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Thyroid and parathyroid glands in humans

The thyroid gland ( Latin: Glandula thyreoidea or Glandula thyroidea ) is a hormonal gland in vertebrates , which in mammals is located on the neck below the larynx in front of the windpipe . In humans it has the shape of a butterfly. It consists of two lobes connected by a narrow bridge called an isthmus.

The main function of the thyroid is to store iodine and to produce the iodine-containing thyroid hormones triiodothyronine and thyroxine as well as the peptide hormone calcitonin . The iodine-containing thyroid hormones are formed by the follicular epithelial cells of the thyroid gland (thyrocytes) and play an important role in the energy metabolism , for the growth of individual cells and for the entire organism. Calcitonin is made by the parafollicular or C cells of the thyroid gland. It inhibits bone breakdown by incorporating calcium and phosphate into the bones and by inhibiting the osteoclasts which, when activated, lead to a reduction in bone substance.

The thyroid gland is the starting point for numerous diseases which, among other things, lead to disorders of the hormone metabolism and can cause an under- or over- functioning of the thyroid gland ( hypothyroidism or hyperthyroidism ). In areas of iodine deficiency , a compensatory goiter (goiter) or lump can arise. In Germany, the German Society for Endocrinology (DGE) deals with this organ and its diseases with its “Thyroid” section.

Anatomy and development

Human thyroid

Thyroid topography

The human thyroid gland consists of two lobes ( lobus dexter and lobus sinister ) that are connected by a narrow strip (isthmus) . This isthmus is located immediately in front of the windpipe (trachea) below the larynx (at the level of the 2nd to 3rd cartilage brace). The two lobes of the thyroid lie on the side surfaces of the windpipe, encompass it and are attached to it by connective tissue . The very variable shape of the thyroid can best be compared with an "H", whereby the lower parts of the longitudinal bars - the lower horns - are short and wide, while the upper parts - the upper horns - are long and narrow and drift slightly apart.

The thyroid is the largest human endocrine gland . On average, the thyroid gland weighs 18–60 g in adults and 2–3 g in newborns. The normal values ​​for the height and thickness of the thyroid lobes are 3–4 and 1–2 cm, respectively. The width is given as 7–11 cm. In terms of volume, a total thyroid volume of up to 18 ml in women and up to 25 ml in men is still considered normal. The weight and size of the thyroid gland also vary intra-individually; for example, small cycle-dependent volume changes are possible in women.

The blood supply is provided by the superior thyroid artery from the external carotid artery and by the inferior thyroid artery from the thyrocervical trunk of the subclavian artery (referred to in animals as the cranial and caudal thyroid arteries ). About five percent of people have an additional, unpaired thyroid artery . This arises directly from the aortic arch and reaches the thyroid at the isthmus or at its lower pole. In addition, small arterial branches from the front and side surfaces of the windpipe supply the thyroid tissue with blood. All small branches of the arteries of the thyroid gland form a network within the organ. After the arterial blood has passed the thyroid cells, it gathers in small veins that form a network beneath the thyroid capsule. The venous outflow is mainly via a venous plexus ( plexus thyroideus impar ), which flows into the vena brachiocephalica via the vena thyroidea inferior .

The tissue fluid ( lymph ) located between the cells of the thyroid gland drains into lymph nodes via lymph vessels . This lymphatic drainage of the thyroid gland is ensured by a well-developed system of lymph vessels. There are many branches between the individual lymph vessels and lymph nodes. The lymph vessels essentially flow into the regional lymph nodes, which are found mainly along the large neck veins ( jugular veins ). The lymph from one side lobe can also reach the downstream lymph nodes of the other thyroid lobe via lymph nodes in front of the windpipe. This is important for thyroid surgery because cancer cells can also spread via lymphatic vessels.

The thyroid is supplied ( innervated ) by nerve fibers of the autonomic nervous system . The sympathetic fibers come from the ganglion cervicale superius (ganglion cervicale craniale) , the parasympathetic ones come from the Nervi laryngei of the Nervus vagus .

