The thyroid gland, or simply the thyroid, is an endocrine gland in the neck, consisting of two lobes connected by an isthmus. It is found at the front of the neck, below the Adam's apple. The thyroid gland secretes three hormones, namely the two thyroid hormones (thyroxine/T4 and triiodothyronine/T3), and calcitonin. The thyroid hormones primarily influence the metabolic rate and protein synthesis, but they also have many other effects, including effects on development. Calcitonin plays a role in calcium homeostasis.[1]

Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) secreted from the anterior pituitary gland, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus.[2]

The thyroid may be affected by several diseases. Hyperthyroidism occurs when the gland produces excessive amounts of thyroid hormones, the most common cause being Graves' disease, an autoimmune disorder. In contrast, hypothyroidism is a state of insufficient thyroid hormone production. Worldwide, the most common cause is iodine deficiency. Thyroid hormones are important for development, and hypothyroidism secondary to iodine deficiency remains the leading cause of preventable intellectual disability.[3] In iodine-sufficient regions, the most common cause of hypothyroidism is Hashimoto's thyroiditis, also an autoimmune disorder. In addition, the thyroid gland may also develop several types of nodules and cancer.

Anterior thyroid
The human thyroid as viewed from the front, with arteries visible
Thyroid dummy
The thyroid is located in the neck, below the Adam's apple.
PrecursorThyroid diverticulum (an extension of endoderm into 2nd pharyngeal arch)
SystemEndocrine system
ArterySuperior, Inferior thyroid arteries
VeinSuperior, middle, Inferior thyroid veins
LatinGlandula thyreoidea
Anatomical terminology


Illu08 thyroid
The thyroid gland surrounds the cricoid and tracheal cartilages, and consists of two lobes. This image shows a variant thyroid with a pyramidal lobe emerging from the middle of the thyroid.

The thyroid gland is a butterfly-shaped organ that sits at the front of the neck. It is composed of two lobes, left and right, connected by a narrow isthmus.[4] The thyroid weighs 25 grams in adults,[4] with each lobe being about 5 cm long, 3 cm wide and 2 cm thick, and the isthmus about 1.25 cm in height and width.[4] The gland is usually larger in women, and increases in size in pregnancy.[4][5]

The thyroid sits near the front of the neck, lying against and around the front of the larynx and trachea.[4] The thyroid cartilage and cricoid cartilage lie just above the gland, below the Adam's apple. The isthmus extends from the second to third rings of the trachea, with the uppermost part of the lobes extending to the thyroid cartilage, and the lowermost around the fourth to sixth tracheal rings.[6] The thyroid gland is covered by a thin fibrous capsule,[4] which has an inner and an outer layer. The outer layer is continuous with the pretracheal fascia, attaching the gland to the cricoid and thyroid cartilages,[5] via a thickening of the fascia to form the posterior suspensory ligament of thyroid gland also known as Berry's ligament.[5] This causes the thyroid to move up and down with swallowing.[5] The inner layer extrudes into the gland and forms the septae that divides the thyroid tissue into microscopic lobules.[4] Typically four parathyroid glands, two on each side, lie on each side between the two layers of the capsule, at the back of the thyroid lobes.[4]

The infrahyoid muscles lie in front of the gland and the sternocleidomastoid muscle to the side.[7] Behind the outer wings of the thyroid lie the two carotid arteries. The trachea, larynx, lower pharynx and esophagus all lie behind the thyroid.[5] In this region, the recurrent laryngeal nerve[8] and the inferior thyroid artery pass next to or in the ligament.[9]

Blood, lymph and nerve supply

The thyroid is supplied with arterial blood from the superior thyroid artery, a branch of the external carotid artery, and the inferior thyroid artery, a branch of the thyrocervical trunk, and sometimes by an anatomical variant the thyroid ima artery,[4] which has a variable origin.[10] The superior thyroid artery splits into anterior and posterior branches supplying the thyroid, and the inferior thyroid artery splits into superior and inferior branches.[4] The superior and inferior thyroid arteries join together behind the outer part of the thyroid lobes.[10] The venous blood is drained via superior and middle thyroid veins, which drain to the internal jugular vein, and via the inferior thyroid veins. The inferior thyroid veins originate in a network of veins and drain into the left and right brachiocephalic veins.[4] Both arteries and veins form a plexus between the two layers of the capsule of the thyroid gland.[10]

Lymphatic drainage frequently passes the prelaryngeal lymph nodes (located just above the isthmus), and the pretracheal and paratracheal lymph nodes.[4] The gland receives sympathetic nerve supply from the superior, middle and inferior cervical ganglion of the sympathetic trunk.[4] The gland receives parasympathetic nerve supply from the superior laryngeal nerve and the recurrent laryngeal nerve.[4]


Sobo 1906 444
Clear pyramidal lobe (center) as viewed from the front.

There are many variants in the size and shape of the thyroid gland, and in the position of the embedded parathyroid glands.[5]

Sometimes there is a third lobe present called the pyramidal lobe.[5] When present, this lobe often stretches up the hyoid bone from the thyroid isthmus and may be one to several divided lobes.[4] The presence of this lobe ranges in reported studies from 18.3%[11] to 44.6%.[12] It was shown to more often arise from the left side and occasionally separated.[11] The pyramidal lobe is also known as Lalouette's pyramid.[13] The pyramidal lobe is a remnant of the thyroglossal duct which usually wastes away during the thyroid gland's descent.[5] Small accessory thyroid glands may in fact occur anywhere along the thyroglossal duct, from the foramen cecum of the tongue to the position of the thyroid in the adult.[4] A small horn at the back of the thyroid lobes, usually close to the recurrent laryngeal nerve and the inferior thyroid artery, is called Zuckerkandl's tubercle.[9]

Other variants include a levator muscle of thyroid gland, connecting the isthmus to the body of the hyoid bone,[5] and the presence of the small thyroid ima artery.[5]


Section of a thyroid gland under the microscope. 1 follicles, 2 follicular cells, 3 endothelial cells

At the microscopic level, there are three primary features of the thyroid—follicles, follicular cells, and parafollicular cells, first discovered by Geoffery Websterson in 1664.[14]


Thyroid follicles are small spherical groupings of cells 0.02–0.9mm in diameter that play the main role in thyroid function.[4] They consist of a rim that has a rich blood supply, nerve and lymphatic presence, that surrounds a core of colloid that consists mostly of thyroid hormone precursor proteins called thyroglobulin, an iodinated glycoprotein.[4][15]

Follicular cells

The core of a follicle is surrounded by a single layer of follicular cells. When stimulated by thyroid stimulating hormone (TSH), these secrete the thyroid hormones T3 and T4. They do this by transporting and metabolising the thyroglobulin contained in the colloid.[4] Follicular cells vary in shape from flat to cuboid to columnar, depending on how active they are.[4][15]

Parafollicular cells

Scattered among follicular cells and in spaces between the spherical follicles are another type of thyroid cell, parafollicular cells.[4] These cells secrete calcitonin and so are also called C cells.[16]


