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{{Goiter}}
{{Goiter}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{ARK}}
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
When the [[Thyrotropin-releasing hormone|thyrotrophin releasing hormone]]-[[Thyroid-stimulating hormone|thyroid stimulating hormone]] axis ([[TRH]]-[[TSH]] [[thyroid hormone]] [[axis]]) is interfered, it results in structural and functional changes in the [[thyroid gland]]. Increased [[TSH]] production is trigerred by a [[deficiency]] in [[thyroid hormone]] [[synthesis]] or intake. In order to normalize [[thyroid hormone]] levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the [[thyroid gland]] and when this process occurs continuously, it leads to goiter.
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Pathophysiology==
==Pathophysiology==


===Pathogenesis===
'''Pathogenesis:'''<ref name="Rapoport1991">{{cite journal|last1=Rapoport|first1=Basil|title=Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism|journal=Annual Review of Medicine|volume=42|issue=1|year=1991|pages=91–96|issn=0066-4219|doi=10.1146/annurev.me.42.020191.000515}}</ref><ref name="Larsen1972">{{cite journal|last1=Larsen|first1=P.R.|title=Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man|journal=Metabolism|volume=21|issue=11|year=1972|pages=1073–1092|issn=00260495|doi=10.1016/0026-0495(72)90038-8}}</ref><ref name="GaitanWahner1969">{{cite journal|last1=Gaitan|first1=Eduardo|last2=Wahner|first2=Heinz W.|last3=Cuello|first3=Carlos|last4=Correa|first4=Pelayo|last5=Jubiz|first5=William|last6=Gaitan|first6=Jorge E.|title=Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=29|issue=5|year=1969|pages=675–683|issn=0021-972X|doi=10.1210/jcem-29-5-675}}</ref><ref name="pmid2114018">{{cite journal |vauthors=Elte JW, Bussemaker JK, Haak A |title=The natural history of euthyroid multinodular goitre |journal=Postgrad Med J |volume=66 |issue=773 |pages=186–90 |year=1990 |pmid=2114018 |pmc=2429462 |doi= |url=}}</ref><ref name="pmid2239979">{{cite journal |vauthors=Berghout A, Wiersinga WM, Smits NJ, Touber JL |title=Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter |journal=Am. J. Med. |volume=89 |issue=5 |pages=602–8 |year=1990 |pmid=2239979 |doi= |url=}}</ref><ref name="SotoImas1967">{{cite journal|last1=Soto|first1=Roberto J.|last2=Imas|first2=Berta|last3=Brunengo|first3=Ana M.|last4=Goldberg|first4=David|last5=Burian|first5=Rosa|last6=Gnocchi|first6=Luisa|title=Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena|journal=The Journal of Clinical Endocrinology & Metabolism|volume=27|issue=11|year=1967|pages=1581–1587|issn=0021-972X|doi=10.1210/jcem-27-11-1581}}</ref><ref name="pmid9677510">{{cite journal |vauthors=Gärtner R, Dugrillon A |title=[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter] |language=German |journal=Internist (Berl) |volume=39 |issue=6 |pages=566–73 |year=1998 |pmid=9677510 |doi= |url=}}</ref><ref name="Peteiro-GonzalezLee2010">{{cite journal|last1=Peteiro-Gonzalez|first1=D.|last2=Lee|first2=J.|last3=Rodriguez-Fontan|first3=J.|last4=Castro-Piedras|first4=I.|last5=Cameselle-Teijeiro|first5=J.|last6=Beiras|first6=A.|last7=Bravo|first7=S. B.|last8=Alvarez|first8=C. V.|last9=Hardy|first9=D. M.|last10=Targovnik|first10=H. M.|last11=Arvan|first11=P.|last12=Lado-Abeal|first12=J.|title=New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter|journal=The Journal of Clinical Endocrinology & Metabolism|volume=95|issue=7|year=2010|pages=3522–3526|issn=0021-972X|doi=10.1210/jc.2009-2109}}</ref><ref name="Capen1992">{{cite journal|last1=Capen|first1=C.C.|title=Pathophysiology of chemical injury of the thyroid gland|journal=Toxicology Letters|volume=64-65|year=1992|pages=381–388|issn=03784274|doi=10.1016/0378-4274(92)90211-2}}</ref><ref name="MaceriSullivan1986">{{cite journal|last1=Maceri|first1=Dennis R.|last2=Sullivan|first2=Michael J.|last3=McClatchney|first3=Kenneth D.|title=AUTOIMMUNE THYROIDITIS|journal=The Laryngoscope|volume=96|issue=1|year=1986|pages=82???86|issn=0023-852X|doi=10.1288/00005537-198601000-00015}}</ref><ref name="NeumannWillgerodt1999">{{cite journal|last1=Neumann|first1=Susanne|last2=Willgerodt|first2=Helmut|last3=Ackermann|first3=Frank|last4=Reske|first4=Andreas|last5=Jung|first5=Martin|last6=Reis|first6=André|last7=Paschke|first7=Ralf|title=Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1|journal=The Journal of Clinical Endocrinology & Metabolism|volume=84|issue=10|year=1999|pages=3750–3756|issn=0021-972X|doi=10.1210/jcem.84.10.6023}}</ref>
*Goiters may can occur as a result of either hypothyroidism, hyperthyroidism, or when the levels of thyroid hormone are normal.
*Goiters may occur as a result of either [[hypothyroidism]], [[hyperthyroidism]], or even with normal levels of [[thyroid hormone]].
*Thyroid enlargement (goiter) and hypothyroidism may occur due to compensatory responses as a result of a severe underlying disorder.
*[[Thyroid enlargement]] (goiter) and [[hypothyroidism]] may occur due to compensatory responses as a result of a severe underlying [[disorder]].
*When the thyroid gland can't secrete enough thyroid hormone to cater too the metabolic requirements, it may lead to simple goiter.
*When the [[thyroid gland]] cannot secrete enough [[thyroid hormone]] to cater to the [[metabolic]] requirements, it may lead to simple goiter (smooth enlargement).
*In order to compensate for inadequate hormone synthesis the thyroid gland enlarges, this type of compensation overcomes mild to moderate hormonal impairment.
*In order to compensate for inadequate [[hormone]] synthesis, the [[thyroid gland]] enlarges, this type of compensation overcomes mild to moderate [[hormonal]] impairment.
*When the [[TRH]]-[[TSH]] [[thyroid hormone]] [[axis]] is interfered, it results in the structural and functional changes of the [[thyroid gland]].
*Increased [[TSH]] production is triggered by a [[deficiency]] in [[thyroid hormone]] [[synthesis]] or intake.
*In order to normalize [[thyroid hormone]] levels, the increase in [[TSH]] leads to increased cellularity and [[hyperplasia]] of the [[thyroid gland]] and when this [[Process (anatomy)|process]] is continuous, it leads to goiter.
*[[Thyroid hormone]] [[deficiency]] may occur secondary to to [[iodine deficiency]], inborn errors of [[thyroid hormone]] [[synthesis]] and goitrogens.
*Goiters may form as a result of many [[TSH]] receptor agonists. The [[TSH]] receptor gets stimulated under the following conditions:
**[[Adenoma]] of the [[pituitary]]
**[[Adenoma]] of the [[hypothalamus]]
**[[Pituitary gland|Pituitary]] resistance to [[thyroid hormone]]
**[[TSH]] receptor [[antibodies]]
**[[Tumors]] producing [[hCG]] ([[human chorionic gonadotropin]])


