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Other names: Goiter
Diffuse hyperplasia of the thyroid
SymptomsSwelling of front of the neck[1]
ComplicationsCough, hoarseness, difficulty swallowing, shortness of breath[1]
TypesDiffuse, nodular, multinodular[2]
CausesIodine deficiency, Grave disease, toxic nodular goiter, thyroid cancer, autoimmune thyroiditis, postpartum thyroiditis, silent thyroiditis, radiation thyroiditis, subacute thyroiditis, suppurative thyroiditis[2]
Diagnostic methodExamination, medical imaging[2]
Differential diagnosisLymphadenopathy, pseudogoiter, branchial cleft cyst, thyroglossal duct cyst, parathyroid adenoma[2]
TreatmentWatchful waiting, iodine supplements, radioactive iodine, surgery[3]
Frequency16% (2004)[4]

Goitre is an enlarged of the thyroid gland.[2] This may result in swelling of the front of the neck.[1] In advanced cases a cough, hoarseness, difficulty swallowing, or shortness of breath may occur.[1] It can occur with normal, low, or high thyroid function.[2]

The most common cause is iodine deficiency.[2] Other causes include Grave disease, toxic nodular goiter, thyroid cancer, autoimmune thyroiditis, postpartum thyroiditis, silent thyroiditis, radiation thyroiditis, subacute thyroiditis, suppurative thyroiditis, sarcoidosis, and certain medications such as amiodarone.[2][5] It can be diagnosed by looking at the neck, feeling the neck, or medical imaging.[2]

Treatment depends on the underlying cause.[1] This may include watchful waiting, iodine supplements, radioactive iodine, or surgery.[3] Rates of goitre globally are about 16% as of 2004.[4] Females are affected four times more often than males.[2] It is more common in Africa and the Mediterranea region, and less common in the Americas.[4] The condition was first described around 2,700 BC in China.[6] The term is from the Latin guttur, meaning throat.[7]

Signs and symptoms

A goitre can present as a palpable or visible enlargement of the thyroid gland at the base of the neck. A goitre, if associated with hypothyroidism or hyperthyroidism, may be present with symptoms of the underlying disorder. For hyperthyroidism, the most common symptoms are associated with adrenergic stimulation: tachycardia (increased heart rate), palpitations, nervousness, tremor, increased blood pressure and heat intolerance. Clinical manifestations are often related to hypermetabolism, (increased metabolism), excessive thyroid hormone, an increase in oxygen consumption, metabolic changes in protein metabolism, immunologic stimulation of diffuse goitre, and ocular changes (exophthalmos).[8] Hypothyroid people commonly have poor appetite, cold intolerance, constipation, lethargy and may undergo weight gain. However, these symptoms are often non-specific and make diagnosis difficult.[citation needed]


Worldwide, the most common cause for goitre is iodine deficiency, commonly seen in countries that scarcely 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.[9] Goitre can also result from cyanide poisoning; this is particularly common in tropical countries where people eat the cyanide-rich cassava root as the staple food.[10]

Cause Mechanism Thyroid activity Growth pattern Treatment Frequency Outcomes
Iodine deficiency Hyperplasia of thyroid to compensate for decreased efficacy Can cause hypothyroidism Diffuse Iodine Constitutes over 90% cases of goitre worldwide[11] 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. Infiltration of lymphocytes. Hypothyroidism Diffuse and lobulated[12] 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[13] Diffuse Pituitary surgery Very rare[13]
Graves' disease—also called Basedow syndrome Autoantibodies (TSHR-Ab) that activate the TSH-receptor (TSHR) Hyperthyroidism Diffuse Antithyroid agents, radioiodine, surgery Will develop in about 0.5% of males and 3% of females 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[14]
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[15]
Benign thyroid neoplasms Usually hyperthyroidism Usually uninodular Mostly harmless[16]
Thyroid hormone insensitivity Secretional hyperthyroidism,
Symptomatic hypothyroidism


Goitre with toxic adenoma

Goitre may be diagnosed via a thyroid function test in an individual suspected of having it.[17]


A goitre may be classified either as nodular or diffuse. Nodular goitres are either of one nodule (uninodular) or of multiple nodules (multinodular).

Growth pattern
  • Uninodular goitre: one thyroid nodule; can be either inactive, or active (toxic) – autonomously producing thyroid hormone.
  • Multinodular goitre: multiple nodules;[18] can likewise be inactive or toxic, the latter is called toxic multinodular goitre and associated with hyperthyroidism. These nodules grow up at varying rates and secrete thyroid hormone autonomously, thereby suppressing TSH-dependent growth and function in the rest of gland. Inactive nodules in the same goitre can be malignant.[19] Thyroid cancer is identified in 13.7% of the patients operated for multinodular goitre.[20]
  • Diffuse goitre: the whole thyroid appearing to be enlarged due to hyperplasia.
  • Class I: the goitre in normal posture of the head cannot be seen; it is only found by palpation.
  • Class II: the goitre is palpable and can be easily seen.
  • Class III: the goitre is very large and is retrosternal (partially or totally lying below the sternum), pressure results in compression marks.


