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Enlargement of the thyroid gland, seen as a swelling in the neck, commonly due to deficiency of iodine in the diet or to the presence of goitrogens in foods. In such cases there is commonly underproduction of the thyroid hormones, i.e. hypothyroid goitre. Euthyroid goitre is a condition in which the enlargement of the thyroid gland is sufficient to compensate for a modest deficiency of iodine, permitting normal production of thyroid hormones.

In infancy, iodine deficiency can also lead to severe mental retardation, goitrous cretinism. Supplementation with iodine often prevents the condition, hence the use of iodized salt. Goitre may be due to other causes, including excessive stimulation of the thyroid gland. In this case there is overproduction of the thyroid hormones, i.e. hyperthyroid goitre.

Goitre is defined as an enlargement of the thyroid gland which can be seen as a swelling in the front of the neck. There are several types of goitre which are features of different thyroid disorders.

Endemic goitre

On a worldwide basis, this is the most notable class of goitre. It arises because of insufficient iodine in the diet. This occurs in regions of the world where the iodine content of the normal diet or drinking water falls below the minimum requirement of about 25 mg/day. At least 1 billion people worldwide are at risk of iodine deficiency. Whereas most of these live in mountainous areas of developing countries, even in Europe 50-100 million people (15-30%) inhabit areas of at least moderate deficiency. In Britain the best recognized region is the Peak District and this is the reason why this goitrous condition is known colloquially as ‘Derbyshire neck’: but iodination of table salt has now made it rare.

The thyroid is unique in its ability to extract iodine from the blood and utilize it for the biosynthesis of hormones. The thyroid gland itself is positively regulated by a hormone from the pituitary gland named ‘thyroid stimulating hormone’, (TSH). The relationship between the pituitary and the thyroid is a classic example of negative feedback: the secretion of thyroid hormones influences TSH secretion from the pituitary; excessive secretion from the thyroid gland raises the concentration of thyroid hormones in the blood, which switches off TSH secretion by the pituitary. Conversely, if the rate of thyroid hormone secretion is inappropriately low, TSH from the pituitary increases.

It is this negative feedback regulation which results in the endemic goitres found in iodine-deficient regions. Iodine is an essential component of both thyroid hormones (T3 and T4). When there is insufficient iodine in the diet the thyroid is unable to synthesize and secrete sufficient quantities of T4 or, in the most restrictive conditions, of T3. As a consequence, pituitary secretion of TSH increases. This ‘trophic’ hormone stimulates both the function and the growth of the thyroid gland, so that it enlarges, eventually forming a goitre. In stimulating growth, TSH acts in conjunction with other growth factors, produced locally within the thyroid gland itself. Endemic goitres are however limited in size, and it is now thought that one of the local growth factors acts as a negative regulator.

Iodine deficiency is prevented by its addition to staple foods such as household salt, bread, and cheese. Iodine can also be effective when given by injection as an intramuscular depot of a slowly resorbable iodized oil. On a long-term basis this leads to the disappearance of goitres, but a more rapid resolution may be obtained surgically.

The correct level of iodine supplementation for household salt was first determined in the 1930s by Purves, in the University of Otago, New Zealand. He showed that when the salt was appropriately supplemented, the levels of iodine excreted in the urine of nurse volunteers in the city of Dunedin increased to equate with those excreted by a control group selected from the inhabitants of an iodine-replete Pacific island. When the suitably iodized salt was subsequently used prophylactically throughout Otago, there was a dramatic decline in the incidence of goitre in the populace of this province.

Goitres in iodine-abundant environments

A variety of goitrous conditions occur which are not due to iodine deficiency in the diet. These range from non-toxic, so-called ‘sporadic’, goitres to those associated with autoimmune hyper- and hypothyroidism. In addition there are rare inborn errors of thyroid hormone biosynthesis which usually cause congenital hypothyroidism, high TSH, and a goitre. Thus a goitre per se does not reveal the thyroid status of the person, as it may be associated with either under- or overactivity of the gland or may be present in a ‘euthyroid’ individual — one with normal hormone levels.

