The medical term hyperthyroidism combines the Latin thyroid name ("glandula thyreoidea") with the Greek term for excessive ("hyper"). Since thyroid hormones play an important role in the body's metabolism, hyperthyroidism often results in increased metabolic activity. Hyperthyroidism is accompanied by symptoms such as restlessness, sleep disturbances, nervousness, increased emotional vulnerability and sweating.
At the beginning of hyperthyroidism, those affected usually feel more active and dynamic, which is why the onset of hyperthyroidism is often perceived as pleasant. However, if the hyperthyroidism tips over, the unpleasant symptoms often come to the fore.
With increasing duration of the disease, the cardiovascular system is also damaged and the risk of osteoporosis increases. Hyperthyroidism is easily treatable in most cases and generally has a good prognosis.
The term hyperthyroidism is not a disease in its own right and merely describes increased hormone production by the thyroid gland. There are various possible causes for this.
Graves' disease describes an autoimmune disease in which the thyroid gland is recognized by the immune system as foreign. About two-thirds of cases manifest after the age of 35, with women being affected about five times as often as men. Here, the immune system produces antibodies against proteins on the thyroid cell surface that have a thyroid-stimulating effect. In particular, the TSH receptor antibody (TRAK), plays an important role in Graves' disease.
TRAKs bind to the TSH receptor of thyroid cells, leading to increased hormone production as well as inflammation. Concomitantly, antibodies against thyroglobulin (Tg-AK) and against thyroid peroxidase (TPO-AK) are occasionally elevated in the blood. The exact cause of the disease is currently unknown. In addition to the classic symptoms of hyperthyroidism, there are sometimes eye complaints (endocrine orbitopathy) or swelling in the area of the lower legs (pretibial myxedema).
Hyperthyroidism can also be caused by thyroid autonomy, with the majority of cases manifesting at older ages. Normally, thyroid hormone production is regulated by a hormone (TSH) produced in the pituitary gland. A small amount of independent (autonomous) - that is, not following TSH - areas in the thyroid gland are normal. However, if these areas increase, hyperthyroidism may result.
The most common cause of thyroid autonomy is iodine deficiency thrombi. The thyroid gland requires the trace element iodine to produce thyroid hormones. A deficiency of iodine leads to increased growth in the thyroid gland as well as nodule formation.
In geographic areas where iodine deficiency is prevalent in the population, the proportion of autonomous areas in the thyroid gland may be large without thyroid dysfunction occurring. However, if normal or excessive intake of iodine (such as from X-ray contrast media) subsequently occurs, this can lead to increased hormone production and subsequently hyperthyroidism due to increased autonomous thyroid tissue.
In the course of thyroiditis, increased thyroid hormones can be released into the blood due to the destruction of thyroid cells. This is the case, for example, at the onset of chronic thyroiditis(Hashimoto's thyroiditis). It can also be caused by acute bacterial thyroiditis or painful subacute thyroiditis de Quervain.
Increased iodine intake can promote hyperthyroidism. In this case, iodine can either be ingested directly or supplied by iodine-containing drugs, such as amiodarone or x-ray contrast media.
Hyperthyroidism caused by an exogenous supply of thyroid hormones is also known as hyperthyroidism factitia. This form of hyperthyroidism can result from either unintentional over-supplementation of thyroid hormones or can be caused by intentional misuse of hormones. Because hyperthyroidism generally leads to weight loss, hyperthyroidism factitia often affects patients with anorexia nervosa.
Hyperthyroidism may also have other rare causes. These include such things as:
Thyroid cancer
TSH production in the context of a tumor (paraneoplastic)
Gestational hyperthyroidism: this often occurs temporarily in early pregnancy (8-20 weeks gestation) and usually does not require treatment.
Disruption of centrally regulating hormones (central hyperthyroidism): Central hyperthyroidism can be caused, for example, by a benign tumor of the pituitary gland (pituitary adenoma).
Hyperthyroidism can cause symptoms of varying severity, mainly triggered by the high hormone levels and the resulting increased metabolic activity.
There are some signs of illness that are typical of hyperthyroidism:
| Body region | Symptoms |
| Cardiovascular system | Palpitations (sinus tachycardia), cardiac arrhythmias |
| Psyche | Nervousness, irritability, inner restlessness, insomnia, emotional vulnerability |
| Vegetative | Heat intolerance, weight loss (despite ravenous appetite), sweating, increased stool frequency, muscle weakness, warm (moist) skin |
| Gynecological and others | Menstrual disorders, thin hair, hair loss, possibly osteoporosis. |
In addition, in the context of Graves' disease, the eyes are also affected in about half of the patients as part of an endocrine orbitopathy. Possible symptoms are increased sensitivity to light, seeing double images (diplopia) and conjunctivitis. A very prominent sign is the so-called exophthalmos. This is the eyes protruding from the eye socket.
Especially in older people, the symptoms can vary and also occur in a milder degree. For example, an accelerated pulse may be the only indication of the presence of hyperthyroidism in the elderly.
Sporadically, hyperthyroidism can precipitate a thyrotoxic crisis, in which there may be high fever, a severely accelerated pulse, circulatory failure, and impaired consciousness or even coma. A thyrotoxic crisis is a life-threatening situation and always requires immediate intensive medical treatment.
A detailed anamnesis interview to ascertain symptoms and the use of iodine-containing medications is important for the diagnosis of hyperthyroidism. If this discussion and a detailed physical examination reveal indications of hyperthyroidism, a blood sample is usually first taken to determine the thyroid hormone concentrations. An increase or decrease in the hormone levels (T3, T4, TSH), for example, can confirm a suspected case of hyperthyroidism. Free T3 (fT3) is almost always elevated in manifest hyperthyroidism. In contrast, free T4 (fT4) is elevated in only about 90% of affected individuals. If Graves' disease is suspected, the blood can also be tested for specific, indicative antibodies (TRAK, TPO-AK).
