gland, but in some cases it can also trigger tissue changes in the eyes, lower legs, hands or feet. What can be done against Graves’ disease?
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Brief overview: Graves’ disease
Definition: Graves’ disease is an autoimmune disease that causes an overactive thyroid gland.
Cause: The development of Graves’ disease has not been clearly clarified, but there seems to be a genetic component. Great stress or trauma can trigger the disease.
Symptoms: Graves’ disease is accompanied by the typical symptoms of an overactive thyroid gland – tachycardia, sweating, inner restlessness. The thyroid gland is often enlarged and the eyeballs protrude.
Diagnosis: With the help of an ultrasound and blood test, Graves’ disease can be diagnosed without a doubt.
Treatment: First, the thyroid function is blocked with medication. If that doesn’t work, the thyroid is surgically removed or overridden with radioiodine therapy.
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What is Graves’ disease?
Graves’ disease (also called Graves’ disease or autoimmune hyperthyroidism) is an autoimmune thyroid disease. The body produces autoantibodies that activate the thyroid gland, which in turn triggers the typical symptoms of an overactive thyroid gland, such as tachycardia, sweating, weight loss and diarrhea.
Graves’ disease is the most common cause of an overactive thyroid gland (hyperthyroidism). In Germany, around 0.5 to two percent of people are affected, women around five times more often than men.
Where does the name come from?
The disease got its name from the Latin word for illness (Morbus) and the doctor Carl von Basedow, who first described it in 1840 in German-speaking countries. The Irish doctor Robert Graves had just recognized it as an independent disease, which is why Graves’ disease is referred to as “Graves’ disease” in English-speaking countries.
Graves’ disease: causes and risk factors
In a healthy body, hormone production in the thyroid gland is controlled by the so-called TSH (thyroid-stimulating hormone). If Graves’ disease is present, antibodies are formed which are similar to TSH and stimulate the thyroid gland to produce more hormones. These autoantibodies are called TSH receptor antibodies (TRAK) and are detectable in the blood of people with Graves’ disease.
The causes of Graves’ disease are not exactly clear. Since there is a familial accumulation, there seems to be a genetic cause – but so far no single gene has been found that is responsible for the development of Graves’ disease.
Whether and when the disease breaks out seems to depend in some cases on external influences:
- a traumatic experience,
- great physical or mental stress
- or a previous viral infection
sometimes precede the disease. Smoking also increases the likelihood of developing Graves’ disease and is considered a risk factor for a severe course.
Typical symptoms of Graves’ disease
Stimulating the thyroid almost always leads to the typical signs of an overactive thyroid. The main symptoms – also known as the “Merseburg triad” – are an enlarged thyroid gland (goiter/goiter), an increased heart rate (tachycardia) and protruding eyeballs (exophthalmos).
The protruding eyeballs are caused by inflammation of the connective tissue in the eye (endocrine orbitopathy), which can also lead to photophobia, itchy and watery eyes, a foreign body sensation or blurred vision. In rare cases, tissue swelling (myxedema) also occurs in the lower legs, hands or feet.
Other symptoms typical of an overactive thyroid are:
Graves’ disease may occur together with other autoimmune diseases:
- White spot disease of the skin (vitiligo)
- Vitamin B12 deficiency (due to autoimmune damage to a certain type of cell in the stomach)
- Gluten intolerance (celiac disease)
- Adrenal hypofunction (Addison’s disease)
- Type 1 diabetes mellitus
In this case one speaks of a polyglandular autoimmune syndrome.
Hypothyroidism: The most common symptoms
This is how Graves’ disease is diagnosed
The diagnosis of Graves’ disease begins with a detailed discussion (anamnesis) in the doctor’s office. Here the specific complaints and any other autoimmune diseases that may be present are asked about. The thyroid gland is then palpated to detect enlargement and to check the sensitivity of the thyroid tissue to pain. The eyes are also examined for swelling and signs of inflammation.
An ultrasound examination (sonography) can be used to identify changes in the thyroid gland that are typical of Graves’ disease. A blood test is also done to determine the thyroid levels and to check for the presence of TSH receptor antibodies (TRAK).
Treatment: How is Graves’ disease treated?
The first step in the treatment of Graves’ disease is always medication: medication that blocks thyroid hormone production (antithyroid drugs) is given for 12 to 18 months. Until they take effect, beta blockers are often used in addition, which eliminate nervous symptoms such as sweating, tachycardia and trembling hands.
If the thyroid values have not improved after 12 to 18 months of drug therapy, another treatment that permanently switches off the thyroid function is recommended. Lifelong therapy with antithyroid drugs is not recommended, as this can lead to undesirable side effects.
To switch off the thyroid function, the thyroid gland is either removed in an operation or subjected to radioiodine therapy. Radioactive iodine is taken, which is stored in the thyroid tissue and destroys the thyroid cells. Since the thyroid no longer works after surgical removal or radioiodine therapy, the thyroid hormones must then be taken in tablet form for life.
Foods containing iodine: The best sources of iodine
Treatment of ocular symptoms in Graves’ disease
Some people with Graves’ disease have endocrine orbitopathy: the eyes become swollen, dry, sensitive to light, and watering. This can result in double vision or blurred vision.
Drops, ointments or gels are prescribed for dry eyes, and cortisone is used for protruding eyeballs or swelling. Smoking should also be stopped as it increases the risk of eye symptoms.
Course and prognosis in Graves’ disease
If Graves’ disease remains untreated, the risk of the typical long-term consequences of hyperthyroidism, including atrial fibrillation and osteoporosis, increases. There is also a risk of what is known as a “thyrotoxic crisis”: This severe imbalance in the thyroid hormone balance is associated with cardiac arrhythmia and circulatory failure and must be treated as an emergency in a hospital. Almost all patients with Graves’ disease show eye symptoms, but only in five percent of cases are they associated with vision loss.
After at least six months of therapy with antithyroid drugs, the disease has healed in more than half of those affected. However, the disease can flare up again (recurrence), usually within the first year after stopping the medication. Then radioiodine therapy or surgical removal of the thyroid gland is required. After that there is a lifelong hypothyroidism, the missing hormones are replaced in tablet form.
Prevention: How can Graves’ disease be prevented?
Since the development of Graves’ disease has not been clearly clarified, the disease cannot really be prevented. However, studies have shown that normal selenium levels can counteract the development of thyroid disorders. The German Society for Nutrition recommends 70 µg selenium daily for men and 60 µg for women.
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