Phylogenetic evolution

The formation and development of the thyroid gland in the course of the tribal history of living things is called phylogenetic development. In this, the thyroid can be traced back to the endostyle present in the basal chordates ; in other invertebrates there are no homologous structures. The Endostyle forms at the acrania , the tunicates and the Ammocoetes larvae of the lamprey a the bottom of the gills intestine preferred Flimmerrinne that hypobranchial, with a glandular epithelium. The cells of the endostyle accumulate iodine from the environment and incorporate this into molecules of the hormone thyroxine. The glandular epithelium produces a web of mucus which is placed over the gill slits and with which food particles filtered in the gill intestine are captured. This is collected in the epibranchial groove and releases the nutrients it contains to the overlying dorsal vessel.

In the further development within the vertebrates, the gill intestine loses its function in terms of food intake and is largely used for breathing, while the food is taken in via the mouth opening, which is now reinforced with jaws, and digested in the intestine . The thyroid tissue is located in the basal vertebrates ( cartilage and bony fish ) ventrally in the area of ​​the gills , while in the terrestrial vertebrates it is located in front of the trachea in the area of ​​the larynx. In all vertebrates, it is embryonic in the ventral gill epithelium. In all vertebrates, the thyroid system is a collection of gland cells surrounded by connective tissue.

In cartilaginous fish, the thyroid gland is a disc-shaped gland in the area of ​​the lower jaw. In many bony fish the compact gland is dissolved and forms several cell clusters in the area of ​​the branching of the ventral aorta, with several small accessory thyroid glands often lying far away from the main thyroid gland. In them, the two paired parathyroid glands (glandulae parathyreoideae) appear for the first time, which develop together with the thymus and the ultimobranchial body in the epithelium of the gill intestine in the area of ​​the fourth and fifth gill pockets . In mammals, the latter are stored in the thyroid gland as calcitonin-producing cells (C cells).

In all terrestrial vertebrates, the thyroid gland forms compact organs again. In amphibians they are formed as unpaired thyroid glands on the side of the larynx, whereby the parathyroid glands are absent in neotene amphibians, which have gills throughout their life. In amphibians, the thyroid hormones are involved in ontogenetic development and control the metamorphosis from larva to adult.

In reptiles , the thyroid is unpaired and is due to the splitting of the large neck vessels. In birds , both thyroid glands are located as small nodules on the windpipe in front of the breast entrance, about at the level of the collarbone and thus much further back ( caudal ) than in other vertebrates.

As in humans, the thyroid gland of most mammals consists of two side lobes, which are connected to one another via a narrow constriction (isthmus). This isthmus can consist of glandular tissue ( isthmus glandularis , e.g. in predators ) or just connective tissue ( isthmus fibrosus , e.g. in horses , sheep and goats ), and in some species it can be completely absent. A remnant of the thyroid duct often occurs in humans in the form of a pyramidal lobe . More rarely, median cervical cysts or fistulas may persist as the remainder of this duct in humans. The shield shape is only typical of humans , monkeys and pigs .

Ontogenetic development

Opening of the thyroglossal duct (thyroid diverticulum) at the level of the second branchial arch

In biology, ontogenetic development is the origin and development of a single individual. It describes all processes that lead from the fertilized egg cell to the adult individual. The structure of the thyroid gland can be demonstrated in the human embryo around the 24th day of development. It develops in the floor of the mouth as a sprouting from the digestive system ("head intestine"). Like a tube formed by a single layer of cells, the sprout, known as the ductus thyreoglossus ("thyroid-tongue duct") , grows downwards. In the lower part of the duct there are two more bulges from which the two thyroid lobes later emerge. The duct itself usually closes up so that the definitive thyroid gland is no longer connected to the floor of the mouth. As a rule, only a triangular depression remains on the base of the tongue, which is known as the foramen caecum . The thyroid gland assumes its final position in front of the windpipe in the 7th week of embryo.

In around 30% of people, a remnant of the thyroid duct remains as the third, unpaired thyroid lobe, even after embryonic development, as the pyramidal lobe . Less often cysts can develop from smaller remaining parts of the duct (for example the Bochdalek cyst ). If such cysts connect to the outer surface of the body or the floor of the mouth, they are called fistulas . Disrupted and hormonally active islands of thyroid tissue can also be preserved along the thyroid's path of development.

