Graves' disease (Basedow-Graves): causes, symptoms, diagnosis and treatment

By Cristiano Antonino On Jul 8, 2023

Graves’ disease, also known as, Basedow-Graves’ disease, Basedow-Graves’ disease or diffuse toxic goiter, is an autoimmune disease affecting the thyroid gland characterised by one or more manifestations such as: hyperthyroidism, increased thyroid volume (goiter), sometimes ocular pathology (ophthalmopathy) and, in rare cases, skin pathology (dermopathy)

This is a more complex condition than common hyperthyroidism and should not, under any circumstances, be confused with it.

Find out everything you need to know about this disease below.

What is Graves’ disease

Graves’ disease is classified as an autoimmune disease, i.e. a disease in which the immune system attacks one or more physiological constituents of the body.

In the course of this disease, the body’s defence system abnormally produces autoantibodies called IST (thyroid-stimulating immunoglobulins), which are directed towards the receptor of the thyroid hormone, known as TSH (thyroid-stimulating hormone), present on thyroid cells.

These antibodies induce the thyroid gland to uncontrolled overproduction of thyroid hormones causing, over time, an enlargement of the thyroid gland and developing a form of hyperthyroidism characterised in many cases by ocular disorders manifesting as swelling, inflammation and protrusion of the eyeball (exophthalmos).

Graves’ disease occurs in about 0.5% of the world’s population and accounts for more than 50% of all cases of hyperthyroidism.

Specifically, in the United States, cases of hyperthyroidism related to Graves’ disease range from about 50% to 80% of cases (source: The New England Journal of Medicine).

Although it can affect anyone, it reportedly occurs more frequently in women than men and is generally seen in 40-60 year olds although it can also affect children and the elderly.

What is the thyroid gland?

The thyroid gland is a butterfly-shaped endocrine gland located at the front of the base of the neck.

Its function is to control certain important functions of the body through the production of two thyroid hormones: thyroxine (T4) and triiodothyronine (T3), which are secreted into the bloodstream and transported to every tissue in the body.

These hormones help regulate metabolism and other important functions such as breathing, heartbeat, growth, development of the central nervous system and body temperature.

The proper functioning of the thyroid gland is managed, in turn, by the pituitary gland, an endocrine gland that controls the body’s activity through the secretion of numerous hormones.

This gland produces the thyroid-stimulating hormone TSH, which stimulates the thyroid gland to produce the hormones T3 and T4.

In hyperthyroidism, the thyroid gland has an ‘excessive’ function in that it produces more hormones than the body needs.

The increased thyroid function, and the resulting excess of thyroid hormones in the blood, leads to a situation of accelerated metabolism that manifests itself with a wide range of symptoms.

Causes of the disease

As explained above, Graves’ disease is caused by a malfunction of the immune system which, in addition to producing antibodies to defend the body against viruses, bacteria and other foreign substances, for reasons that are still unclear tends to produce autoantibodies, i.e. antibodies directed against the body’s own structures.

Although it is unknown in many respects, the origin of Graves’ disease is assumed to be an alteration of the immune system caused by hereditary and genetic factors.

Although anyone can develop the disease, a number of factors have been found to increase the risk of developing the disease.

These include:

Family members suffering from Graves’ disease (genetic predisposition);
Gender, the female sex seems to be more likely to develop the disease;
Age, generally the disease develops in individuals aged 40-60 years;
Presence of other autoimmune diseases such as rheumatoid arthritis or type 1 diabetes;
Emotional and physical stress, which can trigger the onset of the disease in people genetically predisposed to it;
Pregnancy or childbirth can trigger the disease in genetically predisposed women;
Smoking, which can affect the immune system and increase the risk of the onset of Graves’ disease. Smokers with the disease are also more likely to develop Graves’ ophthalmopathy.

What are the symptoms?

Graves’ disease can manifest itself with many symptoms and signs that, however, tend to develop slowly.

In the early stages, in fact, the disease may be almost completely asymptomatic and then progressively worsen.

