Graves’ disease is the name given to autoimmune thyroid disease. The thyroid gland is stimulated by auto-antibodies, which make it overactive, resulting in increased thyroid hormone production. Graves’ disease is named after the doctor who first described it, Robert Graves, and is the most common cause of hyperthyroidism.
The body's immune system reacts to the thyroid gland and produces special proteins (called antibodies) that attack the thyroid gland. This is called an autoimmune reaction. These antibodies then stimulate the thyroid gland causing increased production and release of thyroid hormones. The exact reason for why the autoimmune reaction is initiated is not fully understood but, in some people, it can be triggered by infection, stress or smoking. Most patients however have a family history of thyroid problems thus suggesting that there is a genetic link.
These are the same for any kind of thyroid overactivity, irrespective of the cause. Common symptoms and signs include:
There may also be related swelling of the thyroid gland in the neck causing difficulty in swallowing and breathing.
Graves’ disease can affect the eyes. They may become swollen and red, sometimes becoming more prominent and in severe cases, there may be double vision and squinting. This is called Graves’ ophthalmopathy or thyroid eye disease. See the article on thyoid eye disease for further information.
There may be specific skin changes affecting the front of the legs, where the skin looks red and swollen. This is called Graves’ dermopathy or pretibial myxedema.
If left untreated, Graves’ disease can lead to heart failure.
Just over 1% of people suffer from an overactive thyroid gland from any cause. Women are five times more likely to suffer from it than men.
Graves’ disease affects about 5 in 1,000 people. Like any autoimmune condition, Graves’ disease is more common in women than men.
Graves’ disease is not inherited. However, it has been seen to affect members of the same family. An identical twin is more likely to have Graves’ disease if the other twin is affected. Although there is a tendency for autoimmunity to be inherited, a mother cannot ‘pass on’ an overactive thyroid to her child.
The diagnosis happens in two parts:
Usually these tests are all done as an outpatient.
Symptoms of thyrotoxicosis (high levels of thyroid hormones) can be treated with beta-blockers (provided the patient can tolerate it). This is often the first type of treatment used. Although this can help to settle symptoms, it does not affect the autoimmune process itself or levels of thyroid hormones.
Anti-thyroid drugs, carbimazole or propylthouracil, are used to treat the actual overactivity of the thyroid gland. Carbimazole is the first type of drug chosen and propylthouracil is usually used during pregnancy and breastfeeding. The duration of treatment is variable depending on the individual patient, ranging between 6 months to 24 months.
Some centres use a treatment regime called ‘block and replacement’, which involves ‘blocking’ the action of the thyroid gland completely with carbimazole and then ‘replacing’ the required thyroxine level with thyroid tablets. Alternatively, a titration regime may be used, where enough of the drug is given to partly suppress the thyroid gland and keep the body’s natural thyroid hormone levels within a normal range.
Other kinds of treatment can be used once the acute thyrotoxicosis has settled. This could be in the form of surgery (to remove the gland) or radioiodine treatment (causes gradual destruction of the thyroid gland). There are pros and cons of both these methods and the specialist will discuss these with the patient.
Some patients do not need surgery or radioiodine treatment as the tablets can settle down the thyroid overactivity adequately and the thyroid gland can function normally after that.
Carbimazole can cause joint pain and an itchy rash. Most importantly, carbimazole (as well as propylthiouracil) can acutely reduce the white cell count in the body and thus reduce the body’s ability to fight infections. Should patients develop a fever, sore throat or become more unwell in any way they must contact their GP or be seen in the emergency department for a blood test to check the cell count. Although very rare, this complication can be fatal if the diagnosis is delayed.
Propylthouracil, if used for a long time, can cause inflammation of blood vessels called vasculitis. This can affect all the organs. In addition, propylthiouracil can affect the functioning of the liver in a very small group of patients.
There will be a chance of Graves’ disease returning after one episode but the likelihood will reduce with time. Smoking can worsen thyroid eye disease associated with this condition, so it is important to stop immediately.
Surgery, and in many cases radioiodine, will result in the thyroid becoming underactive, meaning that the patient will have to take thyroid hormone replacement (levothyroxine) for the rest of their life. The alternative to surgery or radioiodine is to take an anti-thyroid drug for a prolonged period of time (up to lifelong). The disadvantage of this approach is that patients can still have a flare of Graves’ disease.
Last reviewed: Mar 2018