In the mammals , cells from the fifth pharynx from which the C cells develop (see below) also migrate into the thyroid system. C-cell precursor cells come from the neural crest . In the other vertebrate classes , the C cells still form their own organ, the ultimobranchial body . In many mammal species, the inner epithelial body ( glandula parathyroidea interna , one of the so-called parathyroid glands) is enclosed in the thyroid gland, in humans it is located as the glandula parathyroidea inferior at the lower pole of the thyroid gland.


Histological image of the human thyroid:
follicle with colloid (1), follicular epithelial cells (2), C-cell (arrow)

The most striking structural feature of the thyroid tissue are microscopic vesicles, which are called thyroid follicles (from the Latin folliculus "vesicles"). The follicles are formed by the cells that produce the thyroid hormones T 3 and T 4 (follicular epithelial cells, also called thyrocytes). The cells are arranged in a single layer ( epithelium ) and enclose the interior (the lumen ) of the follicle. In cross-section, the follicles are usually round to oval in shape. The follicle diameter can also vary widely within an individual gland (between 50 and 200 µm). Within the follicle lumen there is a preliminary stage of the thyroid hormones, the protein thyroglobulin. It forms a cloudy, glassy, ​​gelatinous to viscous mass called a colloid . It is estimated that the hormones contained within the colloid are sufficient to supply the organism of healthy people for about three months. The shape of the follicles and the amount of colloid depend on the age and functional status of the tissue. An activated thyroid is characterized by tall epithelial cells and smaller follicles, while large amounts of colloid and flat epithelium indicate an inactive stage of the cells. This inactive state is also known as the resting or stacking form of the gland.

The thyroid gland is surrounded by a connective tissue capsule (capsula fibrosa) from which connective tissue sheaths (septa) extend and divide the organ into individual lobules. Each lobule consists of several follicles. In mammals, the parafollicular C cells lie between the epithelial cells of the follicles and their basement membrane . These do not extend to the lumen of the follicle. Reticular fibers and a dense capillary network ( blood and lymph capillaries) are formed around the follicles .

The size of the follicles in the histological specimen depends not only on the functional state, but also on the plane of the section through the follicle. The coloring of the colloid is strongly dependent on its water content. Due to shrinkage in the course of the histological work-up, the colloid does not seem to completely fill the follicle, but this is an artifact . The C cells can only be precisely identified by immunohistochemistry .


Structural formula of triiodothyronine
Structural formula of thyroxine
The thyrotropic control loop (simplified representation)

The hormones triiodothyronine (T 3 ) and thyroxine (tetraiodothyronine, T 4 ) produced by the thyroid gland are of great importance for the proper development of the newborn organism. In adults, too, the thyroid hormones influence the metabolism and functional status of almost all organs. Calcitonin , which is also formed in the thyroid, plays a subordinate role in the organism's calcium metabolism .

Outside of mammals, the thyroid hormones T 3 and T 4 fulfill a number of other important functions. They induce for example with frogs the metamorphosis from tadpole to frog and in birds the Mauser .

The thyroid hormones are part of the so-called thyrotropic control circuit . The function of the thyroid gland is regulated by the hypothalamus and the pituitary gland (anterior pituitary gland). The hormone TSH (thyroid stimulating hormone) is formed in the pituitary gland and released into the bloodstream. When it reaches the thyroid cells, it promotes their growth and the release of T 3 and T 4 . T 3 and T 4 themselves in turn inhibit the release of TSH. This mechanism, known as negative feedback, means that the metabolic parameters in the healthy organism are kept constant.

Effects of thyroid hormones

Thyroid hormones affect the heart and circulation. They can lead to an increase in heart rate and blood pressure, as well as to dilation of blood vessels . They affect the sugar, fat and connective tissue metabolism by increasing their turnover. They increase the activity of the sweat and sebum glands of the skin and the activity of the intestinal motor skills. In the nervous system, they lead to increased excitability of the cells. Overall, the effect of the thyroid hormones increases the energy consumption and the basal metabolic rate of the organism. The consequence of this is an increase in body temperature .

