The human thyroid as viewed from the front, with arteries visible.
Precursor Thyroid diverticulum (an extension of endoderm into 2nd pharyngeal arch)
System Endocrine system
Artery Superior, Inferior thyroid arteries
Vein Superior, middle, Inferior thyroid veins
Latin Glandula thyreoidea
MeSH A06.407.900
TA A11.3.00.001
FMA 9603

Anatomical terminology

The thyroid gland, or simply the thyroid /ˈθrɔɪd/, is an endocrine gland in the neck, and consists 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 thyroid hormones, which primarily influence the metabolic rate and protein synthesis. The hormones also have many other effects including those on development. The thyroid hormones T3 and T4 are synthesized from iodine and tyrosine. The thyroid also produces the hormone calcitonin, which plays a role in calcium homeostasis.[1]

Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) secreted from the anterior pituitary, 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 disease. In addition, the thyroid gland may also develop several types of nodules and cancer.


Image showing the thyroid gland surrounding the cricoid cartilage
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, and a narrow connecting thyroid 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.[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] Two parathyroid glands usually 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. Behind the outer wings of the thyroid lie the two carotid arteries. The trachea, laryngx, lower pharynx and esophagus all lie behind the thyroid.[5] In this region, the recurrent laryngeal nerve and the inferior thyroid artery pass next to or in the ligament, and where present Zuckerkandl's tubercle.[7]

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.[8] 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.[8] 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.[8]

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]


There are many variants in the size and shape of the thyroid gland, and 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%[9] to 44.6%.[10] It was shown to more often arise from the left side and occasionally separated.[9] The pyramidal lobe is also known as Lalouette's pyramid.[11] 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]

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.[12]


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 flow, nerve and lymphatic supply, that surrounds a core of colloid that consists mostly of thyroid hormone precursor proteins called thyroglobulin, an iodinated glycoprotein.[4][13]

Follicular cells

The core of follicles 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][13]

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. Because the cytoplasm of these cells is clear, they are also called "C cells".[4]


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 [14] 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.[14]

The fetal hypothalamus and pituitary start to secrete thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH). TSH is first measurable at 11 weeks.[15] By 18–20 weeks, and the production of thyroxine (T4) reaches a clinically significant and self-sufficient level.[15][16] Fetal triiodothyronine (T3) remains low, less than 15 ng/dL until 30 weeks, and increases to 50 ng/dL at full-term.[16] The fetus needs to be self-sufficient in thyroid hormones in order to guard against neurodevelopmental disorders that would arise from maternal hypothyroidism.[17] The presence of sufficient iodine is essential for healthy neurodevelopment.[18] Preterm neonates are at risk of these disorders as their thyroid glands are insufficiently developed to meet their postnatal needs.[19]

The neuroendocrine parafollicular cells, also known as C cells, responsible for the production of calcitonin, are derived from neural crest cells, which migrate to the pharyngeal arches. 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.[20]

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.[15]


Diagram explaining the relationship between the thyroid hormones T3 and T4, thyroid stimulating hormone (TSH), and thyrotropin releasing hormone (TRH)
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

Main article: Thyroid hormones

The primary function of the thyroid is the production of iodine-containing hormones, triiodothyronine (T3) and thyroxine (T4) and peptide hormone calcitonin.[21] T3 is so named because it contains three atoms of iodine per molecule and T4 contains four atoms of iodine per molecule.[22] The thyroid hormones have a wide range of effects on the human body. These include:

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%).[27] Only the 0.03% of T4 and 0.3% of T3 traveling freely has hormonal activity.[28] In addition, up to 85% of the T3 in blood is produced following conversion from T4 by iodothyronine deiodinases in organs around the body.[21]

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.[28][29] 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.[15]

Hormone production

Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell:[30]
- 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.[31]
- 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 formed from the addition of successive iodide ions to thyroglobulin, a precursor molecule,

Iodide from the circulation is taken up by follicular cells through the sodium-iodide symporter. This is an ion channel on the cell membrane which transports two sodium ions and an iodide ion into the cell.[32] From within the cell iodide is then transported to the follicular space from the cell via the iodide-chloride antiporter pendrin. In the follicular space, the iodide is then oxidized to iodine, following which it is attached to thyroglobulin by the enzyme thyroid peroxidase. This forms the precursors of thyroid hormones monoiodotyrosine (MIT), and diiodotyrosine (DIT)).[2]