Floor of pharynx of embryo between 18 and 21 days

In the development of the embryo, at 3–4 weeks gestational age, the thyroid gland appears as an epithelial proliferation in the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula linguae. The copula soon becomes covered over by the hypopharyngeal eminence [17] at a point later indicated by the foramen cecum. The thyroid then descends in front of the pharyngeal gut as a bilobed diverticulum through the thyroglossal duct. Over the next few weeks, it migrates to the base of the neck, passing in front of the hyoid bone. During migration, the thyroid remains connected to the tongue by a narrow canal, the thyroglossal duct. At the end of the fifth week the thyroglossal duct degenerates and the detached thyroid continues on to its final position over the following two weeks.[17]

The fetal hypothalamus and pituitary start to secrete thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH). TSH is first measurable at 11 weeks.[18] By 18–20 weeks, the production of thyroxine (T4) reaches a clinically significant and self-sufficient level.[18][19] Fetal triiodothyronine (T3) remains low, less than 15 ng/dL until 30 weeks, and increases to 50 ng/dL at full-term.[19] The fetus needs to be self-sufficient in thyroid hormones in order to guard against neurodevelopmental disorders that would arise from maternal hypothyroidism.[20] The presence of sufficient iodine is essential for healthy neurodevelopment.[21]

The neuroendocrine parafollicular cells, also known as C cells, responsible for the production of calcitonin, are derived from foregut endoderm. This part of the thyroid then first forms as the ultimopharyngeal body, which begins in the ventral fourth pharyngeal pouch and joins the primordial thyroid gland during its descent to its final location.[22]

Aberrations in prenatal development can result in various forms of thyroid dysgenesis which can cause congenital hypothyroidism, and if untreated this can lead to cretinism.[18]


Thyroid system
The thyroid hormones T3 and T4 have a number of metabolic, cardiovascular and developmental effects on the body. The production is stimulated by release of thyroid stimulating hormone (TSH), which in turn depends on release of thyrotropin releasing hormone (TRH). Every downstream hormone has negative feedback and decreases the level of the hormone that stimulates its release.

Thyroid hormones

The primary function of the thyroid is the production of the iodine-containing thyroid hormones, triiodothyronine (T3) and thyroxine (T4) and the peptide hormone calcitonin.[23] The thyroid hormones are created from iodine and tyrosine. T3 is so named because it contains three atoms of iodine per molecule and T4 contains four atoms of iodine per molecule.[24] The thyroid hormones have a wide range of effects on the human body. These include:

  • Metabolic. The thyroid hormones increase the basal metabolic rate and have effects on almost all body tissues.[25] Appetite, the absorption of substances, and gut motility are all influenced by thyroid hormones.[26] They increase the absorption in the gut, generation, uptake by cells, and breakdown of glucose.[27] They stimulate the breakdown of fats, and increase the number of free fatty acids.[27] Despite increasing free fatty acids, thyroid hormones decrease cholesterol levels, perhaps by increasing the rate of secretion of cholesterol in bile.[27]
  • Cardiovascular. The hormones increase the rate and strength of the heartbeat. They increase the rate of breathing, intake and consumption of oxygen, and increase the activity of mitochondria.[26] Combined, these factors increase blood flow and the body's temperature.[26]
  • Developmental. Thyroid hormones are important for normal development.[27] They increase the growth rate of young people,[28] and cells of the developing brain are a major target for the thyroid hormones T3 and T4. Thyroid hormones play a particularly crucial role in brain maturation during fetal development and first few years of postnatal life[27]
  • The thyroid hormones also play a role in maintaining normal sexual function, sleep, and thought patterns. Increased levels are associated with increased speed of thought generation but decreased focus.[26] Sexual function, including libido and the maintenance of a normal menstrual cycle, are influenced by thyroid hormones.[26]

After secretion, only a very small proportion of the thyroid hormones travel freely in the blood. Most are bound to thyroxine-binding globulin (about 70%), transthyretin (10%), and albumin (15%).[29] Only the 0.03% of T4 and 0.3% of T3 traveling freely have hormonal activity.[30] In addition, up to 85% of the T3 in blood is produced following conversion from T4 by iodothyronine deiodinases in organs around the body.[23]

Thyroid hormones act by crossing the cell membrane and binding to intracellular nuclear thyroid hormone receptors TR-α1,TR-α2,TR-β1 and TR-β2, which bind with hormone response elements and transcription factors to modulate DNA transcription.[30][31] In addition to these actions on DNA, the thyroid hormones also act within the cell membrane or within cytoplasm via reactions with enzymes, including calcium ATPase, adenylyl cyclase, and glucose transporters.[18]

Hormone production

Thyroid hormone synthesis
Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell:[32]
- Thyroglobulin is synthesized in the rough endoplasmic reticulum and follows the secretory pathway to enter the colloid in the lumen of the thyroid follicle by exocytosis.
- Meanwhile, a sodium-iodide (Na/I) symporter pumps iodide (I) actively into the cell, which previously has crossed the endothelium by largely unknown mechanisms.
- This iodide enters the follicular lumen from the cytoplasm by the transporter pendrin, in a purportedly passive manner.
- In the colloid, iodide (I) is oxidized to iodine (I0) by an enzyme called thyroid peroxidase.
- Iodine (I0) is very reactive and iodinates the thyroglobulin at tyrosyl residues in its protein chain (in total containing approximately 120 tyrosyl residues).
- In conjugation, adjacent tyrosyl residues are paired together.
- The entire complex re-enters the follicular cell by endocytosis.
- Proteolysis by various proteases liberates thyroxine and triiodothyronine molecules, which enters the blood by largely unknown mechanisms.

The thyroid hormones are created from thyroglobulin. This is a protein within the follicular space that is originally created within the rough endoplasmic reticulum of follicular cells and then transported into the follicular space. Thyroglobulin contains 123 units of tyrosine, which reacts with iodine within the follicular space.[33]

Iodine is essential for the production of the thyroid hormones. Iodine (I0) travels in the blood as iodide (I), which is taken up into the follicular cells by a sodium-iodide symporter. This is an ion channel on the cell membrane which in the same action transports two sodium ions and an iodide ion into the cell.[34] Iodide then travels from within the cell into the follicular space, through the action of pendrin, an iodide-chloride antiporter. In the follicular space, the iodide is then oxidized to iodine. This makes it more reactive,[32] and the iodine is attached to the active tyrosine units in thyroglobulin by the enzyme thyroid peroxidase. This forms the precursors of thyroid hormones monoiodotyrosine (MIT), and diiodotyrosine (DIT).[2]

When the follicular cells are stimulated by thyroid-stimulating hormone, the follicular cells reabsorb thyroglobulin from the follicular space. The iodinated tyrosines are cleaved, forming the thyroid hormones T4, T3, DIT, MIT, and traces of reverse triiodothyronine. T3 and T4 are released into the blood. The hormones secreted from the gland are about 80–90% T4 and about 10–20% T3.[35][36] Deiodinase enzymes in peripheral tissues remove the iodine from MIT and DIT and convert T4 to T3 and RT3. [33] This is a major source of both RT3 (95%) and T3 (87%) in peripheral tissues.[37]


