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Anterior thyroid.jpg
The human thyroid as viewed from the front, with arteries visible.
Posterior thyroid.jpg
The thyroid as it may be seen from a posterior view, from behind the trachea
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
Thyroid gland
TA A11.3.00.001
FMA 9603
Anatomical terminology

The thyroid gland, or simply the thyroid /ˈθrɔɪd/, is one of the largest endocrine glands in the body, and consists of two connected lobes. It is found in the anterior neck, below the laryngeal prominence (Adam's apple). The thyroid gland controls the metabolic rate, protein synthesis, and controls the body's sensitivity to other hormones. The thyroid hormones regulate the growth and rate of function of many other systems in the body. T3 and T4 are synthesized from iodine and tyrosine. The thyroid also produces calcitonin, which plays a role in calcium homeostasis.

Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) produced by the anterior pituitary, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus.[1]

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.[2] 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.


The thyroid gland wraps round the front of the trachea, seen here with a pyramidal lobe

The thyroid gland is a butterfly-shaped organ and is composed of two lobes, one on the right and the left as the wings, and the narrow connecting isthmus as the body.[3][4]The thyroid is one of the larger endocrine glands, weighing 2-3 grams in neonates[citation needed] and 25 grams in adults, and is increased in pregnancy.[3] Each lobe is about 5 cm long, 3 cm wide and 2 cm thick, with the isthmus about 1.25 cm in length.[3] The lobes though are asymmetrical with the right lobe usually larger. The gland itself is usually larger in women.[4] The thyroid sits near the front of the neck, lying against and around the larynx and trachea.[3] The top of the thyroid lies below the thyroid cartilage (just below the laryngeal prominence, or 'Adam's Apple'), and extends to the fifth or sixth tracheal ring. It is difficult to demarcate the gland's upper and lower border with vertebral levels because it moves position in relation to these during swallowing.[5] However it usually spans from C5 to C7.[4]

The thyroid gland is covered by a thin fibrous sheath, the capsule of the thyroid.[3] The external layer is anteriorly continuous with the pretracheal fascia and posterolaterally continuous with the carotid sheath.[citation needed] The capsule extrudes into the gland itself and forms the septae that divides the thyroid tissue into microscopic lobules.[3]

The gland is covered anteriorly with infrahyoid muscles and laterally with the sternocleidomastoid muscle also known as sternomastoid muscle. On the posterior side, the gland is fixed to the cricoid and tracheal cartilage and cricopharyngeus muscle by a thickening of the fascia to form the posterior suspensory ligament of thyroid gland also known as Berry's ligament.[6][7] The thyroid gland's firm attachment to the underlying trachea is the reason behind its movement with swallowing.[8]

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.[9]

Two parathyroid glands usually lie on each side between the two layers of the capsule, at the back of the thyroid lobes.[3]

Blood, lymph, and nerve supply[edit]

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, branching directly from the subclavian artery.[3] The superior thyroid artery splits into anterior and posterior branches supplying the thyroid, and the inferior thyroid artery splits into superior and inferior branches.[3] 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.[3]

Lymphatic drainage passes frequently the deep lateral cervical lymph nodes, and the pretracheal and paratracheal lymph nodes. The gland is supplied by parasympathetic nerve input from the superior laryngeal nerve and the recurrent laryngeal nerve.


Isthmus showing pyramidal lobe position

Sometimes there is a third lobe present called the pyramidal lobe of the thyroid gland.[10] One study showed an 18.3% presence of this extra lobe.[11] Another study showed a presence of 44.6%.[12]The pyramidal lobe grows upwards from the isthmus to the hyoid bone. It was shown to more often arise from the left side and also to be mostly attached to the main gland with 9.2% shown to be separated.[11] The pyramidal lobe is a remnant of the thyroglossal duct (fetal thyroid stalk) which usually wastes away during the thyroid gland’s descent.[13]The pyramidal lobe is also known as Lalouette's pyramid.[14]

The thyroid isthmus is variable in its situation and size and can also change in shape. It can encompass the pyramidal lobe (lobus or processus pyramidalis.[citation needed] In variable extent, the pyramidal lobe is present at the most anterior side of the lobe.