Goitre is treated according to the cause. If the thyroid gland is producing an excess of thyroid hormones (T3 and T4), radioactive iodine is given to the patient to shrink the gland. If goitre is caused by iodine deficiency, small doses of iodide in the form of Lugol's iodine or KI solution are given. If the goitre is associated with an underactive thyroid, thyroid supplements are used as treatment. Sometimes a partial or complete thyroidectomy is required.[21]


Disability-adjusted life year for iodine deficiency per 100,000 inhabitants in 2002.[22]
  no data
  fewer than 50
  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.[23]


Goitre and cretinism in Styria, copper engraving, 1815
Women in Miesbacher Tracht, including a goitre choker

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.[24] This was outlined in Zhen Quan's (d. 643 AD) book, as well as several others.[24] 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.[24]

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 a displacement of the eye known as exophthalmos in his Thesaurus of the Shah of Khwarazm, the major medical dictionary of its time.[25][26] Al-Jurjani also established an association between goitre and palpitation.[27] 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,[28] and by the English physician Caleb Hillier Parry (a friend of Edward Jenner) in the late 18th century.[29]

Paracelsus (1493–1541) was the first person to propose a relationship between goitre and minerals (particularly lead) in drinking water.[30] 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 is now practically absent in affluent nations, where table salt is supplemented with iodine. However, it is still prevalent in India, China,[31] 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.[32]

Society and culture

In the 1920s wearing bottles of iodine around the neck was believed to prevent goitre.[33]

Notable cases


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 ("Kropf").[37]