Examination procedures such as thyroid ultrasound (sonography) are suitable for visualizing the thyroid tissue and its structure as well as blood flow. Ultrasound of the neck area is also part of the basic diagnosis of thyroid disease. In addition, changes suspicious of malignancy can be assessed with the help of this examination. Thyroid nodules are often graded according to a standardized scoring system such as TIRADS (Thyroid Imaging Reporting And Data System).
Thyroid scintigraphy, on the other hand, is a nuclear medicine procedure used to determine thyroid metabolism. In this procedure, the patient is administered a contrast medium (usually technetium - Tc 99m) via the arm vein, which is absorbed primarily by the thyroid gland. The contrast medium accumulates in the thyroid gland like natural iodine. Subsequent imaging with a special gamma camera can show the accumulation of the radioactive contrast agent. In the case of autonomy, a strong accumulation of the tracer is generally seen in the autonomous thyroid areas.
In some cases, thyroid tissue sampling (biopsy) is also indicated to examine the nature of the thyroid tissue. For example, a suspicious thyroid nodule can be evaluated for malignancy by biopsy.
The treatment of hyperthyroidism generally depends on the patient's age and the form of hyperthyroidism. In most cases, the therapeutic approaches are well tolerated and are also satisfactory for many affected persons. A rough distinction is made between four possible therapeutic options for hyperthyroidism:
Symptomatic therapy of an increased heart rate with beta blockers
Medicinal thyrostatic therapy
Surgical therapy
Radioiodine therapy
Thyrostatic drugs interfere with hormone production and inhibit it at various levels. Any hyperthyroidism is treated with thyroid inhibitors until a normal thyroid hormone level is reached. Often, this can bring the hormone concentration into the normal range within a few weeks and normalize the metabolic state. Possible agents include thiamazole, propylthiouracil, carbimazole and sodium perchlorate. Since thyrostatic therapy can also lead to hypothyroidism, the treatment should be continuously monitored by the treating physician. Possible side effects of thyrostatic drugs include liver enzyme elevations or blood count changes (thrombocytopenia/leukocytopenia).
In a surgical procedure, either nodes of the thyroid gland, parts of the thyroid gland or the entire organ can be removed. Furthermore, surgical removal is indicated for thyroid nodules suspected of malignancy. Surgery to treat hyperthyroidism should not be performed before hormone concentrations have normalized with medication. A disadvantage of this form of treatment is often subsequent hypothyroidism, which must be treated with lifelong use of thyroid hormones. Surgery is recommended for the following thyroid disorders:
Large goiter
Displacement symptoms by the thyroid gland
Suspected malignancy (for example, cold nodules)
After a thyrotoxic crisis
In this therapy option, the affected person is administered radioactive iodine, which accumulates in the thyroid gland. The radioactive iodine destroys the hormone-producing cells of the thyroid gland. As a result, normalization of thyroid function is achieved. Since the effect of radioiodine therapy only sets in after weeks, thyrostatic drugs should generally be used before or after treatment. After radioiodine therapy, substitution of thyroid hormones (L-thyroxine) is generally required to prevent hypothyroidism. Radioiodine therapy is contraindicated in affected individuals of growing age, pregnant women and lactating women.
We speak of an incipient hyperthyroidism (latent hyperthyroidism) when only the TSH value in the blood is reduced and the values for free T3 and free T4 are still within the normal range. Patients with incipient hyperthyroidism should avoid iodine-containing drugs (e.g. amiodarone) and X-ray contrast media, as these can trigger manifest hyperthyroidism. If an examination with iodine-containing contrast medium is absolutely necessary, a two-week therapy with sodium perchlorate, possibly in combination with thiamazole, should precede the administration.
Hyperthyroidism can usually be treated well with the right therapy, which depends on the exact trigger of the disease. As a rule, symptoms subside some time after the start of therapy.
To prevent thyroid dysfunction in the context of thyroid autonomy, sufficient iodine intake is essential. In contrast, there are currently no effective preventive measures against hyperthyroidism caused by Graves' disease.
Iodine is a vital trace element that cannot be produced by the body itself. For adults, a daily intake of 150-200 micrograms of iodine is therefore recommended. Children and infants, on the other hand, usually require about 40-180 micrograms of iodine per day.
During pregnancy or breastfeeding, the iodine requirement is increased. Although table salt is fortified with iodine in Austria, Germany and Switzerland, an additional diet of iodine-rich foods such as fish should be consumed. Sea fish is the best known source of iodine. Iodine deficiency can cause non-specific symptoms such as fatigue and can also lead to the formation of an enlarged thyroid gland (goiter).
Iodine deficiency in pregnancy, in addition to thyroid dysfunction, can also lead to physical or neuronal developmental disorders in infancy and early childhood. Pregnant and breastfeeding women are therefore often recommended supplemental iodine therapy with iodine tablets, often in combination with other trace elements and vitamins, after discussion with their physician.
If Graves' disease is already known, strict nicotine abstinence should be observed. Smoking generally worsens the disease and also possible eye involvement (endocrine orbitopathy). In addition, affected individuals should not ingest iodine excessively.
Thyroid function should be determined prior to administration of an x-ray contrast agent. In some cases, worsening of hyperthyroidism and thyrotoxic crisis can be avoided by concomitant administration of thyroid inhibitors with the contrast agent. Patients who are treated with thyroid hormones should have their hormone levels checked regularly by their physician to avoid excessive hormone concentrations and thus hyperthyroidism.
Dr. med. univ. Moritz Wieser
Thomas Hofko
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