The production of thyroxine and triiodothyronine is primarily regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary gland. TSH release in turn is stimulated by thyrotropin releasing hormone (TRH), released in a pulsatile manner from the hypothalamus.[38] The thyroid hormones provide negative feedback to the thyrotropes TSH and TRH: when the thyroid hormones are high, TSH production is suppressed. This negative feedback also occurs when levels of TSH are high, causing TRH production to be suppressed.[39]

TRH is secreted at an increased rate in situations such as cold exposure in order to stimulate thermogenesis.[40] In addition to being suppressed by the presence of thyroid hormones, TSH production is blunted by dopamine, somatostatin, and glucocorticoids.[41]


The thyroid gland also produces the hormone calcitonin, which helps regulate blood calcium levels. Parafollicular cells produce calcitonin in response to high blood calcium. Calcitonin decreases the release of calcium from bone, by decreasing the activity of osteoclasts, cells which break down bone. Bone is constantly reabsorbed by osteoclasts and created by osteoblasts, so calcitonin effectively stimulates movement of calcium into bone. The effects of calcitonin are opposite those of the parathyroid hormone (PTH) produced in the parathyroid glands. However, calcitonin seems far less essential than PTH, as calcium metabolism remains clinically normal after removal of the thyroid (thyroidectomy), but not the parathyroid glands.[42]

Gene and protein expression

About 20,000 protein coding genes are expressed in human cells and 70% of these genes are expressed in the normal thyroid.[43][44] Some 250 of these genes are more specifically expressed in the thyroid with about 20 genes being highly thyroid specific. The corresponding specific proteins are mainly involved in thyroid hormone synthesis, such as thyroglobulin, TPO and IYD, and expressed in follicular cells. Other proteins elevated in the thyroid are calcitonin related proteins such as CALCA and CALCB, expressed in the parafollicular c-cells.

Clinical significance



Excessive production of the thyroid hormones is called hyperthyroidism, which is most commonly a result of Graves' disease, a toxic multinodular goitre, a solitary thyroid adenoma, or inflammation. Other causes include drug-induced excess of iodine, particularly from amiodarone, an antiarrhythmic medication; an excess caused by the preferential uptake of iodine by the thyroid following iodinated contrast imaging; or from pituitary adenomas which may cause an overproduction of thyroid stimulating hormone.[45] Hyperthyroidism often causes a variety of non-specific symptoms including weight loss, increased appetite, insomnia, decreased tolerance of heat, tremor, palpitations, anxiety and nervousness. In some cases it can cause chest pain, diarrhoea, hair loss and muscle weakness.[46] Such symptoms may be managed temporarily with drugs such as beta blockers.[47]

Long-term management of hyperthyroidism may include drugs that suppress thyroid function such as propylthiouracil, carbimazole and methimazole.[48] Radioactive iodine-131 can be used to destroy thyroid tissue. Radioactive iodine is selectively taken up by the thyroid, which over time destroys the cells involved in its uptake. The chosen first-line treatment will depend on the individual and on the country where being treated. Surgery to remove the thyroid can sometimes be performed as a transoral thyroidectomy, a minimally-invasive procedure.[49] Surgery does however carry a risk of damage to the parathyroid glands and the nerves controlling the vocal cords. If the entire thyroid gland is removed, hypothyroidism will naturally result, and thyroid hormone substitutes will be needed.[50][47]


An underactive thyroid gland results in hypothyroidism. Typical symptoms are abnormal weight gain, tiredness, constipation, heavy menstrual bleeding, hair loss, cold intolerance, and a slow heart rate.[46] Iodine deficiency is the most common cause of hypothyroidism worldwide,[51] and the autoimmune disease Hashimoto's thyroiditis is the most common cause in the developed world.[52] Other causes include congenital abnormalities, diseases causing transient inflammation, surgical removal or radioablation of the thyroid, the drugs amiodarone and lithium, amyloidosis, and sarcoidosis.[53] Some forms of hypothyroidism can result in myxedema and severe cases can result in myxedema coma.[54]

Hypothyroidism is managed with replacement of the hormone thyroxine. This is usually given daily as an oral supplement, and may take a few weeks to become effective.[54] Some causes of hypothyroidism, such as Postpartum thyroiditis and Subacute thyroiditis may be transient and pass over time, and other causes such as iodine deficiency may be able to be rectified with dietary supplementation.[55]


Thyroid nodules are often found on the gland, with a prevalence of 4–7%.[56] The majority of nodules do not cause any symptoms and are non-cancerous.[57] Non-cancerous cases include simple cysts, colloid nodules, and thyroid adenomas. Malignant nodules, which only occur in about 5% of nodules, include follicular, papillary, medullary carcinomas and metastases from other sites [58] Nodules are more likely in females, those who are exposed to radiation, and in those who are iodine deficient.[56]

When a nodule is present, thyroid function tests are performed and reveal whether a person has a normal amount of thyroid hormones ("euthyroid") or an excess of hormones, usually secreted by the nodule, causing hyperthyroidism.[57] When the thyroid function tests are normal, an ultrasound is often used to investigate the nodule, and provide information such as whether the nodule is fluid-filled or a solid mass, and whether the appearance is suggestive of a benign or malignant cancer.[56] A needle aspiration biopsy may then be performed, and the sample undergoes cytology, in which the appearance of cells is viewed to determine whether they resemble normal or cancerous cells.[58]

There can be many nodules, which is termed a multinodular goitre, and this can sometimes be a toxic multinodular goitre.[58]


An enlarged thyroid gland is called a goitre.[59] Goitres are present in some form in about 5% of people,[58] and are the result of a large number of causes, including iodine deficiency, autoimmune disease (both Grave's disease and Hashimoto's thyroiditis), infection, inflammation, and infltrative disease such as sarcoidosis and amyloidosis. Sometimes no cause can be found, a state called "simple goitre".[60]

Some forms of goitre are associated with pain, whereas many do not cause any symptoms. Enlarged goitres may extend beyond the normal position of the thyroid gland to below the sternum, around the airway or esophagus.[58] Goitres may be associated with hyperthyoidism or hypothyroidism, relating to the underlying cause of the goitre.[58] Thyroid function tests may be done to investigate the cause and effects of the goitre. The underlying cause of the goitre may be treated, however many goitres with no associated symptoms are simply monitored.[58]


Disorders of the thyroid are functional–caused by dysfunction in the production of hormones, and nodes and tumors either benign or malignant. Functional disorders can cause inflammation as can some other forms of thyroiditis. Functional disorders can result in the overproduction or underproduction of hormones. Any of the functional thyroid disorders can result in the gland's enlargement and cause a swollen neck termed a goitre.