Thyroid hormones regulate the growth of the newborn and the development of cells, especially in the central nervous system ( brain and spinal cord ). Thyroid hormones act on growth through other hormones such as the growth hormone somatotropin and IGF-1 . In the nervous system, thyroid hormones promote the shedding (myelination) of nerve cells. If there is a deficiency of thyroid hormones in the first months of life, changes in the structure and function of the glial cells of the nervous system can be detected. Furthermore, thyroid hormones influence the development (differentiation) of nerve cells and many other cells of the organism by controlling the expression of genes at the molecular level . If a thyroid hormone deficiency in the newborn is not recognized and treated, severe neurological disorders (movement disorders and disorders of cognitive development) develop.

T 3 and T 4 mediate their effects via receptors in the target cells . T 3 is here many times more effective than T 4 . The thyroid cells mainly produce T 4 , which is converted ( deiodized ) to T 3 in the target cells . The receptors for the thyroid hormones are mainly located in the cell nuclei and the mitochondria of the cells. These are proteins that are bound to the DNA of the genes they regulate and thus inhibit gene expression. By binding the thyroid hormones, the receptors are activated, so that the gene expression of a whole range of proteins is facilitated or made possible in the first place.

The parafollicular C cells produce calcitonin. It lowers the calcium level in the blood and thus serves as an antagonist of the parathyroid hormone (PTH) as a regulator of the extracellular calcium concentration.

Formation of thyroid hormones

Iodine transport and synthesis in the thyroid cells of the thyroid gland. 1st step: Na + / I - - Symporter actively absorbs iodide from the blood plasma into the thyrocytes ("iodination"). Step 2: Thyroid peroxidase (TPO) catalyzes the oxidation of iodide to iodine . Subsequent binding to the thyroglobulin on the apical cell membrane . The two thyroglobulin-bound hormone precursors monoiodothyrosine and diiodothyrosine are released into the follicle lumen through exocytosis.

The hormones triiodothyronine (T 3 ) and thyroxine / tetraiodothyronine (T 4 ) produced by the thyroid are iodine compounds . They are formed by the follicular epithelial cells, which are dependent on a sufficient supply of iodine through food. The follicular epithelial cells first produce the protein thyroglobulin and release it into the follicular cavity. With the blood vessels, iodine reaches the follicular epithelial cells (thyrocytes) in the form of its ion iodide. With the help of a specialized protein - the so-called sodium iodide cotransporter (NIS) - the cells absorb the iodide basolaterally. The iodide gets from the blood through an ion channel (pendrin) apically into the follicle lumen ( iodination ).

The enzymes thyrooxidase (an NADPH / H + oxidase for the synthesis of hydrogen peroxide; an integral membrane protein) and thyroid peroxidase are necessary for the next steps in hormone synthesis . This is located in the membrane of the thyroid cell adjacent to the follicle cavity. This hydrogen peroxide then oxidizes iodide from the oxidation number −1 to elemental iodine with an oxidation number ± 0 ( iodization ). In the next step, the iodine atoms are bound to the tyrosine components of the thyroglobulin ( iodination , coupling ). Tyrosine is an amino acid and part of thyroglobulin. The iodinated thyroglobulin is taken up again by the follicular epithelial cell ( storage ) and broken down by enzymes. The iodinated tyrosine compounds (now called thyroxine and triiodothyronine) are also released. They can freely pass through the cell membrane and reach their target cells ( hormone incretion ) via the blood vessel system , where they develop their biological effects.

Investigation methods

Ultrasound examination of the thyroid gland - here a large thyroid nodule

The thyroid gland in humans can be by scanning (palpation) of the neck to be examined. In dogs , a palpable thyroid is already considered enlarged. A pronounced goiter is visible in humans. In principle, any doctor should be able to carry out an exploratory examination of the thyroid, since thyroid diseases are very common in humans and there are points of contact with almost all branches of medicine. Endocrinologists and nuclear medicine specialists usually have particular experience in this area .