There is a range of techniques for investigating the nature of a goitre, from manual examination by a skilled thyroidologist (needle aspiration biopsy), to imaging techniques such as radiology, ultrasound, radionuclide scanning, computed tomography, and, more recently, magnetic resonance imaging. These are useful both in discriminating the goitre type and also in observing changes such as shrinking of thyroid volume following treatment. Conventional radiology provides information on the effects of goitre growth on surrounding tissues; for example it identifies goitres which are pressing on the windpipe, causing breathing difficulties, and require prompt surgical intervention.

A large proportion of patients who have either an over- or an underactive thyroid suffer from autoimmune conditions and their thyroids exhibit varying degrees of infiltration by lymphocytes. In the hyperthyroidism of Grave's disease we have a unique example of antibodies (known as thyroid stimulating antibodies) which mimic the action of a pituitary trophic hormone, namely TSH. This leads to persistent and unregulated stimulation of the thyroid. A diffuse and symmetrical goitre is often present. Conversely in the hypothyroidism of Hashimoto's disease there is autoimmune destruction of thyroid follicular cells, leading to underproduction of the hormones and eventually to thyroid failure. Large multinodular goitres are characteristic of this condition; there is extensive lymphocytic infiltration and with the passage of time mere remnants of thyroid follicles.

Aberrant growth within the thyroid may produce solitary nodules. These can be ‘hot’, when they avidly accumulate orally administered radioactive isotopes of iodine and usually suppress the activity of the surrounding thyroid tissue. Alternatively they may be non-functional — ‘cold’ — when iodine uptake is abnormally low. About 10% of these ‘cold’ nodules are malignant; however the overall incidence of thyroid cancer is very low, with only about 750 newly diagnosed cases reported annually in all of England and Wales.

Thus goitres occur in several different forms, due to a variety of widely differing causes, some of which are at present only poorly understood. It is likely that advances in our knowledge of local regulators of thyroid growth, including some subtle effects of iodine which have recently come to light, will lead to improved understanding and management.

Goitres are long-recognized clinical and cosmetic problems: they influenced even male fashions in the Regency period when high collars were adopted to alleviate the embarrassment of the Prince Regent who suffered from an unsightly goitre. Indeed his search for a cure, by daily drinking several pints of sea water, presumably influenced his choice of Brighton for the location of his Pavilion. Conversely, small goitres, particularly in women, have been considered marks of beauty. Examples are seen in some of Lely's portraits of ladies of the seventeenth century Dutch court.

— N. J. Marshall

See also hormones; hyperthyroidism; hypothyroidism; thyroid.

Goiter is an enlargement of the thyroid gland. It may be diffuse, involving all thyroid tissue, or it may be caused by one or more lumps (nodules)—called nodular goiter. Diffuse goiter reflects an underlying thyroid problem, most commonly iodine deficiency in iodine-deficient areas of the world, where nearly 1 billion people may be subject to the disorder. In the United States, iodine deficiency is rare (because of widespread use of iodized salt) and goiter is most commonly caused by Graves' disease or Hashimoto's disease. Nodular goiter affects 3 to 5 percent of adults, mainly women. Nodules may reflect thyroid cancer (in 5% of cases), but the remainder are benign processes due to multiple causes. Cancers can be distinguished from benign disease by microscopic evaluation of thyroid tissue obtained by fine-needle aspiration biopsy.

(SEE ALSO: Hyperthyroidism; Hypothyroidism; Iodine; Thyroid Disorders; Thyroid Function Tests)

Bibliography

Gharib, H. (1999). "Nontoxic Diffuse and Nodular Goiter." In Atlas of Clinical Endocrinology, Vol. 1: Thyroid Diseases, ed. M. I. Surks. Philadelphia, PA: Current Medicine.

— MARTIN I. SURKS

A goiter is an enlargement of the thyroid gland caused by hypothyroidism (too little thyroxin). An insufficient dietary intake of iodine is a common cause of goiter.

An enlargement of the thyroid gland.

• Afflictions and Conditions - goiter: swollen neck due to enlarged thyroid gland

Goiter
Classification and external resources
ICD-10	E01-E05
ICD-9	240.9
DiseasesDB	5332
MedlinePlus	001178
MeSH	D006042

A goitre or goiter (Latin gutteria, struma), is a swelling in the thyroid gland,^[1] which can lead to a swelling of the neck or larynx (voice box). Goitre is a term that refers to an enlargement of the thyroid (thyromegaly) and can be associated with a thyroid gland that is functioning properly or not.