Thyrogobulin is a protein within the follicular space that has 123 tyrosine residues, only 4–6 of which are active. When the follicular cells are stimulated by thyroid-stimulating hormone (TSH), the follicular cells reabsorb thyroglobulin and cleave the iodinated tyrosines, forming free T4, (fT4), DIT, MIT, T3 and traces of reverse triiodothyronine (rT3), and releasing T3 and T4 into the blood. Deiodinase enzymes releases the iodine from MIT and DIT and convert T4 to T3 and RT3, [33] which is a major source of both RT3 (95%) and T3 (87%) in peripheral tissues.[34] Thyroid hormone secreted from the gland is about 80–90% T4 and about 10–20% T3.[35][36]


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.[37] 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.[38]

TRH is secreted at an increased rate in situations such as cold exposure (to stimulate thermogenesis) which is prominent in case of infants. TSH production is blunted by dopamine and somatostatin which act as local regulators at the level of the pituitary, in response to rising levels of glucocorticoids and sex hormones (estrogen and testosterone), and excessively high blood iodide concentration.


Main article: Calcitonin

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 bone down. 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, 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.[39]

Clinical significance


Main article: Hyperthyroidism

Excessive production of the thyroid hormone due to an overactive thyroid is called hyperthyroidism, which is most commonly a result of Graves' disease, a toxic multinodular goitre, a solitary thyroid adenoma, and 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.[40] 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.[41] Such symptoms may be managed temporarily with drugs such as beta blockers.[42]

Long-term management of hyperthyroidism may include drugs that suppress thyroid function such as propylthiouracil, carbimazole and methimazole.[43] 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.[44] 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 hormone therapy will be needed.[45][42]


Main article: Hypothyroidism

An underactive thyroid gland results in hypothyroidism. Typical symptoms are abnormal weight gain, tiredness, constipation, heavy menstrual bleeding, baldness, cold intolerance, and a slow heart rate.[41] Hypothyroid disorders may occur as a result of autoimmune disease such as Hashimoto's thyroiditis; iodine deficiency; as a result of medical treatments such as surgical removal or radioablation of the thyroid, amiodarone and lithium; as a result of congenital thyroid abnormalities; or as a result of diseases such as amyloidosis or sarcoidosis or because of transient inflammation of the thyroid.[46] Some forms of hypothyroidism can result in myxedema and severe cases can result in myxedema coma.[47]

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.[47] 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.[48]


Main article: Thyroid nodule

Thyroid nodules are often found on the gland, with a prevalence of 4–7%.[49] The majority of nodules do not cause any symptoms and are non-cancerous.[50] 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 [51] Nodules are more likely in females, those who are exposed to radiation, and in those who are iodine deficient.[49]

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.[50] 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.[49] 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.[51] Investigations of a malignant nodule, or when hyperthyroidism is present, is discussed in the "Cancer" section below.

There can be many nodules, which is termed a multinodular goiter, and this can sometimes be a toxic multinodular goiter.[51]


Main article: Goiter

An enlarged thyroid gland is called a goiter.[52] Goiters are present in some form in about 5% of people,[51] 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, infltrative disease such as sarcoidosis and amyloidosis. Sometimes no cause can be found, a state called "simple goiter".[53]

Some forms of goiter are associated with pain, whereas many do not cause any symptoms. Enlarged goiters may extend beyond the normal position of the thyroid gland to below the sternum, around the airway or esophagus.[51] Goiters may be associated with causes or hyperthyoidism, hypothyroidism, relating to the underlying cause.[51] Thyroid function tests may be done to investigate the cause and effects of the goiter. The underlying cause of the goiter may be treated, however many goiters with no associated symptoms are simply monitored.[51]


Main article: Thyroid disease

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 goiter.


Main article: Thyroiditis

Inflammation of the thyroid is called thyroiditis. There are two types of thyroiditis where initially hyperthyroidism presents which is followed by a period of hypothyroidism; (the overproduction of T3 and T4 followed by the underproduction of T3 and T4). These are Hashimoto's thyroiditis and postpartum thyroiditis.