In imaging diagnostics , ultrasound is mainly used and scintigraphy is used for further clarification in the event of lumps and functional disorders, and computer tomography and magnetic resonance tomography are also used for special issues .

A fine needle puncture of the thyroid gland is used to obtain samples for cytology , a biopsy for samples for histological examination .

The free T 3 and T 4 levels as well as the TSH and thyroglobulin levels can be determined in the laboratory . A determination of thyroid autoantibodies ( TRAK , Tg-AK, TPO-AK ) can also be carried out.


Both the causes and the sequelae of diseases of the thyroid gland, which are also known as thyroid disorders, are diverse. Tumor-like diseases ( goiter (goiter), thyroid autonomy ), inflammation , benign and malignant neoplasms ( benign and malignant neoplasms ) and disorders of organ development can be differentiated according to the frequency . All thyroid diseases can lead to disorders of the hormone metabolism. These functional disorders are known as overactive thyroid ( hyperthyroidism ) or underactive thyroid ( hypothyroidism ), depending on the effect of the thyroid hormones on the organism .


Enlarged thyroid with a visible and palpable lump in front of the windpipe
The situs during thyroid surgery; the enlarged thyroid lobe was raised.
The situs in the further course; the enlarged thyroid lobe is dissected out, the ligatures for hemostasis visible .

As goiter (goiter) any enlargement of the thyroid is known about their normal volume addition. Such enlargements can be objectively determined with the help of a sonographic examination of the thyroid gland. In principle, any of the thyroid diseases can be associated with an increase in volume. By far the most common cause of goiter is with around 90% the diet-related iodine deficiency (also known as bland goiter ). The symptom of goiter was already known in ancient times.

Iodine-deficient goiter
Since sufficient thyroid hormones are usually still synthesized in iodine-deficient goiter, there is no dysfunction of the thyroid in the sense of under or overfunction. This is why iodine-deficient
goiter is also known as euthyroid goiter . Iodine deficiency goiter mainly affects women (ratio of affected women to men: 7: 1). In areas where the incidence of goiter exceeds 10%, it is also known as endemic goiter . With regard to the disease mechanism, it is known that the iodine deficiency leads to an increased release of so-called growth factors by the thyrocytes. These proteins lead to an increased rate of division of the thyrocytes, as a result of which the thyroid gland increases in volume. If this hyperplasia affects the entire thyroid evenly at the beginning of the process (diffuse goiter) , it can later lead to a nodular remodeling of individual areas of the thyroid (nodular goiter) . The most important measure to prevent iodine deficiency goiter is the general use of iodized table salt. Since in iodine-deficient areas such as Austria, Switzerland and Germany the use of iodinated table salt alone in the household is not sufficient, industrially produced ready-made foods must also contain iodinated table salt in order to ensure a sufficient supply of iodine through the diet. While iodine prophylaxis for the population is regulated by law in Switzerland, Austria and the USA, in Germany only voluntary iodine prophylaxis is permitted.

Thyroid autonomy

A thyroid autonomy is when the thyroid cells are in their growth and their function is no longer subject to the regulation by the pituitary gland. Increased growth leads to the formation of single or multiple nodes ( unifocal or multifocal autonomy), rarely also to a disseminated autonomy, in which there is diffuse growth. The autonomic nodes can produce increased amounts of thyroid hormone, which often leads to an overactive thyroid. Thyroid autonomy occurs more frequently in iodine-deficient regions than in countries with an adequate iodine supply. Their frequency increases with age: it is mainly found in people over the age of 40.


Inflammation of the thyroid is known as thyroiditis . (Acute) purulent inflammations that develop within a short time are rare. They are caused by bacteria or fungi that reach the thyroid gland through blood vessels ( hematogenous ) . A weakening of the immune system due to chemotherapy for cancer diseases or an infection with HIV can be beneficial.

Chronic Hashimoto's thyroiditis is common: it affects around 3% of the population and more women than men (around a 10: 1 ratio). This leads to the destruction of the thyroid tissue mediated by the immune system. It is the most common cause of adult hypothyroidism in non-iodine deficiency areas worldwide.