Worldwide, over 90% cases of goitre are caused by iodine deficiency.^[2]

Contents 1 Signs and symptoms 2 Morphology 3 Causes 4 Epidemiology 5 Treatment 6 History 7 Society and culture 7.1 Famous goitre sufferers 8 Heraldry 9 See also 10 References 11 External links

Signs and symptoms

Goitre associated with hypothyroidism or hyperthyroidism may be present with symptoms of the underlying disorder, although the symptoms are often unspecific and hard to diagnose, weight loss despite increased appetite, and heat intolerance.

Morphology

Struma nodosa (Class II)

Struma with autonomous adenoma

Struma Class III

Regarding morphology, goitres may be classified either as the growth pattern or as the size of the growth:

Growth pattern

• Uninodular (struma uninodosa) - can be either inactive or a toxic nodule
• Multinodular (struma nodosa) - can likewise be inactive or toxic, the latter called toxic multinodular goitre
• Diffuse (struma diffuse), with the whole thyroid appearing to be enlarged.

Size

• Class I - palpation struma - in normal posture of the head, it cannot be seen; it is only found by palpation.
• Class II - the struma is palpative and can be easily seen.
• Class III - the struma is very large and is retrosternal; pressure results in compression marks.

Causes

Worldwide, the most common cause for goitre is iodine deficiency, usually seen in countries that do not use iodized salt. Selenium deficiency is also considered a contributing factor. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause.^[3]

Cause	Pathophysiology	Resultant thyroid activity	Growth pattern	Treatment	Incidence and prevalence	Prognosis
Iodine deficiency	Hyperplasia of thyroid to compensate for decreased efficacy	Can cause hypothyroidism	Diffuse	Iodine	Constitutes over 90% cases of goitre worldwide[2]	Increased size of thyroid may be permanent if untreated for around five years
Congenital hypothyroidism	Inborn errors of thyroid hormone synthesis	Hypothyroidism
Goitrogen ingestion
Adverse drug reactions
Hashimoto's thyroiditis	Autoimmune disease in which the thyroid gland is gradually destroyed	Hypothyroidism	Diffuse and lobulated[4]	Thyroid hormone replacement	Prevalence: 1 to 1.5 in a 1000	Remission with treatment
Pituitary disease	Hypersecretion of thyroid stimulating hormone, almost always by a pituitary adenoma[5]		Diffuse	Pituitary surgery	Very rare[5]
Graves' disease - also called Basedow syndrome	Autoantibodies (TSHR-Ab) that activate the TSH-receptor (TSHR)	Hyperthyroidism	Diffuse	Antithyroid agents, radioiodine, surgery	1 to 2 cases per 1,000 population per year	Remission with treatment, but still lower quality of life for 14 to 21 years after treatment, with lower mood and lower vitality, regardless of the choice of treatment[6]
Thyroiditis	Acute or chronic inflammation	Can be hyperthyroidism initially, but progress to hypothyroidism
Thyroid cancer			Usually uninodular			Overall relative 5-year survival rate of 85% for females and 74% for males[7]
Benign thyroid neoplasms		Usually hyperthyroidism	Usually uninodular			Mostly harmless
Thyroid hormone insensitivity		Secretional hyperthyroidism, Symptomatical hypothyroidism	Diffuse

• Sarcoidosis
• amyloidosis
• hydatiform mole
• cysts
• acromegaly

Epidemiology

Disability-adjusted life year for iodine deficiency per 100,000 inhabitants in 2002.^[8]

  no data

  less than 50

  50-100

  100-150

  150-200

  200-250

  250-300

  300-350

  350-400

  400-450

  450-500

  500-800

  more than 800

Goitre is more common among women, but this includes the many types of goitre caused by autoimmune problems, and not only those caused by simple lack of iodine.

Some researchers ^[9] showed a correlation between Iodine-deficient goitre and gastric cancer, and reported in goitrous territories a decrease of the incidence of goitre and of stomach cancer after implementation of iodine-prophylaxis.^[10] The proposed mechanism of action is that iodide ion (I-) can function in thyroid gland and in gastric mucosa as an antioxidant ^[11] reducing species that can detoxify poisonous reactive oxygen species, such as hydrogen peroxide.