Inflammation of the thyroid is called thyroiditis. Inflamed thyroids may cause symptoms of hyperthyroidism or hypothyroidism. Two types of thyroiditis initially present with hyperthyroidism and are sometimes followed by a period of hypothyroidism – Hashimoto's thyroiditis and postpartum thyroiditis. There are other disorders that cause inflammation of the thyroid, and these include subacute thyroiditis, acute thyroiditis, silent thyroiditis, Riedel's thyroiditis and traumatic injury, including palpation thyroiditis.[61]

Hashimoto's thyroiditis is an autoimmune disorder in which the thyroid gland is infltrated by the lymphocytes B-cell and T-cells. These progressively destroy the thyroid gland.[62] In this way, Hasimoto's thyroiditis may have occurred insidiously, and only be noticed when thyroid hormone production decreases, causing symptoms of hypothyroidism.[62] Hashimoto's is more common in females than males, much more common after the age of 60, and has known genetic risk factors.[62] Also more common in individuals with Hashimoto's thyroiditis are type 1 diabetes, pernicious anaemia, Addison's disease vitiligo.[62]

Postpartum thyroiditis occurs in some females following childbirth. After delivery, the gland becomes inflamed and the condition initially presents with a period of hyperthyroidism followed by hypothyroidism and, usually, a return to normal function. [63] The course of the illness takes place over several months, and is characterised by a painless goitre. Antibodies against thyroid peroxidase can be found on testing. The inflammation usually resolves without treatment, although thyroid hormone replacement may be needed during the period of hypothyroidism.[63]


The most common neoplasm affecting the thyroid gland is a benign adenoma, usually presenting as a painless mass in the neck.[64] Malignant thyroid cancers are most often carcinomas, although cancer can occur in any tissue that the thyroid consists of, including cancer of C-cells and lymphomas. Cancers from other sites also rarely lodge in the thyroid.[64] Radiation of the head and neck presents a risk factor for thyroid cancer, and cancer is more common in women than men, occurring at a rate of about 2:1.[64]

In most cases, thyroid cancer presents as a painless mass in the neck. It is very unusual for thyroid cancers to present with other symptoms, although in some cases cancer may cause hyperthyroidism.[65] Most malignant thyroid cancers are papillary, followed by follicular, medullary, and thyroid lymphoma.[64][65] Because of the prominence of the thyroid gland, cancer is often detected earlier in the course of disease as the cause of a nodule, which may undergo fine needle aspiration. Thyroid function tests will help reveal whether the nodule produces excess thyroid hormones. A radioactive iodine uptake test can help reveal the activity and location of the cancer and metastases.[64][66]

Thyroid cancers are treated by removing the whole or part of thyroid gland. Radioactive Iodine 131 may be given to radioablate the thyroid. Thyroxine is given to replace the hormones lost and to suppress TSH production, as TSH may stimulate recurrence.[66] With the exception of the rare anaplastic thyroid cancer, which carries a very poor prognosis, most thyroid cancers carry an excellent prognosis and can even be considered curable.[67]


A persistent thyroglossal duct is the most common clinically significant congenital disorder of the thyroid gland. A persistent sinus tract may remain as a vestigial remnant of the tubular development of the thyroid gland. Parts of this tube may be obliterated, leaving small segments to form thyroglossal cysts.[22] Preterm neonates are at risk of hypothyroidism as their thyroid glands are insufficiently developed to meet their postnatal needs.[68] In order to detect hypothyroidism in newborn babies, to prevent growth and development abnormalities in later life, many countries have newborn screening programs at birth.[69]

Infants with thyroid hormone deficiency (congenital hypothyroidism) can manifest problems of physical growth and development as well as brain development, termed cretinism.[70][21] Children with congenital hypothyroidism are treated supplementally with levothyroxine, which facilitates normal growth and development.[71]

Mucinous, clear secretions may collect within these cysts to form either spherical masses or fusiform swellings, rarely larger than 2 to 3 cm in diameter. These are present in the midline of the neck anterior to the trachea. Segments of the duct and cysts that occur high in the neck are lined by stratified squamous epithelium, which is essentially identical to that covering the posterior portion of the tongue in the region of the foramen cecum. The disorders that occur in the lower neck more proximal to the thyroid gland are lined by epithelium resembling the thyroidal acinar epithelium. Characteristically, next to the lining epithelium, there is an intense lymphocytic infiltrate. Superimposed infection may convert these lesions into abscess cavities, and rarely, give rise to cancers.

Another disorder is that of thyroid dysgenesis which can result in various presentations of one or more misplaced accessory thyroid glands.[4] These can be asymptomatic.


The thyroid gland in health and disease (1917) (14780980651)
Child affected by cretinism, associated with a lack of iodine.[72]

Iodine deficiency, most common in inland and mountainous areas, can predispose to goitre – if widespread, known as endemic goitre.[70] Pregnant women deficient of iodine can give birth to infants with thyroid hormone deficiency.[70][21] The use of iodised salt used to add iodine to the diet[21] has eliminated endemic cretinism in most developed countries,[73] and over 120 countries have made the iodination of salt mandatory.[74]

Because the thyroid concentrates iodine, it also concentrates the various radioactive isotopes of iodine produced by nuclear fission. In the event of large accidental releases of such material into the environment, the uptake of radioactive iodine isotopes by the thyroid can, in theory, be blocked by saturating the uptake mechanism with a large surplus of non-radioactive iodine, taken in the form of potassium iodide tablets. One consequence of the Chernobyl disaster was an increase in thyroid cancers in children in the years following the accident.[75]

As with most substances, either too much or too little can cause problems. Recent studies on some populations are showing that excess iodine intake could cause an increased prevalence of autoimmune thyroid disease, resulting in permanent hypothyroidism.[76]

Graves' disease

Graves' disease is an autoimmune disorder that is the most common cause of hyperthyroidism.[77] In Graves' disease, for an unknown reason autoantibodies develop against the thyroid stimulating hormone receptor. These antibodies activate the receptor, leading to development of a goitre and symptoms of hyperthyroidism, such as heat intolerance, weight loss, diarrhoea and palpitations. Occasionally such antibodies block but do not activate the receptor, leading to symptoms associated with hypothyroidism.[77] In addition, gradual protrusion of the eyes may occur, called Graves' ophthalmopathy, as may swelling of the front of the shins.[77] Graves' disease can be diagnosed by the presence of pathomnomonic features such as involvement of the eyes and shins, or isolation of autoantibodies, or by results of a radiolabelled uptake scan. Graves' disease is treated with anti-thyroid drugs such as propylthiouracil, which decrease the production of thyroid hormones, but hold a high rate of relapse. If there is no involvement of the eyes, then use of radioactive isotopes to ablate the gland may be considered. Surgical removal of the gland with subsequent thyroid hormone replacement may be considered, however this will not control symptoms associated with the eye or skin.[77]


Physicians who specialise in the treatment of thyroid disorders are known generally as endocrinologists, thyroid specialists or thyroidologists. Thyroid surgeons or otolaryngologists may play a role in the surgical management of thyroid disease and general practitioners and family physicians may play a role in monitoring and identifying symptoms related to thyroid disease.