The manifestations of the disease vary significantly from person to person.

Generally, the first disorders that appear in the patient are psychological such as:

Anxiety states;
Difficulty falling asleep (insomnia);
Excessive emotionality;
Irritability;
Depression;
Tremors;
Mental fatigue.

Other symptoms that may develop as a direct or indirect effect of hyperthyroidism are:

Hyperactivity;
Excessive hair loss;
Excessive sweating and heat intolerance;
Unexplained weight loss despite increased appetite;
Diarrhoea or frequent defecation;
Tachycardia, arrhythmia or palpitations;
In women, irregularity of the menstrual cycle up to amenorrhoea;
Decreased libido and fertility;
Enlargement of the thyroid gland (goiter);
Thickening and redness of the skin on the backs of the feet and shins (Graves’ dermopathy);
Fragility of the nails with a tendency to fissure (onycholysis)
In children, delays in growth, development and puberty.

Complications due to Basedow-Graves disease include exophthalmos or Graves’ ophthalmopathy, a condition that causes the eyes to bulge outwards and the eyelids to swell.

In addition to irritation and dryness of the eyes, the condition can lead to visual impairment or other more serious complications such as damage to the cornea or optic nerve, resulting in loss of vision.

Furthermore, if not properly treated, prolonged exposure to excessive amounts of thyroid hormones can lead to the development of osteoporosis.

Finally, if left unchecked, the disease can cause a sudden increase in thyroid hormones, triggering a ‘thyroid storm’ that can prove fatal.

How is the diagnosis made?

The doctor to refer to for the diagnosis of Graves’ disease is the endocrinologist, who will subject the patient to a thorough clinical test looking for the symptoms of the disease and the risk factors listed above.

Subsequently, it will be of crucial importance to measure the levels of TSH (thyroid-stimulating hormone), T3 and T4 (thyroid hormones) in the blood.

Typically, patients with Graves’ disease have lower than normal TSH values and higher levels of T3 and T4

The doctor will also check for the presence of TSI and TRAb antibodies in the blood.

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If the result is positive, the diagnosis is confirmed without the need for further tests.

A negative result, on the other hand, could indicate that the cause of hyperthyroidism is not Graves’ disease, although in some cases it can happen that the result is negative even in individuals with the disease.

An ultrasound of the gland using echocolordoppler may be required to measure the size, observe the shape and vascularity of the thyroid gland.

This is a viable alternative to radioactive iodine uptake (RAIU), a test in which a capsule or beverage containing a small amount of radioactive iodine is administered to the patient and, subsequently, the amount of iodine absorbed by the thyroid gland is measured using an instrument called a scanner.

Although this test is particularly useful in cases where thyroid nodules are present, for obvious reasons it is contraindicated in pregnant women, for whom ultrasound scanning tends to be used.

Possible treatments for the disease

The main aims of treatment are to inhibit the excessive production of thyroid hormones and reduce and mitigate the severity of symptoms.

Three types of treatment strategies are possible:

Radioiodine therapy;
Administration of specific drugs;
Surgical treatment of the thyroid gland.
Radioiodine therapy consists of the oral administration of large doses of radioactive iodine (iodine-131) with the aim of damaging most of the thyroid gland, thus reducing hormone levels and, consequently, eliminating the symptoms of hyperthyroidism.

The therapy may also not be effective immediately and may last for weeks or months.

Those who undergo this type of therapy may develop reduced thyroid function (hypothyroidism) even after many years, which will have to be treated with synthetic thyroid hormones.

Anti-thyroid medication is useful in reducing thyroid hormone production and is prescribed for periods of time no longer than 1-2 years.

Some patients tend to have normal thyroid activity even after the drugs are discontinued, although, in most cases, further treatment is required.

Beta-blockers help reduce the symptoms caused by hyperthyroidism, keeping tachycardia, anxiety and restlessness under control.

However, they can be used for a limited time, pending more appropriate solutions.

With surgical treatment, most of the thyroid gland is removed, leading to the need to make up for the hormone deficiency through replacement therapy.

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