Treatment

Goitre only needs to be treated if it is causing the enlargement of the thyroid or thyroid gland. If the thyroid is producing too much T3 and T4, radioactive iodine is exposed to the victim to shrink the gland. If it is caused by iodine deficiency, small doses of Lugol’s Iodine or KI solution are given. If the goitre is due to underactive thyroid, thyroid supplements are used as treatment. In extreme cases, a partial or complete thyroidectomy is required. ^[12]

History

Chinese physicians of the Tang Dynasty (618–907) were the first to successfully treat patients with goitre by using the iodine-rich thyroid gland of animals such as sheep and pigs—in raw, pill, or powdered form.^[13] This was outlined in Zhen Quan's (d. 643 AD) book, as well as several others.^[14] One Chinese book, The Pharmacopoeia of the Heavenly Husbandman, asserted that iodine-rich sargassum was used to treat goitre patients by the 1st century BC, but this book was written much later.^[15]

In the 12th century, Zayn al-Din al-Jurjani, a Persian physician, provided the first description of Graves' disease after noting the association of goitre and exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time.^[16][17] Al-Jurjani also established an association between goitre and palpitation.^[18] The disease was later named after Irish doctor Robert James Graves, who described a case of goitre with exophthalmos in 1835. The German Karl Adolph von Basedow also independently reported the same constellation of symptoms in 1840, while earlier reports of the disease were also published by the Italians Giuseppe Flajani and Antonio Giuseppe Testa, in 1802 and 1810 respectively,^[19] and by the English physician Caleb Hillier Parry (a friend of Edward Jenner) in the late 18th century.^[20]

Paracelsus (1493–1541) was the first person to propose a relationship between goitre and minerals (particularly lead) in drinking water.^[21] Iodine was later discovered by Bernard Courtois in 1811 from seaweed ash.

Goitre was previously common in many areas that were deficient in iodine in the soil. For example, in the English Midlands, the condition was known as Derbyshire Neck. In the United States, goitre was found in the Great Lakes, Midwest, and Intermountain regions. The condition now is practically absent in affluent nations, where table salt is supplemented with iodine. However, it is still prevalent in India, China^[22] Central Asia and Central Africa.

Goitre had been prevalent in the alpine countries for a long time. Switzerland reduced the condition by introducing iodised salt in 1922. The Bavarian tracht in the Miesbach and Salzburg regions, which appeared in the 19th century, includes a choker, dubbed Kropfband (struma band) which was used to hide either the goitre or the remnants of goitre surgery.^[23]

Society and culture

Famous goitre sufferers

• Former President George H. W. Bush and his wife Barbara Bush both were diagnosed with Graves' disease and goitres, within two years of each other. In the president's case, the disease caused hyperthyroidism and cardiac dysrhythmia.^[24][25] Scientists said that the odds of both George and Barbara Bush having Graves’ disease might be 1 in 100,000 or as low as 1 in 3,000,000^[26]
• Andrea True (according to an interview on VH1)^[27]

Heraldry

The coat of arms and crest of Die Kröpfner, of Tyrol showed a man "afflicted with a large goitre," an apparent pun on the German for the word.^[28]

See also

Wikimedia Commons has media related to: Goiter

• Struma ovarii (a kind of teratoma)
• David Marine conducted substantial research on the treatment of goitre with iodine.
• Endemic goitre