The thyroid itself is examined by observation of the gland and surrounding neck for swelling or enlargement.[78] It is then felt, usually from behind, and a person is often asked to swallow to better feel the gland against the fingers of the examiner.[78] The gland moves up and down with swallowing because of its attachments to the thyroid and cricoid cartilages.[5] In a healthy person the gland is not visible yet is palpable as a soft mass. Examination of the thyroid gland includes the search for abnormal masses and the assessment of overall thyroid size.[79] The character of the thyroid, swellings, nodules, and their consistency may all be able to be felt. If a goitre is present, an examiner may also feel down the neck consider tapping the upper part of the chest to check for extension. Further tests may include raising the arms (Pemberton's sign), listening to the gland with a stethoscope for bruits, testing of reflexes, and palpation of the lymph nodes in the head and neck. A medical examination of the thyroid will also include observation of the person as a whole, to look for systemic signs such as weight gain or loss, hair loss, and signs in other locations – such as protrusion of the eyes or swelling of the calves in Grave's disease.[80][78]


A number of tests can be used to test the function of the thyroid, for the presence of diseases, and for the success or failure of treatment. Blood tests in general aim to measure thyroid function or determine the cause of thyroid dysfunction. Thyroid function tests include a battery of blood tests including the measurement of the thyroid hormones T3 and T4, as well as the measurement of TSH.[81] They may reveal hyperthyroidism (high T3 and T4), hypothyroidism (low T3, T4), or subclinical hyperthyroidism (normal T3 and T4 with a low TSH).[81]

TSH levels are considered the most sensitive marker of thyroid dysfunction.[81] They are however not always accurate, particularly if the cause of hypothyroidism is thought to be related to insufficient TRH secretion, in which case it may be low or falsely normal. In such a case a TRH stimulation test, in which TRH is given and TSH levels are measured at 30 and 60-minutes after, may be conducted.[81]

T3 and T4 can be measured directly. However, as the two thyroid hormones travel bound to other molecules, and it is the "free" component that is biologically active, free T3 and free T4 levels can be measured.[81] T4 is preferred, because in hypothyroidism T3 levels may be normal.[81] The ratio of bound to unbound thyroid hormones is known as the thyroid hormone binding ratio (THBR).[82] It is also possible to measure directly the main carriers of the thyroid hormones, thryoglobulin and throxine-binding globulin.[83] Thyroglobulin will also be measurable in a healthy thyroid, and will increase with inflammation, and may also be used to measure the success of thyroid removal or ablation. If successful, thyroglobulin should be undetectable.[82] Lastly, antibodies against components of the thyroid, particularly anti-TPO and anti-thyroglobulin, can be measured. These may be present in normal individuals but are highly sensitive for autoimmune-related disease.[82]

Ultrasound of the thyroid may be used to reveal whether structures are solid or filled with fluid, helping to differentiate between nodules and goitres and cysts. It may also help differentiate between malignant and benign lesions.[84] A fine needle aspiration biopsy may be taken concurrently of thyroid tissue to determine the nature of a lesion. These biopsies are then sent for histopathology and cytology.[85] When further imaging is required, a radiolabelled iodine-123 or technetium-99 uptake scan may take place. This can determine the size and shape of lesions, reveal whether nodules or goitres are metabolically active, and reveal and monitor sites of thyroid disease or cancer deposits outside the thyroid.[86]

Computed tomography of the thyroid plays an important role in the evaluation of thyroid cancer.[87] CT scans often incidentally find thyroid abnormalities, and thereby practically becomes the first investigation modality.[87]


Thespiae 431-424 BC
The thyroid was named by Thomas Wharton after the ancient Greek shield of a similar pronunciation. Shown is an example, as engraved on an obol dating from 431–424 BCE.

The presence and diseases of the thyroid have been noted and treated for thousands of years, although the gland itself has only been described and named since the renaissance.[88] In 1600 BCE burnt sponge and seaweed were used within China for the treatment of goitres, a practice which has developed in many parts of the world.[88][89] In Ayurvedic medicine, the book Sushruta Samhita written about 1400 BCE describes hyperthyroidism, hypothyroidism and goitre.[89] Aristotle and Xenophon in the fifth century BCE describe cases of Grave's disease, which receives its name over two millennia later owing to descriptions provided by Robert James Graves in 1834,[89] Hippocrates and Plato in the fourth century BCE provided some of the first descriptions of the gland itself, proposing its function as a salivary gland.[89] Pliny the Elder in the first century BCE referred to epidemics of goitre in the Alps and proposed treatment with burnt seaweed,[88] a practice also referred to by Galen in the second century, referred to burnt sponge for the treatment of goitre.[88] The Chinese pharmacology text Shennong_Ben_Cao_Jing, written ca. 200-250, also refers to goitre.[88][89]

In 1500 polymath Leonardo da Vinci provides the first illustration of the thyroid.[88] In 1543 Anatomist Andreas Vesalius gave the first anatomic description and illustration of the gland.[88] In 1656 the thyroid received its name, by the anatomist Thomas Wharton.[88] The gland was named thyroid, meaning shield, as its shape resembled the shields commonly used in Ancient Greece.[88] The English name thyroid gland[90] is derived from the medical Latin used by Wharton – glandula thyreoidea.[91] Glandula means gland in Latin,[92] and thyreoidea can be traced back to the Ancient Greek word θυρεοειδής, meaning shield-like/shield-shaped.[93]

French chemist Bernard Courtois discovered Iodine in 1811,[89] and in 1896 Eugen Baumann documented it as the central ingredient in the thryoid gland. He did this by boiling the thyroid glands of a thousand sheep, and named the precipitate, a combination of the thyroid hormones, 'iodothyrin'.[89] David Marine in 1907 provided iodine is necessary for thyroid function.[89][88] Thyroxine itself was first isolated in 1914 and synthesized in 1927, and trirodothyroxine in 1952.[89][94] The conversion of T4 to T3 was discovered in 1970.[88] The process of discovering TSH took place over the early to mid twentieth century.[95] TRH was discovered by Polish endocrinologist Andrew Schally in 1970, contributing in part to his Nobel Prize in Medicine in 1977.[88][96]

Either Aetius in the sixth century CE[89] or Persian Ali ibn Abbas al-Magusi in 990 CE conducted the first recorded thyroidectomy as a treatment for goitre.[88][97] Operations remained risky and generally were not successful until the 19th century, when descriptions emerged from a number of authors including Prussian surgeon Theodor Billroth, Swiss surgeon and physiologist Theodor Kocher, American physician Charles Mayo, William Halsted and George Crile. These descriptions provided the basis for modern thyroid surgery.[98] Theodor Kocher went on to win the Nobel Prize in Physiology or Medicine in 1909 "for his work on the physiology, pathology and surgery of the thyroid gland".[99]

Numerous authors described cretinism, myxoedema their relationship with the thyroid in the nineteenth century.[89] Charles Mayo coined the term hyperthyroidism in 1910,[88] Hakaru Hashimoto documented a case of Hashimoto's thyroiditis in 1912, and autoantibodies were demonstrated in 1956.[89] Knowledge of the thyroid and its conditions developed throughout the late nineteenth and twentieth centuries, with many modern treatments and investigative modalities evolving throughout the mid twentieth century, including the use of radioactive iodine, thiouracil and fine needle aspiration.[88]