The Graves' disease is an autoimmune disease of the thyroid gland, with the formation of stimulating antibodies associated to thyroid cells. In addition to hyperfunction with the corresponding symptoms, the consequence is often an enlargement of the thyroid gland. The disease affects about 1–2% of the population, with women five times more likely to be affected than men. The immune process that underlies Graves 'disease can also lead to symptoms in other organs ( extrathyroidal manifestation of Graves' disease). So-called endocrine orbitopathy occurs in around 60% of patients , which is characterized by an increase in the volume of the connective tissue behind the eye. This can push the eyeballs forward ( exophthalmos ). Less common (in less than 3% of patients) is a manifestation in the skin in front of the shin (pretibial myxedema ) , in which there is a non-compressible swelling of the skin.

In the rare subacute thyroiditis ( Thyreoiditis de Quervain ) (which develops within a few days to weeks ), an immune-mediated destruction of thyroid tissue usually occurs following a viral infection. There is often a painful swelling of the thyroid gland. The inflammation usually subsides spontaneously after a few weeks or months.

Riedel's thyroiditis (also known as “iron-hard goiter”), which is associated with a pronounced scarring of the thyroid gland, is very rare . The inflammation spreads from the surrounding tissue to the thyroid organ.

The inflammation of the thyroid that can be traced back to autoimmune processes is summarized under the term autoimmune thyroid disease .

Thyroid cysts

Cysts are fluid-filled cavities that are often asymptomatic and incidental. Depending on the development (see above), cysts from thyroid tissue can appear as median cervical cysts .

Thyroid cysts can occur in the context of iodine deficiency goiter, which is common in Germany, but also in benign and malignant tumors or systemic diseases and after injuries. Therapy depends on the cause of the cyst and the symptoms it is causing. It ranges from clinical observation to drug treatment or sclerotherapy with alcohol to surgical removal of large cysts with symptoms or suspected cancer.

As a rule, cysts can be visualized and assessed very well on ultrasound . A diagnostic fine needle puncture can also be performed under ultrasound control.

Thyroid cancer

Most malignant thyroid tumors are adenocarcinomas . The malignant neoplasms of the thyroid gland (malignant neoplasms) usually originate from the thyrocytes or from the calcitonin- producing C cells. Thyroid cancer ( sarcoma ) originating in connective tissue is very rare . Radiation exposure is the only proven cause of thyroid cancer. According to pathological criteria, thyroid cancer is divided into the following subgroups:

Follicular carcinoma
In this carcinoma , the structure of the tissue largely resembles the structure of a mature or developing thyroid. The cancer cells start from the thyrocytes and form settlements (hematogenous metastasis) in the lungs, skeleton and brain , mainly via the bloodstream . Follicular carcinoma accounts for 20–50% of all thyroid carcinomas. It often affects women in their 4th and 5th decades of life.

Papillary carcinoma
These carcinomas also originate from the thyrocytes and form finger-like (papillary) structures. They are the most common malignant neoplasms of the thyroid gland, accounting for 50–80% of all thyroid carcinomas. They metastasize mainly via the lymph vessels (lymphogenic metastasis) into the lymph nodes of the neck. These can then increase in size and can be felt. Papillary carcinomas often affect women in their 3rd to 4th grade. Decade of life. Radiation exposure (for example, in the context of therapeutic radiation to the head and neck region or the Chernobyl reactor disaster ), Hashimoto's thyroiditis and various genetic syndromes ( FAP syndrome and Cowden syndrome ) are considered to be favorable factors for its development .

Anaplastic carcinoma
In its fine structure, this carcinoma no longer shows any similarities with the original thyroid tissue and is therefore also referred to as undifferentiated carcinoma. It grows very aggressively into the surrounding tissue and metastasizes both lymphogenically and hematogenously. This type accounts for around 5–10% of thyroid carcinomas. It rarely develops before the age of 60; a gender preference does not show it.