Hashimoto's thyroiditis or Hashimoto's disease is an autoimmune disorder whereby the body's own immune system reacts with the thyroid tissues in an attempt to destroy it. At the beginning, the gland may be overactive, and then becomes underactive as the gland is damaged resulting in too little thyroid hormone production or hypothyroidism. Some patients may experience "swings" in hormone levels that can progress rapidly from hyper-to-hypothyroid (sometimes mistaken as severe mood swings, or even being bipolar, before the proper clinical diagnosis is made). Some patients may experience these "swings" over a longer period of time, over days or weeks or even months.Hashimoto's is more common in females than males, usually appearing after the age of 30, and tends to run in families, meaning it can be seen as a genetic disease. Also more common in individuals with Hashimoto's thyroiditis are type 1 diabetes and celiac disease.[54]

Postpartum thyroiditis occurs in some females following childbirth due to the development of immune tolerance in pregnancy. After delivery, the gland becomes inflamed and the condition initially presents with overactivity of the gland followed by underactivity. In some cases, the gland may recover with time and resume its functions. In others it may not. The etiology is not always known, but can sometimes be attributed to an autoimmune disorder, such as Hashimoto's thyroiditis or Graves' disease.

There are other disorders that cause inflammation of the thyroid, and these include subacute thyroiditis, acute thyroiditis, silent thyroiditis, Riedel's thyroiditis.[55] and palpation thyroiditis.[56]


Main article: Thyroid cancer

The most common neoplasm affecting the thyroid gland is a benign adenoma, usually presenting as a painless mass in the neck.[57] Malignant thyroid cancers are most often carcinomas, although cancer can occur in any tissue that the thyroid consists of, including C-cells, lymphomas. Cancers from other sites also rarely lodge in the thyroid.[57] 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.[57]

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.[58] Most malignant thyroid cancers are papillary, followed by follicular, medullary, and thyroid lymphoma.[57][58] 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.[57][59]

Thyroid cancers are treated by removing the whole thyroid gland with the cancer in it. A large amount of radioactive Iodine 131 is given to radioablate the thyroid. Thyroxine is given to replace the hormones lost and to suppress TSH production, which may stimulate recurrence.[59]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.[60]


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.[20]

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.

Iodine deficiency and excess

Child affected by cretinism, associated with a lack of iodine.[61]

In areas of the world where iodine is lacking in the diet, particularly in mountainous regions and inland, iodine deficiency can cause the thyroid gland to become considerably enlarged, a condition called an endemic goiter.[62] Pregnant women on a diet that is severely deficient of iodine can give birth to infants with thyroid hormone deficiency (congenital hypothyroidism), manifesting in problems of physical growth and development as well as brain development (a condition referred to as endemic cretinism).[62][18] In many developed countries, newborns are routinely tested for congenital hypothyroidism as part of newborn screening. Children with congenital hypothyroidism are treated supplementally with levothyroxine, which facilitates normal growth and development.[63]

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.[64]

The use of iodised salt is an efficient way to add iodine to the diet.[18] It has eliminated endemic cretinism in most developed countries,[65] and some governments have made the iodination of flour, cooking oil, and salt mandatory. Potassium iodide and sodium iodide are typically used forms of supplemental iodine.

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.[66]

Grave's disease

Main article: Grave's disease

Graves' disease is an autoimmune disorder that is the most common cause of hyperthyroidism.[67] 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 cold intolerance, weight loss, diarrhoea and palpitations . Occasionally such antibodies block but do not activate the receptor, leading to symptoms associated with hypothyroidism.[67] In addition, gradual protrusion of the eyes may occur, called Graves' ophthalmopathy, as may swelling of the front of the shins.[67] 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.[67]


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

The thyroid itself is examined by observation of the gland and surrounding neck for swelling or enlargement.[68] 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.[68] 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.[69] The character of the thyroid, swellings, nodules, and their consistency may all be able to be felt. If a goiter 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.[70][68]


Blood tests

There are a number of blood tests that can be used to test the function of the thyroid. 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.[71] They may reveal hyperthyroidism (high T3 and T4), hypothyroidism (low T3, T4), or subclinical hyperthyroidism (normal T3 and T4 with a low TSH).[71]