Other animals

The thyroid gland in health and disease (1917) (14780977681)
Goat affected by a goitre

The thyroid gland is found in all vertebrates. In fish, it is usually located below the gills and is not always divided into distinct lobes. However, in some teleosts, patches of thyroid tissue are found elsewhere in the body, associated with the kidneys, spleen, heart, or eyes.[100]

In tetrapods, the thyroid is always found somewhere in the neck region. In most tetrapod species, there are two paired thyroid glands – that is, the right and left lobes are not joined together. However, there is only ever a single thyroid gland in most mammals, and the shape found in humans is common to many other species.[100]

In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the gut, and associated with the larva's filter-feeding apparatus. In the adult lamprey, the gland separates from the gut, and becomes endocrine, but this path of development may reflect the evolutionary origin of the thyroid. For instance, the closest living relatives of vertebrates, the tunicates and Amphioxus, have a structure very similar to that of larval lampreys (the endostyle), and this also secretes iodine-containing compounds (albeit not thyroxine).[100]

Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom. For example, iodine and T4 trigger the change from a plant-eating water-dwelling tadpole into a meat-eating land-dwelling frog, with better neurological, visuospatial, smell and cognitive abilities for hunting, as seen in other predatory animals. A similar phenomenon happens in the neotenic amphibian salamanders, which, without introducing iodine, don't transform into land-dwelling adults, and live and reproduce in the larval form of aquatic axolotl. Among amphibians, administering a thyroid-blocking agent such as propylthiouracil (PTU) can prevent tadpoles from metamorphosing into frogs; in contrast, administering thyroxine will trigger metamorphosis. In amphibian metamorphosis, thyroxine and iodine also exert a well-studied experimental model of apoptosis on the cells of gills, tail, and fins of tadpoles. Iodine, via iodolipids, has favored the evolution of terrestrial animal species and has likely played a crucial role in the evolution of the human brain.[101][102]

See also


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External links


Calcitonin is a 32 amino acid peptide hormone secreted by parafollicular cells (also known as C cells) of the thyroid gland in humans, and in many other animals in the ultimopharyngeal body. It acts to reduce blood calcium (Ca2+), opposing the effects of parathyroid hormone (PTH).Calcitonin has been found in fish, reptiles, birds, and mammals. Its importance in humans has not been as well established as its importance in other animals, as its function is usually not significant in the regulation of normal calcium homeostasis. It belongs to the calcitonin-like protein family.

Historically calcitonin has also been called thyrocalcitonin.


Endocrinology (from endocrine + -ology) is a branch of biology and medicine dealing with the endocrine system, its diseases, and its specific secretions known as hormones. It is also concerned with the integration of developmental events proliferation, growth, and differentiation, and the psychological or behavioral activities of metabolism, growth and development, tissue function, sleep, digestion, respiration, excretion, mood, stress, lactation, movement, reproduction, and sensory perception caused by hormones. Specializations include behavioral endocrinology and comparative endocrinology.

The endocrine system consists of several glands, all in different parts of the body, that secrete hormones directly into the blood rather than into a duct system. Therefore, endocrine glands are regarded as ductless glands. Hormones have many different functions and modes of action; one hormone may have several effects on different target organs, and, conversely, one target organ may be affected by more than one hormone.


A goitre, or goiter, is a swelling in the neck resulting from an enlarged thyroid gland. A goitre can be associated with a thyroid that is not functioning properly.

Worldwide, over 90% of goitre cases are caused by iodine deficiency. The term is from the Latin gutturia, meaning throat. Most goitres are of a benign nature.

Graves' disease

Graves' disease, also known as toxic diffuse goiter, is an autoimmune disease that affects the thyroid. It frequently results in and is the most common cause of hyperthyroidism. It also often results in an enlarged thyroid. Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea, and unintentional weight loss. Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy. About 25 to 80% of people with the condition develop eye problems.The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. A person is more likely to be affected if they have a family member with the disease. If one twin is affected, a 30% chance exists that the other twin will also have the disease. The onset of disease may be triggered by stress, infection, or giving birth. Those with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis are more likely to be affected. Smoking increases the risk of disease and may worsen eye problems. The disorder results from an antibody, called thyroid-stimulating immunoglobulin (TSI), that has a similar effect to thyroid stimulating hormone (TSH). These TSI antibodies cause the thyroid gland to produce excess thyroid hormone. The diagnosis may be suspected based on symptoms and confirmed with blood tests and radioiodine uptake. Typically, blood tests show a raised T3 and T4, low TSH, increased radioiodine uptake in all areas of the thyroid, and TSI antibodies.The three treatment options are radioiodine therapy, medications, and thyroid surgery. Radioiodine therapy involves taking iodine-131 by mouth, which is then concentrated in the thyroid and destroys it over weeks to months. The resulting hypothyroidism is treated with synthetic thyroid hormone. Medications such as beta blockers may control some of the symptoms, and antithyroid medications such as methimazole may temporarily help people while other treatments are having effect. Surgery to remove the thyroid is another option. Eye problems may require additional treatments.Graves' disease will develop in about 0.5% of males and 3% of females. It occurs about 7.5 times more often in women than in men. Often, it starts between the ages of 40 and 60, but can begin at any age. It is the most common cause of hyperthyroidism in the United States (about 50 to 80% of cases). The condition is named after Robert Graves, who described it in 1835. A number of prior descriptions also exist.

Hashimoto's thyroiditis

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. Early on there may be no symptoms. Over time the thyroid may enlarge, forming a painless goiter. Some people eventually develop hypothyroidism with accompanying weight gain, feeling tired, constipation, depression, and general pains. After many years the thyroid typically shrinks in size. Potential complications include thyroid lymphoma.Hashimoto's thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, T4, and anti-thyroid autoantibodies. Other conditions that can produce similar symptoms include Graves’ disease and nontoxic nodular goiter.Hashimoto's thyroiditis is typically treated with levothyroxine. If hypothyroidism is not present, some may recommend no treatment while others may treat to try to reduce the size of the goiter. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.Hashimoto's thyroiditis affects about 5% of the population at some point in their life. It typically begins between the ages of 30 and 50 and is much more common in women than men. Rates of the disease appear to be increasing. It was first described by the Japanese physician Hakaru Hashimoto in 1912. In 1957 it was recognized as an autoimmune disorder.


Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormone by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature and often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.Graves' disease is the cause of about 50% to 80% of the cases of hyperthyroidism in the United States. Other causes include multinodular goiter, toxic adenoma, inflammation of the thyroid, eating too much iodine, and too much synthetic thyroid hormone. A less common cause is a pituitary adenoma. The diagnosis may be suspected based on signs and symptoms and then confirmed with blood tests. Typically blood tests show a low thyroid stimulating hormone (TSH) and raised T3 or T4. Radioiodine uptake by the thyroid, thyroid scan, and TSI antibodies may help determine the cause.Treatment depends partly on the cause and severity of disease. There are three main treatment options: radioiodine therapy, medications, and thyroid surgery. Radioiodine therapy involves taking iodine-131 by mouth which is then concentrated in and destroys the thyroid over weeks to months. The resulting hypothyroidism is treated with synthetic thyroid hormone. Medications such as beta blockers may control the symptoms, and anti-thyroid medications such as methimazole may temporarily help people while other treatments are having effect. Surgery to remove the thyroid is another option. This may be used in those with very large thyroids or when cancer is a concern. In the United States hyperthyroidism affects about 1.2% of the population. It occurs between two and ten times more often in women. Onset is commonly between 20 and 50 years of age. Overall the disease is more common in those over the age of 60 years.