References

1. ^ "goiter" at Dorland's Medical Dictionary
2. ^ ^{a b} R. Hörmann: Schilddrüsenkrankheiten. ABW-Wissenschaftsverlag, 4. Auflage 2005, Seite 15-37. ISBN 3-936072-27-2
3. ^ Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7.  8th edition.
4. ^ Babademez, M. A.; Tuncay, K. S.; Zaim, M.; Acar, B.; Karaşen, R. M. (2010). "Hashimoto Thyroiditis and Thyroid Gland Anomalies". Journal of Craniofacial Surgery 21 (6): 1807–1809. doi:10.1097/SCS.0b013e3181f43e32. PMID 21119426.  edit
5. ^ ^{a b} Thyrotropin (TSH)-secreting pituitary adenomas. By Roy E Weiss and Samuel Refetoff. Last literature review version 19.1: January 2011. This topic last updated: July 2, 2009
6. ^ Abraham-Nordling, Torring, Hamberger, Lundell, Tallstedt, Calissendorff, Wallin. Graves' Disease: A long-term quality-of-life follow-up of patients randomized to treatment with antithyroid drugs, radioiodine, or surgery, Thyroid 15, no. 11(2005), 1279-86
7. ^ Numbers from EUROCARE, from Page 10 in: F. Grünwald; Biersack, H. J.; Grںunwald, F. (2005). Thyroid cancer. Berlin: Springer. ISBN 3-540-22309-6. 
8. ^ "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. http://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls. 
9. ^ Abnet CC; Fan JH; Kamangar F et al (September 2006). "Self-reported goitre is associated with a significantly increased risk of gastric noncardia adenocarcinoma in a large population-based Chinese cohort". Int. J. Cancer 119 (6): 1508–10. doi:10.1002/ijc.21993. PMID 16642482. 
   Venturi S, Venturi A, Cimini D, Arduini C, Venturi M, Guidi A (January 1993). "A new hypothesis: iodine and gastric cancer". Eur. J. Cancer Prev. 2 (1): 17–23. doi:10.1097/00008469-199301000-00004. PMID 8428171. 
   Venturi S, Donati FM, Venturi A, Venturi M, Grossi L, Guidi A (January 2000). "Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach". Adv Clin Path 4 (1): 11–7. PMID 10936894. 
   
10. ^ Goł Kowski f, Szybiń Ski z, Rachtan J et al (August 2007). "Iodine prophylaxis--the protective factor against stomach cancer in iodine deficient areas". Eur J Nutr 46 (5): 251–6. doi:10.1007/s00394-007-0657-8. PMID 17497074. 
11. ^ Venturi S, Venturi M (April 1999). "Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?". Eur. J. Endocrinol. 140 (4): 371–2. doi:10.1530/eje.0.1400371. PMID 10097259. http://eje-online.org/cgi/pmidlookup?view=long&pmid=10097259. 
    
12. ^ http://health.nytimes.com/health/guides/disease/goiter/overview.html
13. ^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0-671-62028-2. Pages 133–134.
14. ^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0-671-62028-2. Page 134.
15. ^ Temple, Robert. (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. With a forward by Joseph Needham. New York: Simon and Schuster, Inc. ISBN 0-671-62028-2. Pages 134–135
16. ^ Basedow's syndrome or disease at Who Named It? - the history and naming of the disease
17. ^ Ljunggren JG (August 1983). "[Who was the man behind the syndrome: Ismail al-Jurjani, Testa, Flagani, Parry, Graves or Basedow? Use the term hyperthyreosis instead]". Lakartidningen 80 (32–33): 2902. PMID 6355710. 
18. ^ Nabipour, I. (2003). "Clinical Endocrinology in the Islamic Civilization in Iran". International Journal of Endocrinology and Metabolism 1: 43–45 [45] 
19. ^ Giuseppe Flajani at Who Named It?
20. ^ Hull G (1998). "Caleb Hillier Parry 1755-1822: a notable provincial physician". Journal of the Royal Society of Medicine 91 (6): 335–8. PMC 1296785. PMID 9771526. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1296785. 
21. ^ "Paracelsus" Britannica
22. ^ "In Raising the World’s I.Q., the Secret’s in the Salt", article by Donald G. McNeil, Jr., December 16, 2006, New York Times
23. ^ Kropfband bei planet-wissen.de
24. ^ Robert G. Lahita and Ina Yalof. Women and Autoimmune Disease: The Mysterious Ways Your Body Betrays Itself. Page 158.
25. ^ Lawrence K. Altman, M.D. “Doctors Say Bush Is in Good Health.” The New York Times. September 14, 1991.
26. ^ Lawrence K. Altman, M.D. “The Doctor’s World; A White House Puzzle: Immunity Ailments.”, The New York Times. May 28, 1991]
27. ^ “Andrea True.” Elle.
28. ^ Fox-Davies, Arthur Charles (1904). The Art of Heraldry: An Encyclopædia of Armory. New York and London: Benjamin Blom, Inc.. p. 413. 