See also


  1. 1.0 1.1 1.2 1.3 1.4 "Goitre - NHS Choices". NHS Choices. 2017-10-19. Archived from the original on 2017-07-05. Retrieved 2017-07-03.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Can, AS; Rehman, A (January 2020). "Goiter". PMID 32965832. {{cite journal}}: Cite journal requires |journal= (help)
  3. 3.0 3.1 "Goitre - Treatment". nhs.uk. 19 October 2017. Archived from the original on 7 February 2021. Retrieved 19 December 2020.
  4. 4.0 4.1 4.2 Sharma, Manoj; Atri, Ashutosh. Essentials of International Health. Jones & Bartlett Learning. p. 206. ISBN 978-0-7637-6529-3. Archived from the original on 2021-07-11. Retrieved 2020-12-20.
  5. Ferri, Fred F. (2020). Ferri's Clinical Advisor 2020 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 1548. ISBN 978-0-323-67977-0. Archived from the original on 2021-07-11. Retrieved 2020-12-20.
  6. Welbourn, Richard Burkewood; Friesen, Stanley R.; Johnston, Ivan D. A.; Sellwood, Ronald A. (1990). The History of Endocrine Surgery. Greenwood Publishing Group. p. 19. ISBN 978-0-275-92586-4. Archived from the original on 2021-07-11. Retrieved 2020-12-20.
  7. Bland, Kirby I.; Sarr, Michael G.; Büchler, Markus W.; Csendes, Attila; Garden, Oliver James; Wong, John (2008). General Surgery: Principles and International Practice. Springer Science & Business Media. p. 1632. ISBN 978-1-84628-832-6. Archived from the original on 2021-07-11. Retrieved 2020-12-20.
  8. Porth CM, Gaspard KJ, Noble KA (2011). Essentials of pathophysiology: Concepts of altered health states (3rd ed.). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins.
  9. Mitchell RS, Kumar V, Abbas AK, Fausto N (2007). Robbins Basic Pathology (8th ed.). Philadelphia: Saunders. ISBN 978-1-4160-2973-1.
  10. "Toxicological Profile For Cyanide" (PDF). Atsdr.cdc.gov. Archived (PDF) from the original on 2010-12-31. Retrieved 2017-03-16.
  11. Hörmann R (2005). Schilddrüsenkrankheiten Leitfaden für Praxis und Klinik (4., aktualisierte und erw. Aufl ed.). Berlin. pp. 15–37. ISBN 3-936072-27-2.
  12. Babademez MA, Tuncay KS, Zaim M, Acar B, Karaşen RM (November 2010). "Hashimoto thyroiditis and thyroid gland anomalies". The Journal of Craniofacial Surgery. 21 (6): 1807–9. doi:10.1097/SCS.0b013e3181f43e32. PMID 21119426.
  13. 13.0 13.1 Thyrotropin (TSH)-secreting pituitary adenomas. Archived 2011-02-18 at the Wayback Machine By Roy E Weiss and Samuel Refetoff. Last literature review version 19.1: January 2011. This topic last updated: July 2, 2009
  14. Abraham-Nordling M, Törring O, Hamberger B, Lundell G, Tallstedt L, Calissendorff J, Wallin G (November 2005). "Graves' disease: a long-term quality-of-life follow up of patients randomized to treatment with antithyroid drugs, radioiodine, or surgery". Thyroid. 15 (11): 1279–86. doi:10.1089/thy.2005.15.1279. PMID 16356093.
  15. Numbers from EUROCARE, from Page 10 Archived 2016-05-13 at the Wayback Machine in: Grünwald F, Biersack HJ (2005). Thyroid cancer. Berlin: Springer. ISBN 978-3-540-22309-2.
  16. Bukvic BR, Zivaljevic VR, Sipetic SB, Diklic AD, Tausanovic KM, Paunovic IR (August 2014). "Improvement of quality of life in patients with benign goiter after surgical treatment". Langenbeck's Archives of Surgery. 399 (6): 755–64. doi:10.1007/s00423-014-1221-7. PMID 25002182. S2CID 34137703.
  17. "Goitre". nhs.uk. 19 October 2017. Archived from the original on 27 March 2019. Retrieved 27 March 2019.
  18. Frilling A, Liu C, Weber F (2004). "Benign multinodular goiter". Scandinavian Journal of Surgery. 93 (4): 278–81. doi:10.1177/145749690409300405. PMID 15658668. S2CID 38834260.
  19. "Toxic multinodular goitre - Symptoms, diagnosis and treatment | BMJ Best Practice". bestpractice.bmj.com. Archived from the original on 2018-11-27. Retrieved 2018-11-26.
  20. Gandolfi PP, Frisina A, Raffa M, Renda F, Rocchetti O, Ruggeri C, Tombolini A (August 2004). "The incidence of thyroid carcinoma in multinodular goiter: retrospective analysis". Acta Bio-Medica. 75 (2): 114–7. PMID 15481700.
  21. "Goiter – Simple". The New York Times. Archived from the original on 2013-07-29. Retrieved 2012-03-21.
  22. "Mortality and Burden of Disease Estimates for WHO Member States in 2002" (xls). World Health Organization. 2002. Archived from the original on 2006-03-24. Retrieved 2020-10-04.
  23. 1
  24. 24.0 24.1 24.2 Temple R (1986). The Genius of China: 3,000 Years of Science, Discovery, and Invention. New York: Simon and Schuster, Inc. pp. 134–5. ISBN 0-671-62028-2.
  25. Basedow's syndrome or disease at Who Named It? – the history and naming of the disease
  26. 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.
  27. Nabipour I (2003). "Clinical Endocrinology in the Islamic Civilization in Iran". International Journal of Endocrinology and Metabolism. 1: 43–45 [45].
  28. Giuseppe Flajani at Who Named It?
  29. Hull G (June 1998). "Caleb Hillier Parry 1755-1822: a notable provincial physician". Journal of the Royal Society of Medicine. 91 (6): 335–8. doi:10.1177/014107689809100618. PMC 1296785. PMID 9771526.
  30. "Paracelsus" Archived 2008-12-23 at the Wayback Machine Britannica
  31. "In Raising the World's I.Q., the Secret's in the Salt" Archived 2008-12-09 at the Wayback Machine, article by Donald G. McNeil, Jr., December 16, 2006, The New York Times
  32. Wissen, Planet (16 March 2017). "Planet Wissen". Archived from the original on 8 July 2009. Retrieved 24 December 2010.
  33. "ARCHIVED – Why take iodine?". Nrc-cnrc.gc.ca. 2011-09-30. Archived from the original on 2012-01-21. Retrieved 2012-11-01.
  34. Lahita RG, Yalof I (2004-07-20). Women and Autoimmune Disease. HarperCollins. p. 158. ISBN 978-0-06-008149-2. Archived from the original on 2021-08-29. Retrieved 2022-03-14.
  35. Altman LK (14 September 1991). "A White House Puzzle: Immunity Ailments". The New York Times. Archived from the original on 24 February 2020. Retrieved 5 November 2020. Doctors Say Bush Is in Good Health
  36. Altman LK (28 May 1991). "The Doctor's World; A White House Puzzle: Immunity Ailments". The New York Times. Archived from the original on 8 May 2013. Retrieved 5 November 2020.
  37. Fox-Davies AC (1904). The Art of Heraldry: An Encyclopædia of Armory. New York and London: Benjamin Blom, Inc. p. 413.

External links

External resources