Medullary carcinoma
The medullary carcinoma originates from the calcitonin-producing cells of the thyroid gland. It is a neuroendocrine carcinoma that can produce other hormones (such as somatostatin , serotonin and vasoactive intestinal peptide ) in addition to calcitonin . It is responsible for about 5% of all thyroid cancers. The disease can occur sporadically in individual individuals or in the context of genetic syndromes ( MEN syndrome ). This carcinoma metastasizes both lymphogenically and hematogenously and occurs with the same frequency overall in women and men.

Organ disorders

Dystopic goiter on the base of the tongue

The complete absence of the thyroid gland ( aplasia of the thyroid or athyreosis ) is very rare in newborns. The cause is usually genetically determined, wherein an autosomal - recessive mode of inheritance is present. An embryonic developmental disorder in which the migration of the thyroid gland from the floor of the mouth to its definitive position in front of the windpipe does not take place or does not take place completely is known as dystopia . Here the thyroid gland in the base of the tongue can grow into a goiter. Aplasias and dystopias are the most common causes of an underactive thyroid in the newborn ( congenital hypothyroidism ) .


Over and underactive thyroid is an increased or decreased effect of thyroid hormones on the metabolism and the organs of the body. Since receptors for thyroid hormones are present everywhere in the organism, symptoms in almost all organ systems can occur as a result of functional disorders of the thyroid gland. Often there are disorders that affect the cardiovascular system, the nervous system and the psyche, the gastrointestinal tract and general metabolism, the skin, the muscular and skeletal system and sexual functions. For example, being overactive can cause the heart to beat faster ( tachycardia ), involuntary weight loss, nervousness and tremors. Symptoms of being underactive can include a slow heartbeat ( bradycardia ), weight gain, constipation, and a loss of libido . An underactive function can trigger depression . In pregnant women, cretinism can be caused in the child .

The most common causes of hyperthyroidism (hyperfunction) are Graves' disease , thyroid autonomy and an increased supply of thyroid hormones from outside in the form of hormone preparations.

The most common causes of hypothyroidism (underactive) are Hashimoto's thyroiditis and measures (surgery, radioiodine therapy , medication) that were carried out as part of the treatment of thyroid disease.

A distinction is made between subclinical (latent) and manifest hyper- and hypothyroidism. In the case of a manifest dysfunction, the concentration of free thyroid hormones (fT3 and fT4) is increased or decreased beyond the normal range. In contrast, in the case of a subclinical dysfunction, the concentration of the free hormones is still in the normal range, while the concentration of the thyroid-stimulating hormone TSH is decreased or increased beyond the normal range.

Hyperthyroidism is the most common hormonal disorder in domestic cats over ten years old ( feline hyperthyroidism ). Thyroid autonomy is almost always the cause.

Medical historical aspects

The understanding of the function of the thyroid gland developed slowly. Until the second half of the 19th century, it was regarded as the "secondary gland of the respiratory organs ", the function of which was unclear.

The Dublin doctor Robert Graves described in his work "Palpitation of the heart with enlargement of the thyroid gland" in 1835 as the first to describe the symptom constellation of the disease later named after him in English-speaking countries (Graves' disease) : palpitations, goiter and exophthalmus. Graves assumed that the cause of these symptoms was heart disease. Independently of this, Carl Adolf von Basedow described the triad of symptoms of goiter, exophthalmos and tachycardia (also known as the Merseburg triad ) in his publication "Exophthalmus due to hypertrophy of the cell tissue in the eye socket" in Merseburg in 1840 . For therapy, he recommended the intake of mineral water containing iodide . In German-speaking countries, the term Basedow's disease prevailed. The determination of Graves' disease as a disease of the thyroid was not made until 1886 by the Leipzig neurologist Paul Julius Möbius .

The Bern surgeon and professor Theodor Kocher , who performed the first strumectomy in 1876 , received the Nobel Prize in 1909 for research into the thyroid gland . In contrast to Kocher, who preferred the complete removal of the thyroid gland, in 1885 Johann von Mikulicz-Radecki recommended leaving some thyroid tissue and the posterior thyroid capsule in place.

George R. Murray carried out the first successful therapy for myxedema with thyroid extracts in 1891. In 1896, Eugen Baumann isolated an insoluble, non- protein substance in which almost all of the iodine present in the thyroid was found - the so-called iodothyrin (or thyreoiodine) - and characterized it as the active component of the thyroid. 1899 was Adolph Oswald the thyroglobulin .