Hypothyroidism, also called underactive thyroid or low thyroid, is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormone. It can cause a number of symptoms, such as poor ability to tolerate cold, a feeling of tiredness, constipation, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goiter. Untreated hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.Worldwide, too little iodine in the diet is the most common cause of hypothyroidism. In countries with enough iodine in the diet, the most common cause of hypothyroidism is the autoimmune condition Hashimoto's thyroiditis. Less common causes include: previous treatment with radioactive iodine, injury to the hypothalamus or the anterior pituitary gland, certain medications, a lack of a functioning thyroid at birth, or previous thyroid surgery. The diagnosis of hypothyroidism, when suspected, can be confirmed with blood tests measuring thyroid-stimulating hormone (TSH) and thyroxine levels.Salt iodization has prevented hypothyroidism in many populations. Hypothyroidism can be treated with levothyroxine. The dose is adjusted according to symptoms and normalization of the thyroxine and TSH levels. Thyroid medication is safe in pregnancy. While a certain amount of dietary iodine is important, excessive amounts can worsen certain types of hypothyroidism.Worldwide about one billion people are estimated to be iodine deficient; however, it is unknown how often this results in hypothyroidism. In the United States, hypothyroidism occurs in 0.3–0.4% of people. Subclinical hypothyroidism, a milder form of hypothyroidism characterized by normal thyroxine levels and an elevated TSH level, is thought to occur in 4.3–8.5% of people in the United States. Hypothyroidism is more common in women than men. People over the age of 60 are more commonly affected. Dogs are also known to develop hypothyroidism and in rare cases cats and horses. The word "hypothyroidism" is from Greek hypo- meaning "reduced", thyreos for "shield", and eidos for "form".


Iodine-131 (131I) is an important radioisotope of iodine discovered by Glenn Seaborg and John Livingood in 1938 at the University of California, Berkeley. It has a radioactive decay half-life of about eight days. It is associated with nuclear energy, medical diagnostic and treatment procedures, and natural gas production. It also plays a major role as a radioactive isotope present in nuclear fission products, and was a significant contributor to the health hazards from open-air atomic bomb testing in the 1950s, and from the Chernobyl disaster, as well as being a large fraction of the contamination hazard in the first weeks in the Fukushima nuclear crisis. This is because I-131 is a major fission product of uranium and plutonium, comprising nearly 3% of the total products of fission (by weight). See fission product yield for a comparison with other radioactive fission products. I-131 is also a major fission product of uranium-233, produced from thorium.

Due to its mode of beta decay, iodine-131 is notable for causing mutation and death in cells that it penetrates, and other cells up to several millimeters away. For this reason, high doses of the isotope are sometimes less dangerous than low doses, since they tend to kill thyroid tissues that would otherwise become cancerous as a result of the radiation. For example, children treated with moderate dose of I-131 for thyroid adenomas had a detectable increase in thyroid cancer, but children treated with a much higher dose did not. Likewise, most studies of very-high-dose I-131 for treatment of Graves disease have failed to find any increase in thyroid cancer, even though there is linear increase in thyroid cancer risk with I-131 absorption at moderate doses. Thus, iodine-131 is increasingly less employed in small doses in medical use (especially in children), but increasingly is used only in large and maximal treatment doses, as a way of killing targeted tissues. This is known as "therapeutic use".

Iodine-131 can be "seen" by nuclear medicine imaging techniques (i.e., gamma cameras) whenever it is given for therapeutic use, since about 10% of its energy and radiation dose is via gamma radiation. However, since the other 90% of radiation (beta radiation) causes tissue damage without contributing to any ability to see or "image" the isotope, other less-damaging radioisotopes of iodine such as iodine-123 (see isotopes of iodine) are preferred in situations when only nuclear imaging is required. The isotope I-131 is still occasionally used for purely diagnostic (i.e., imaging) work, due to its low expense compared to other iodine radioisotopes. Very small medical imaging doses of I-131 have not shown any increase in thyroid cancer. The low-cost availability of I-131, in turn, is due to the relative ease of creating I-131 by neutron bombardment of natural tellurium in a nuclear reactor, then separating I-131 out by various simple methods (i.e., heating to drive off the volatile iodine). By contrast, other iodine radioisotopes are usually created by far more expensive techniques, starting with reactor radiation of expensive capsules of pressurized xenon gas.

Iodine-131 is also one of the most commonly used gamma-emitting radioactive industrial tracer. Radioactive tracer isotopes are injected with hydraulic fracturing fluid to determine the injection profile and location of fractures created by hydraulic fracturing.Much smaller incidental doses of iodine-131 than those used in medical therapeutic procedures, are supposed by some studies to be the major cause of increased thyroid cancers after accidental nuclear contamination. These studies suppose that cancers happen from residual tissue radiation damage caused by the I-131, and should appear mostly years after exposure, long after the I-131 has decayed. Other studies can't find a correlation.


Levothyroxine, also known as L-thyroxine, is a manufactured form of the thyroid hormone thyroxine (T4). It is used to treat thyroid hormone deficiency, including the severe form known as myxedema coma. It may also be used to treat and prevent certain types of thyroid tumors. It is not indicated for weight loss. Levothyroxine is taken by mouth or given by injection into a vein. Maximum effect from a specific dose can take up to six weeks to occur.Side effects from excessive doses include weight loss, trouble tolerating heat, sweating, anxiety, trouble sleeping, tremor, and fast heart rate. Use is not recommended in people who have had a recent heart attack. Use during pregnancy has been found to be safe. It is recommended that dosing be based on regular measurements of thyroid-stimulating hormone (TSH) and T4 levels in the blood. Much of the effect of levothyroxine is following its conversion to triiodothyronine (T3).Levothyroxine was first made in 1927. It is on the World Health Organization's List of Essential Medicines, which lists the most effective and safe medicines needed in a health system. Levothyroxine is available as a generic medication. The wholesale cost in the developing world is about US$0.58 to US$12.28 per month. In the United States, a typical month of treatment costs less than US$25. Levothyroxine was the most commonly prescribed medication in the United States as of 2016, with more than 114 million prescriptions.