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.[15]


Follicles are small spherical groupings of cells 0.02-0.9mm in diameter that play the main role in thyroid function.[3] 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.[3][16]

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.[3] Follicular cells vary in shape from flat to cuboid to columnar, depending on how active they are.[3][16]

Parafollicular cells

Scattered among follicular cells and in spaces between the spherical follicles are another type of thyroid cell, parafollicular cells.[3] These cells secrete calcitonin. Because the cytoplasm of these cells is clear, they are also called "C cells".[3]


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) at 18-20 weeks, and the production of thyroxine (T4) reaches a clinically significant level at this time.[18] Fetal triiodothyronine (T3) remains low (less than 15 ng/dL) until 30 weeks, and increases to 50 ng/dL at full-term.[18] Fetal self-sufficiency of thyroid hormones protects the fetus against (e.g., brain development abnormalities caused by maternal hypothyroidism).[19] However, preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones due their own thyroid being insufficiently developed to meet their postnatal needs.[20]

While it was originally thought that the portion of the thyroid containing the neuroendocrine parafollicular cells, also known as C cells, responsible for the production of calcitonin, are derived from neural crest, more recent research suggests that C-cells originate from pharyngeal endoderm. This is first seen 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 in the anterior neck.

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.


Thyroid hormones[edit]

Main article: Thyroid hormone

The primary function of the thyroid is production of the thyroid hormones triiodothyronine (T3) and thyroxine (T4) and calcitonin which plays a part in calcium metabolism.[21] T3 contains three atoms of iodine per molecule and T4 contains four atoms of iodine per molecule.[22] After it has been secreted, up to 85% of the T3 in blood is converted from T4 by deiodinase enzymes in organs around the body.[21] T3 is several times more powerful than T4, which is largely a prohormone, perhaps four[23] or even ten times more active.[24]

Only a very small proportion of the thyroid hormones travel freely in the blood. Most T4 and T3 hormones are bound to thyroxine-binding globulin, transthyretin, and albumin. Only 0.03% of T4 and 0.3% of T3 travels freely and it is only the free fraction that has hormonal activity.[25]

The thyroid hormones increase the basal metabolic rate and have affects on almost all body tissues.[26] Appetite, the absorption of substances, and gut motility are all influenced by thyroid hormones.[27] They increase the absorption in the gut, creation, uptake by cells and breakdown of glucose.[28] They stimulate the breakdown of fats, and increase free fatty acids.[28] Despite increasing free fatty acids, thyroid hormones decrease cholesterol levels, perhaps by increasing the rate of secretion of cholesterol in bile.[28]

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.[27] Combined, these factors increase blood flow and the body's temperature.[27]

Thyroid hormones are important for normal development.[28] They increase the growth rate of young people,[29] 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.[28]

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.[27] Sexual function, including libido and the maintenance of a normal menstrual cycle, are influenced by thyroid hormones.[27] In addition:

  • It is helps in conversion of carotene into vitamin A in hepatic cells, therefore, hypothyroidism may lead to high levels of carotene in the blood, resulting in yellowish tint of only skin (and not the mucous membrane, like sclera) called as carotenemia. It increases vitamin requirements.
  • Decreased level of thyroid hormone result in retention of glycoproteins in the skin, which results in water retention (due to polyolic nature) and myxedema.
  • The hormones decrease reflex time.

Thyroid hormones cross the cell membrane and bind to intracellular receptors1, α2, β1 and β2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription.[25]

In addition to these actions on DNA, the thyroid hormones also act within the plasma membrane or within cytoplasm. Plasma membrane-initiated actions begin at a receptor on the integrin alpha-v beta-3 that activates ERK1/2. This binding culminates in local membrane actions on ion transport systems such as the Na+/H+ exchanger or complex cellular events including cell proliferation. These integrins are concentrated on cells of the vasculature and on some types of tumor cells, which in part explains the proangiogenic effects of iodothyronines and proliferative actions of thyroid hormone on some cancers including gliomas. T4 also acts on the mitochondrial genome via imported isoforms of nuclear thyroid receptors to affect several mitochondrial transcription factors. Regulation of actin polymerization by T4 is critical to cell migration in neurons and glial cells and is important to brain development.

T3 can activate phosphatidylinositol 3-kinase by a mechanism that may be cytoplasmic in origin or may begin at integrin alpha V beta3.

Hormone production[edit]

The system of the thyroid hormones T3 and T4.[30]
Synthesis of the thyroid hormones, as seen on an individual thyroid follicular cell:[31]
- 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.[32]
- 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.