The total level of T3 and T4 may be measured. The two thyroid hormones travel bound to other molecules, and it is the "free" component that is biologically active - hence free T3 and free T4 levels may be measured instead.[71] T4 is preferred, because in hypothyroidism T3 levels may be normal.[71] The levels of thryoglobulin and throxine-binding globulin change (TBG, for example, may be elevated in pregnancy) may also be measured, as this will affect how much of the hormones are bound and unbound.[72]

TSH levels are considered the most sensitive marker of thyroid dysfunction.[71] 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.[71]

Test Abbreviation Normal ranges[73]
Thyroid hormone binding ratio THBR 0.9–1.1
Thyroid microsomal antibody titer TMAb Varies with method
Thyroglobulin antibody titer TgAb Varies with method


Ultrasound of the thyroid may be used to reveal whether structures are solid or filled with fluid, helping to differentiate between nodules and goiters and cysts. It may also help differentiate between malignant and benign lesions.[74] When further imaging is required, a radiolabelled iodine-123 or technetium-99 uptake scan may take place. This can the size and shape of lesions, reveal whether nodules or goiters are metabolically active, and reveal and monitor sites of thyroid disease or cancer deposits outside the thyroid.[75]


A fine needle aspiration biopsy may be taken of thyroid tissue to determine the nature of a lesion. These biopsies are then sent for histopathology and cytology.[76]


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 BC.

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.[77] Treatment of goitre was mentioned in 2700 BC in the Compendium of Materia Medica (本草纲目).[77] In Ayurvedic medicine, the book Sushruta Samhita written about 1400 BC mentions the disease goitre as 'Galaganda' along with its treatment.[78] In 1600 BC the Chinese were using burnt sponge and seaweed for the treatment of goitres, a practice which has developed in many parts of the world.[77][78] Hippocrates and Plato both described the thyroid gland as a salivary gland. Pliny referred to epidemics of goitre in the Alps and proposed treatment with burnt seweed.[77] In Galen, an instrumental figure in the transition from ancient to modern medicine, referred to 'spongia usta' (burnt sponge) for the treatment of goitre.[77] Ali ibn Abbas al-Magusi in 990 conducted the first recorded thyroidiectomy.[79]

In 1110 a Persian scientist was the first to describe symptoms associated with Grave's disease, describing protruding eyes and goitre,[79] although Robert Graves himself only described it in 1834.[78]

There are several findings that evidence a great interest for thyroid disorders just in the Medieval Medical School of Salerno (12th century). Rogerius Salernitanus, the Salernitan surgeon and author of "Post mundi fabricam" (around 1180) was considered at that time the surgical text par excellence all over Europe. In the chapter "De bocio" of his magnum opus, he describes several pharmacological and surgical cures, some of which nowadays are reappraised as scientifically effective.[80]

A Chinese physician Wang Hei recommended that the treatment of goitre should be dried minced thyroid.[77] Paracelsus, some fifty years later, attributed goitre to mineral impurities in the water.

In 1500 Leonardo da Vinci first recognised and drew the thyroid.[77] In 1543 Andreas Vesalius gave the first description and illustration of the gland.[77] In 1956 the thyroid received its name, by the anatomist Thomas Wharton.[81] The gland was named thyroid, meaning shield, as its shape resembled the shields commonly used in Ancient Greece.[77][82] The English name thyroid gland[83] is derived from the medical Latin used by Wharton - glandula thyreoidea.[84] Glandula means gland in Latin,[85] and thyreoidea can be traced back to the Ancient Greek word θυρεοειδής, meaning shield-like/shield-shaped.[86]

In 1909, Theodor Kocher from Switzerland won the Nobel Prize in Physiology or Medicine "for his work on the physiology, pathology and surgery of the thyroid gland".[87] Thyroxine was first isolated in 1914 and synthesized in 1927.[88]

Other animals

Dog affected by a goiter

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.[89]

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.[89]

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).[89]

Thyroxine is critical to the regulation of metabolism and growth throughout the animal kingdom. Among amphibians, for example, 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. Iodine (and T4) trigger the amphibian metamorphosis that transforms the vegetarian aquatic tadpole into a carnivorous terrestrial adult frog, with better neurological, visuospatial, olfactory 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 terrestrial adults, and live and reproduce in the larval form of aquatic axolotl.[90][91]

Additional images

See also



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