Robert Hutchison presented the knowledge of his time in his work on the physiology of the thyroid gland in 1898. The iodine content of the colloid of the follicle was estimated and only the iodine-containing components were shown as active. Experiments at that time had shown that the intravenous administration of the colloid had no effect exercised on blood pressure or heart activity. However, a drop in blood pressure was observed after injection of thyroid extracts. Animal experiments have shown that the blood did not clump after injection of the colloid in the vessels, that keeping it warm after surgical removal of the thyroid gland did not delay the occurrence or change the course of acute symptoms, although no toxins in the bile or CNS could be detected, but oral administration of Thyroid tissue decreased the mortality rate. In addition, it was found in the experiments that neither the surgical removal of testes or ovaries, nor the oral administration of the parathyroid gland had a curative effect on the myxedema . Iodothyrin was used for experimental purposes in the late 19th and early 20th centuries. From the opposing effects of different thyroid extracts on the circulatory system, a dispute that was called polemical at the time developed around the turn of the century. In 1909, John H. King was able to establish that iodothyrin had an independent, retarding effect on the carbohydrate metabolism that was superior to the extract of the entire thyroid gland . In 1911, Harry E. Alderson described the opposing effects of hypo- and hyperthyroidism on the skin and treatment options. He described extracts of the whole thyroid gland, iodine and substances containing iodine, arsenic, salicylates , phosphorus, alcohol, pilocarpine , tea, coffee, meat, sexual activity, uterine ailments, pregnancy and great emotional excitement as effective in terms of thyroid stimulation. He described opioids , bromides , hypnotics in general , linden tree glycerophosphates , calcium, milk, a diet rich in cereals and sexual abstinence as effective in reducing thyroid function . Lewellys F. Barker described iodothyrin in 1913 as the hormone of the thyroid gland and counted it among the sympatheticotrophic substances of endocrine origin. He described the effects as an acceleration of the heart rate, a widening of the eyelid, the exophthalmos and an increased response of the pupil to adrenaline .

The discovery of the thyroid hormone thyroxine is attributed to Edward Calvin Kendall . He had crystallized an active component out of iodothyrin and named it thyroxin. To diagnose a thyroid disease in the blood, indirect parameters such as blood coagulation and differential blood count were used during this period . In 1922, Henry Stanley Plummer described a reduction in hyperthyroidism signs in patients with Graves' disease , the so-called "Plumming" , achieved using Lugol's solution . This iodine preparation enabled a far less risky resection of a hyperfunctional goiter than it was first performed in 1884 by Ludwig Rehn . Emil Abderhalden and Ernst Wertheimer showed in 1929 that muscle tissue absorbed a thyroxine solution to a far greater extent than liver tissue, but could not determine "what happens to the thyroxine absorbed by the tissues." As recently as 1930 it was suspected that thyroxine was formed in the organism it could be composed of two molecules of diiodotyrosine . In 1933, I. Abelin and A. Florin described that thyroid hormones greatly increase the basal metabolic rate, cause glycogen and fat depletion, and accelerate heart and respiratory rates. The artificial production of thyroxine was first carried out in 1927 by Charles Robert Harington in London.

In 1965, Beverley EP Murphy applied for his patent for the direct measurement of thyroxine in body fluids, which was accepted by the patent authority on December 3, 1968. Up to this point in time, only indirect thyroid function tests, such as measuring the absolute iodine content or the protein-bound iodine in the blood, had been carried out.


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  • Ludwig Weissbecker: Diseases of the thyroid. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 1033-1051.

Web links

Commons : Thyroid  - Collection of pictures, videos and audio files
Wiktionary: Thyroid gland  - explanations of meanings, word origins, synonyms, translations
Wikibooks: Thyroid  - Learning and Teaching Materials

Individual evidence

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  22. Fine needle aspiration
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  43. Patent specification of the United States Patent Office 3.414.383 (pdf)
This article was added to the list of excellent articles on July 8, 2008 in this version .