Potassium iodide

Potassium iodide is a chemical compound, medication, and dietary supplement. As a medication it is used to treat hyperthyroidism, in radiation emergencies, and to protect the thyroid gland when certain types of radiopharmaceuticals are used. In the developing world it is also used to treat skin sporotrichosis and phycomycosis. As a supplement it is used in those who have low intake of iodine in the diet. It is given by mouth.Common side effects include vomiting, diarrhea, abdominal pain, rash, and swelling of the salivary glands. Other side effects include allergic reactions, headache, goitre, and depression. While use during pregnancy may harm the baby, its use is still recommended in radiation emergencies. Potassium iodide has the chemical formula KI. Commercially it is made by mixing potassium hydroxide with iodine.Potassium iodide has been used medically since at least 1820. It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system. Potassium iodide is available as a generic medication and over the counter. In the United States a course of treatment is less than 25 USD. Potassium iodide is also used for the iodization of salt.

Thyroid-stimulating hormone

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid. In 1916, Bennett M. Allen and Philip E. Smith found that the pituitary contained a thyrotropic substance.

Thyroid cancer

Thyroid cancer is cancer that develops from the tissues of the thyroid gland. It is a disease in which cells grow abnormally and have the potential to spread to other parts of the body. Symptoms can include swelling or a lump in the neck. Cancer can also occur in the thyroid after spread from other locations, in which case it is not classified as thyroid cancer.Risk factors include radiation exposure at a young age, having an enlarged thyroid, and family history. The four main types are papillary thyroid cancer, follicular thyroid cancer, medullary thyroid cancer, and anaplastic thyroid cancer. Diagnosis is often based on ultrasound and fine needle aspiration. Screening people without symptoms and at normal risk for the disease is not recommended as of 2017.Treatment options may include surgery, radiation therapy including radioactive iodine, chemotherapy, thyroid hormone, targeted therapy, and watchful waiting. Surgery may involve removing part or all of the thyroid. Five-year survival rates are 98% in the United States.Globally as of 2015, 3.2 million people have thyroid cancer. In 2012, 298,000 new cases occurred. It most commonly occurs between the ages of 35 and 65. Women are affected more often than men. Those of Asian descent are more commonly affected. Rates have increased in the last few decades, which is believed to be due to better detection. In 2015, it resulted in 31,900 deaths.

Thyroid disease

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.There are five general types of thyroid disease, each with their own symptoms. A person may have one or several different types at the same time. The five groups are:

1) Hypothyroidism (low function) caused by not having enough free thyroid hormones2) Hyperthyroidism (high function) caused by having too much free thyroid hormones3) Structural abnormalities, most commonly a goiter (enlargement of the thyroid gland)4) Tumors which can be benign (not cancerous) or cancerous5) Abnormal thyroid function tests without any clinical symptoms (subclinical hypothyroidism or subclinical hyperthyroidism).In some types, such as subacute thyroiditis or postpartum thyroiditis, symptoms may go away after a few months and laboratory tests may return to normal. However most types of thyroid disease do not resolve on their own. Common hypothyroid symptoms include fatigue, low energy, weight gain, inability to tolerate the cold, slow heart rate, dry skin and constipation. Common hyperthyroid symptoms include irritability, anxiety, weight loss, fast heartbeat, inability to tolerate the heat, diarrhea, and enlargement of the thyroid. Structural abnormalities may not produce symptoms, however some people may have hyperthyroid or hypothyroid symptoms related to the structural abnormality or notice swelling of the neck. Rarely goiters can cause compression of the airway, compression of the vessels in the neck, or difficulty swallowing. Tumors, often called thyroid nodules, can also have many different symptoms ranging from hyperthyroidism to hypothyroidism to swelling in the neck and compression of the structures in the neck.Diagnosis starts with a history and physical examination. Screening for thyroid disease in patients without symptoms is a debated topic although commonly practiced in the United States. If dysfunction of the thyroid is suspected, laboratory tests can help support or rule out thyroid disease. Initial blood tests often include thyroid-stimulating hormone (TSH) and free thyroxine (T4). Total and free triiodothyronine (T3) levels are less commonly used. If autoimmune disease of the thyroid is suspected, blood tests looking for Anti-thyroid autoantibodies can also be obtained. Procedures such as ultrasound, biopsy and a radioiodine scanning and uptake study may also be used to help with the diagnosis, particularly if a nodule is suspected.

Treatment of thyroid disease varies based on the disorder. Levothyroxine is the mainstay of treatment for people with hypothyroidism, while people with hyperthyroidism caused by Graves' disease can be managed with iodine therapy, antithyroid medication, or surgical removal of the thyroid gland. Thyroid surgery may also be performed to remove a thyroid nodule or to reduce the size of a goiter if it obstructs nearby structures or for cosmetic reasons.

Thyroid hormone receptor

The thyroid hormone receptor (TR) is a type of nuclear receptor that is activated by binding thyroid hormone. TRs act as transcription factors, ultimately affecting the regulation of gene transcriptionand translation. These receptors also have non-genomic effects that lead to second messenger activation, and corresponding cellular response.

Thyroid hormone receptor alpha

Thyroid hormone receptor alpha (TR-alpha) also known as nuclear receptor subfamily 1, group A, member 1 (NR1A1), is a nuclear receptor protein that in humans is encoded by the THRA gene.

Thyroid hormone receptor beta

Thyroid hormone receptor beta (TR-beta) also known as nuclear receptor subfamily 1, group A, member 2 (NR1A2), is a nuclear receptor protein that in humans is encoded by the THRB gene.

Thyroid hormones

Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3. In humans, the ratio of T4 to T3 released into the blood is approximately 14:1. T4 is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T3 production.

Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915. In 2016 desiccated thyroid was the 119th most prescribed medication in the United States with more than 6 million prescriptions.

Thyrotropin-releasing hormone

Thyrotropin-releasing hormone (TRH), is a hypophysiotropic hormone, produced by neurons in the hypothalamus, that stimulates the release of thyroid-stimulating hormone (TSH) and prolactin from the anterior pituitary.

TRH has been used clinically for the treatment of spinocerebellar degeneration and disturbance of consciousness in humans. Its pharmaceutical form is called protirelin (INN) ().


Triiodothyronine, also known as T3, is a thyroid hormone. It affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate.Production of T3 and its prohormone thyroxine (T4) is activated by thyroid-stimulating hormone (TSH), which is released from the anterior pituitary gland. This pathway is part of a closed-loop feedback process: Elevated concentrations of T3, and T4 in the blood plasma inhibit the production of TSH in the anterior pituitary gland. As concentrations of these hormones decrease, the anterior pituitary gland increases production of TSH, and by these processes, a feedback control system stabilizes the amount of thyroid hormones that are in the bloodstream.

T3 is the true hormone. Its effects on target tissues are roughly four times more potent than those of T4. Of the thyroid hormone that is produced, just about 20% is T3, whereas 80% is produced as T4. Roughly 85% of the circulating T3 is later formed in the liver and anterior pituitary by removal of the iodine atom from the carbon atom number five of the outer ring of T4. In any case, the concentration of T3 in the human blood plasma is about one-fortieth that of T4. The half-life of T3 is about 2.5 days. The half-life of T4 is about 6.5 days.

Anatomy of the endocrine system
Pituitary gland
Parathyroid gland
Adrenal gland
Islets of pancreas
Pineal gland

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