Thyroxine (T4) is synthesised by the follicular cells from the tyrosine residues of the protein called thyroglobulin (Tg). It has 123 tyrosine residues, but only 4-6 are active. Iodine is captured with the "iodine trap" by the hydrogen peroxide generated by the enzyme thyroid peroxidase (TPO)[33] and linked to the 3' and 5' sites of the benzene ring of the tyrosine residues on Tg sequentially on tyrosine residue forming monoiodotyrosine (MIT) and then diiodotyrosine (DIT) (iodination). Two DIT can couple (coupling) to form T4 hormone attached to thyroglobulin releasing one alanine. Upon stimulation by the thyroid-stimulating hormone (TSH), the follicular cells reabsorb Tg and cleave the iodinated tyrosines from Tg in lysosomes, forming free T4, (fT4), DIT, MIT, T3 and traces of reverse triiodothyronine (rT3) (in T3 and rT3 has three iodine atom while T4 has four), and releasing T3 and T4 into the blood. Deiodinase releases the sequestred iodine from MIT and DIT. Deiodinase enzymes convert T4 to T3 and RT3, [34] which is a major source of both RT3 (95%) and T3 (87%) in peripheral tissues.[35] Thyroid hormone secreted from the gland is about 80-90% T4 and about 10-20% T3.[23][24]

Iodide—the ionized form of iodine—is essential for proper thyroid function. Iodide is taken up by follicular cells through the sodium-iodide symporter (NIS) present on the basolateral membrane, which transports two sodium cations and one iodide ion into the cell. It works against the iodide concentration gradient and uses energy of sodium gradient (maintained by the sodium-potassium pump) and therefore acts by secondary active transport. Thus, NIS help to maintain a 20- to 40-fold difference in iodide concentration across the membrane.[36] This iodide is transported to the follicular space through the apical membrane of the follicular cell with the help of the iodide-chloride antiporter pendrin. This iodide is then oxidized to iodine and attached to thyroglobulin by the enzyme thyroid peroxidase to form the precursors of thyroid hormones.[1]


The production of thyroxine and triiodothyronine is primarily regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary. The thyroid, and thyrotropes in the anterior pituitary, form a negative feedback loop: TSH production is suppressed when the free T4 levels are high. The negative feedback occurs on both the hypothalamus and the pituitary, but it is of particular importance at the level of the pituitary[37] The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus. This 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 (SRIH) 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.

An additional hormone produced by the thyroid contributes to the regulation of blood calcium levels. Parafollicular cells produce calcitonin in response to hypercalcemia. Calcitonin stimulates movement of calcium into bone, in opposition to the effects of parathyroid hormone (PTH). However, calcitonin seems far less essential than PTH, as calcium metabolism remains clinically normal after removal of the thyroid (thyroidectomy), but not the parathyroids.

Clinical significance[edit]

Main article: Thyroid disease

Thyroid disorders include

All these disorders may give rise to a goiter, that is, an enlarged thyroid.



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.[38] 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.[39] Such symptoms may be managed temporarily with drugs such as beta blockers.[40]

Long-term management of hyperthyroidism may include drugs that suppress thyroid function such as propylthiouracil, carbimazole and methimazole.[41] 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.[42] 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.[43][40]


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.[39] 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.[44] Some forms of hypothyroidism can result in myxedema and severe cases can result in myxedema coma.

Hypothyroidism is treated with hormone therapy, such as the synthetic levothyroxine, which is typically required for the rest of the patient's life. Thyroid hormone treatment is given under the care of a physician and may take a few weeks to become effective.[45]

Negative feedback mechanisms result in growth of the thyroid gland when thyroid hormones are being produced in sufficiently low quantities, as a means of increasing the thyroid output; however, where hypothyroidism is caused by iodine insufficiency, the thyroid is unable to produce T3 and T4 and as a result, the thyroid may continue to grow to form a non-toxic goiter. It is termed non-toxic as it does not produce toxic quantities of thyroid hormones, despite its size.


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.[46]

Thyroid function tests[edit]

There are a number of blood tests that can be used to test the function of the thyroid:

Test Abbreviation Normal ranges[47]
Serum thyrotropin/thyroid-stimulating hormone TSH 0.5–6.0 μU/ml
Free thyroxine fT4 7–18 ng/l = 0.7–1.8 ng/dl
Serum triiodothyronine T3 0.8–1.8 μg/l = 80–180 ng/dl
Radioactive iodine-123 uptake RAIU 10–30%
Radioiodine scan (gamma camera) N/A N/A - thyroid contrasted images
Free thyroxine fraction fT4F 0.03–0.005%
Serum thyroxine T4 46–120 μg/l = 4.6–12.0 μg/dl
Thyroid hormone binding ratio THBR 0.9–1.1
Free thyroxine index fT4I 4–11
Free triiodothyronine l fT3 230–619 pg/d
Free T3 Index fT3I 80–180
Thyroxine-binding globulin TBG 12–20 ug/dl T4 +1.8 μg
TRH stimulation test Peak TSH 9–30 μIU/ml at 20–30 min.
Serum thyroglobulin l Tg 0-30 ng/m
Thyroid microsomal antibody titer TMAb Varies with method
Thyroglobulin antibody titer TgAb Varies with method
  • μU/ml = mU/l, microunit per milliliter
  • ng/dl, nanograms per deciliter
  • μg, micrograms
  • pg/d, picograms per day
  • μIU/ml = mIU/l, micro-international unit per milliliter
  • See [1] for more information on medical units of measure