External links

Wikimedia Commons has media related to: Goiters

• National Health Services, UK
• Network for Sustained Elimination of Iodine Deficiency
• Network for Sustained Elimination of Iodine Deficiency - alternate site at Emory University's School of Public Health
• A case and photograph of a huge goitre from Photobucket.com and Doctorkhodadoust.net

v t e Endocrine pathology: endocrine diseases (E00–E35, 240–259) Pancreas/ glucose metabolism Hypofunction Diabetes mellitus types: (type 1, type 2, MODY 1 2 3 4 5 6) · complications (coma, angiopathy, ketoacidosis, nephropathy, neuropathy, retinopathy, cardiomyopathy) insulin receptor (Rabson–Mendenhall syndrome) · Insulin resistance Hyperfunction Hypoglycemia · beta cell (Hyperinsulinism) · G cell (Zollinger–Ellison syndrome) Hypothalamic/ pituitary axes Hypothalamus gonadotropin (Kallmann syndrome, Adiposogenital dystrophy) · CRH (Tertiary adrenal insufficiency) · vasopressin (Neurogenic diabetes insipidus) · general (Hypothalamic hamartoma) Pituitary Hyperpituitarism anterior (Acromegaly, Hyperprolactinaemia, Pituitary ACTH hypersecretion) · posterior (SIADH) · general (Nelson's syndrome) Hypopituitarism anterior (Kallmann syndrome, Growth hormone deficiency, ACTH deficiency/Secondary adrenal insufficiency) · posterior (Neurogenic diabetes insipidus) · general (Empty sella syndrome, Pituitary apoplexy, Sheehan's syndrome, Lymphocytic hypophysitis) Thyroid Hypothyroidism Iodine deficiency · Cretinism (Congenital hypothyroidism) · Myxedema · Euthyroid sick syndrome Hyperthyroidism Hyperthyroxinemia (Thyroid hormone resistance, Familial dysalbuminemic hyperthyroxinemia) · Hashitoxicosis · Thyrotoxicosis factitia · Graves' disease Thyroiditis Acute infectious · Subacute (De Quervain's, Subacute lymphocytic) · Autoimmune/chronic (Hashimoto's, Postpartum, Riedel's) Goitre Endemic goitre · Toxic nodular goitre · Toxic multinodular goiter Thyroid nodule Parathyroid Hypoparathyroidism Pseudohypoparathyroidism Hyperparathyroidism Primary · Secondary · Tertiary · Osteitis fibrosa cystica Adrenal Hyperfunction aldosterone: Hyperaldosteronism/Primary aldosteronism (Conn syndrome, Bartter syndrome, Glucocorticoid remediable aldosteronism) · AME · Liddle's syndrome · 17α CAH cortisol: Cushing's syndrome (Pseudo-Cushing's syndrome) sex hormones: 21α CAH · 11β CAH Hypofunction/ Adrenal insufficiency (Addison's, WF) aldosterone: Hypoaldosteronism (21α CAH, 11β CAH) cortisol: CAH (Lipoid, 3β, 11β, 17α, 21α) sex hormones: 17α CAH Gonads ovarian: Polycystic ovary syndrome · Premature ovarian failure testicular: enzymatic (5-alpha-reductase deficiency, 17-beta-hydroxysteroid dehydrogenase deficiency) · Androgen receptor (Androgen insensitivity syndrome) general: Hypogonadism (Delayed puberty) · Hypergonadism (Precocious puberty) Height Gigantism · Dwarfism/Short stature (Laron syndrome, Psychosocial) Multiple Autoimmune polyendocrine syndrome (APS1, APS2) · Carcinoid syndrome · Multiple endocrine neoplasia (1, 2A, 2B) · Progeria (Werner syndrome, Acrogeria, Metageria) · Woodhouse-Sakati syndrome M: END anat/phys/devp/horm noco(d)/cong/tumr, sysi/epon proc, drug (A10/H1/H2/H3/H5)

This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

Dansk (Danish)
n. - struma, Basedowsk syge

Français (French)
n. - goitre

Deutsch (German)
n. - Kropf

Ελληνική (Greek)
n. - βρογχοκήλη

Italiano (Italian)
gozzo

Português (Portuguese)
n. - bócio (m) (Med.)

Русский (Russian)
зоб, базедова болезнь

Español (Spanish)
n. - bocio, coto

Svenska (Swedish)
n. - struma (med.)

中文（简体）(Chinese (Simplified))
甲状腺肿, 肿物

中文（繁體）(Chinese (Traditional))
n. - 甲狀腺腫, 腫物

한국어 (Korean)
n. - 갑상선 종양

日本語 (Japanese)
n. - 甲状腺腫

עברית (Hebrew)
n. - ‮זפקת (מחלה)‬

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