The thyroid gland is the largest hormone-producing gland in humans, sits on the neck below the larynx and has the shape of a butterfly. It produces the thyroid hormones T3 (triiodothyronine) and T4 (thyroxine), which regulate many functions. These messenger substances are very important for the body's energy metabolism and influence, among other things, physical and mental performance, cardiovascular system, body temperature, digestion and also the mental state. In addition, the thyroid gland produces the hormone calcitonin, which regulates the calcium content of the blood. In children, the thyroid gland also controls physical growth as well as brain development. An excess or deficiency of thyroid hormones can therefore have strong effects.
In the case of pathological thyroid hypofunction (hypothyroidism), too few hormones are produced in the thyroid gland and the body is accordingly undersupplied. This slows down many metabolic processes.
Affected people feel tired, less active and complain of weak concentration and memory. Other symptoms of hypofunction are increased sensitivity to cold, slower pulse and low blood pressure, menstrual disorders in women, constipation, dull hair, and hair loss as well as brittle fingernails. The skin is cool and dry. Hypothyroidism does not necessarily have to be accompanied by all these symptoms. In the case of pronounced deficiency, the skin acquires a typical doughy texture and non-inflammable swelling occurs (myxedema).
Strictly speaking, hypothyroidism is not an independent thyroid disease, but a symptom of various other diseases. However, by far the most common cause of thyroid hypofunction is chronic immune thyroiditis Hashimoto (Hashimoto's disease), an inflammatory autoimmune disease of the thyroid gland. The hypofunction usually develops gradually over years, often unnoticed. Additionally, there are other, but more rare, diseases that can lead to hypothyroidism. More frequently, therapeutic interventions lead to hypofunction if there is no or insufficient thyroid tissue for the production of thyroid hormones after thyroid gland surgery or radioiodine therapy.
The level of free thyroid hormones (fT4, fT3) and the TSH hormone (thyroid-stimulating hormone) in the blood is important for assessing thyroid function. TSH is produced in the pituitary gland and regulates the production of thyroid hormones. If there are very few thyroid hormones in the body in a hypoactive state, more TSH is produced to stimulate the thyroid gland. In subclinical hypothyroidism (latent hypothyroidism), only the hormone TSH is initially elevated and the free thyroid hormones are normal. The pituitary gland tries to stimulate the affected thyroid gland, which initially succeeds. In the case of manifest hypofunction (manifest hypothyroidism), the free hormones in the blood are also reduced.
In order to find out the exact cause of the hypofunction, however, further examinations must be carried out (determination of additional blood parameters, clinical examination, ultrasound, scintigraphy, etc.).
In most cases, the treatment of hypothyroidism involves lifelong substitution of thyroid hormones with medication. Thyroid function should be monitored regularly, as the need for thyroid hormones may change with age. In practice, unfortunately, patients with a hypofunction are often not well treated.
In the case of hyperthyroidism, excess hormones are produced in the thyroid gland and the body is accordingly oversupplied. The metabolism is working at full speed.
Hyperfunction of the thyroid gland is associated with a variety of symptoms, although not all symptoms necessarily occur. These include weight loss despite unchanged or even increased appetite, nervousness, restlessness, poor concentration, tremors, insomnia, hair loss, muscle pain and weakness, increased sweating, heat intolerance, and warm, moist skin. In women, menstrual disorders can indicate hyperthyroidism. Thyroid hormones have a stimulating effect on the cardiovascular system, which leads to a fast pulse and elevated blood pressure. In the long run, this condition is associated with an increased risk of cardiac arrhythmia and stroke.
Similar to hypothyroidism, hyperthyroidism is not an independent thyroid disease, but a symptom of various other diseases. In younger people between the ages of 20 and 40, the most common cause is an autoimmune disease called Graves' disease. Certain antibodies directed against the thyroid gland (autoantibodies) stimulate the thyroid cells to produce more thyroid hormones. Women suffer from this type of immune hyperthyroidism five times more than men. The thyroid gland is then mostly enlarged. Many patients also suffer from eye problems, ranging from dry eyes to double vision. In some cases, the eyes also protrude visibly. In older people, the cause of hyperfunction is usually , which produce thyroid hormones independently (autonomously) from the regulatory mechanism of the pituitary gland and thyroid gland (autonomous adenoma).
Bei einer Überfunktion ist der Spiegel an Schilddrüsenhormone im Blut (fT3, fT4) im Blut erhöht. Der Körper versucht gegenzusteuern, iIn the case of hyperfunction, the level of thyroid hormones in the blood (fT3, fT4) is elevated. The body tries to counteract this by reducing the release of TSH. In subclinical hyperthyroidism (latent hyperthyroidism), the thyroid hormones are still in the normal range and only the TSH is reduced. In manifest hyperthyroidism, the free thyroid hormones in the blood are also increased.
In order to find out the exact cause of the hyperfunction, however, further examinations must be carried out (determination of additional blood parameters, clinical examination, ultrasound, scintigraphy, etc.). This is the only way to ensure targeted treatment of the underlying disease.
The excessive production of thyroid hormones can be reduced with so-called thyroid inhibitors (thyrostatic drugs). Common thyroid inhibitors are carbimazole, thiamazole, and propylthiouracil. In about 50 % of Graves' disease patients, spontaneous healing of the disease can be achieved. If drug treatment is not successful, the possibilities of surgery or radioiodine therapy should be discussed. In the case of autonomy of the thyroid gland as a result of a hormone-producing thyroid nodule (autonomous adenoma), self-healing by medication is not to be expected. This usually serves as preparation for the causal treatment. The options here are also surgery, radioiodine therapy but also a minimally invasive treatment of the thyroid nodule by means of thermal ablation. The affected thyroid tissue is immediately destroyed by heat and the thyroid function returns to normal. Radioiodine therapy or surgery is intended to reduce the amount of active thyroid tissue and thus prevent the body from being flooded with thyroid hormones. In a few cases, however, extensive surgery or radioiodine therapy can lead to thyroid hypofunction (hypothyroidism), which in turn must be treated with medication. This is practically impossible with a treatment with thermal ablation since the healthy thyroid tissue is spared.