As of early 2015, in the United States, new guidelines for TSH levels have been implemented as endorsed by The American Association of Clinical Endocrinologists. The new range is a TSH of 0.45 to 4.12.[48]



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.[49]

Postpartum thyroiditis occurs in some females following the birth of a child. 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 autoimmunity, 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 and Riedel's thyroiditis.[50]


Main article: Thyroid cancer

In most cases, thyroid cancer presents as a painless mass in the neck. It is very unusual for thyroid cancers to present with symptoms, unless they have been neglected. One may be able to feel a hard nodule in the neck. Diagnosis is made using a needle biopsy and various radiological studies.[51]

Non-cancerous nodules[edit]

Further information: Thyroid nodule

Thyroid nodules are often found on the gland. The majority of these nodules are benign (non cancerous), and their presence does not necessarily indicate disease. Most thyroid nodules do not cause any symptoms, and are mostly discovered on an incidental examination. Often there can be many nodules, which is termed a multinodular goiter. Doctors usually perform a needle aspiration biopsy of the thyroid to determine the status of the nodules. If the nodule is found to be non-cancerous, no other treatment is required. If the nodule is suspicious then surgery is recommended.

Congenital disorders[edit]

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. These occur at any age and might not become evident until adult life. 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.[citation needed]

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

Iodine deficiency and excess[edit]

Child affected by Cretinism, associated with a lack of iodine. [52]

In areas of the world where iodine is lacking in the diet, the thyroid gland can become considerably enlarged, a condition called endemic goiter. 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). 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.

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.[53]

The use of iodised salt is an efficient way to add iodine to the diet. It has eliminated endemic cretinism in most developed countries, 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.[54]


Historical references to what we now know as the thyroid gland arise early in medical history. In Ayurvedic medicine, the book Sushruta Samhita written about 1500 BC mentions the disease goitre as 'Galaganda' along with its treatment. In 1600 BC the Chinese were using burnt sponge and seaweed for the treatment of goitres (enlarged thyroid glands). Celsus first described a bronchoceole (a tumour of the neck) in 15 AD. Around this time Pliny referred to epidemics of goitre in the Alps and also mentioned the use of burnt seaweed in their treatment, in the same way as the Chinese had done 1600 years earlier. In 150 AD Galen, an instrumental figure in the transition from ancient to modern medicine, referred to 'spongia usta' (burnt sponge) for the treatment of goitre. He also suggested (incorrectly, as it turns out) that the role of the thyroid was to lubricate the larynx.

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.[55]

It was not until 1475 that Wang Hei anatomically described the thyroid gland and recommended that the treatment of goitre should be dried thyroid. Paracelsus, some fifty years later, attributed goitre to mineral impurities in the water.

In modern times, the thyroid was first identified in 1656 by the anatomist Thomas Wharton (whose name is also eponymised in Wharton's duct of the submandibular gland).[56] In 1656 Thomas Wharton named the gland the thyroid, meaning shield, as its shape resembled the shields commonly used in Ancient Greece.

In 1909, Theodor Kocher from Switzerland won the Nobel Prize in Medicine "for his work on the physiology, pathology and surgery of the thyroid gland".[57]


The English name thyroid gland[58] is derived from Latin glandula thyreoidea.[59] Glandula means gland in Latin,[60] and thyreoidea can be traced back to the Ancient Greek word θυρεοειδής, meaning shield-like/shield-shaped.[61]

Other animals[edit]

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.[62]

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.[62]

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).[62]

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.[63][64]

Additional images[edit]

See also[edit]


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  2. ^ Longo, D; Fauci, A; Kasper, D; Hauser, S; Jameson, J; Loscalzo, J (2012). Harrison's Principles of Internal Medicine (18th ed.). New York: McGraw-Hill. pp. 2913, 2918. ISBN 978-0071748896. 
  3. ^ a b c d e f g h i j k l m n o p editor-in-chief, Susan Standring ; section editors, Neil R. Borley; et al. (2008). Gray's anatomy : the anatomical basis of clinical practice (40th ed.). London: Churchill Livingstone. pp. 462–464. ISBN 978-0-8089-2371-8. 
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  • Longo, Dan; Fauci, Anthony; Kasper, Dennis; Hauser, Stephen; Jameson, J.; Loscalzo, Joseph (August 11, 2011). Harrison's Principles of Internal Medicine (18 ed.). McGraw-Hill Professional. ISBN 978-0-07-174889-6. 
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