*'''<u>The pathophysiological consequences of goitres results from one of the following</u>:'''
*'''<u>The pathophysiological consequences of goitres results from one of the following</u>:'''
**''The effect of thyroid hormone dysfunction''
**''[[Thyroid hormone]] dysfunction''
**''The effect of enlarged thyroid gland''
**''[[Enlarged thyroid gland]]''
**''The effect of primary disease causing goitre''
**''The effect of primary disease causing goiter''


*'''''The effect of thyroid hormone dysfunction:'''''
*'''''The effect of thyroid hormone dysfunction:'''''
**Thyroid hyperfunction (hyperthyroidism) → Features of hyperthyroidism
**Thyroid [[hyperfunction]] ([[hyperthyroidism]]) → Features of [[hyperthyroidism]]
**Thyroid hypofunction (hypothyroidism) → Features of hypothyroidism
**[[Hypofunctioning thyroid|Thyroid hypofunction]] ([[hypothyroidism]]) → Features of [[hypothyroidism]]


*'''''The effect of enlarged thyroid gland:'''''
*'''''The effect of enlarged thyroid gland:'''''
**Effect on the trachea → dyspnea
**Effect on the [[trachea]] results in [[dyspnea]]
**Effect on the esophagus → dysphagia
**Effect on the [[esophagus]] results in [[dysphagia]]
**Effect on the superior venacava → distended neck veins
**Effect on the [[superior vena cava]] results in distended [[neck veins]]
**Effect on the recurrent laryngeal nerve → horsiness of voice
**Effect on the [[recurrent laryngeal nerve]] results in [[hoarseness]] of voice


*'''''The effect of primary disease causing goitre:'''''
*'''''The effect of primary disease causing goitre:'''''
**The effect depends on the underlying disease
**The effect depends on the underlying [[disease]]


==Genetics==
==Genetics==
*Goiter may be caused by a mutation in the following genes which vary from one family to the other: <ref name="pmid10821321">{{cite journal |vauthors=Brix TH, Hegedüs L |title=Genetic and environmental factors in the aetiology of simple goitre |journal=Ann. Med. |volume=32 |issue=3 |pages=153–6 |year=2000 |pmid=10821321 |doi= |url=}}</ref>
*Goiter may be caused by a [[mutation]] in the following [[genes]] which vary from one [[family]] to the other: <ref name="pmid10821321">{{cite journal |vauthors=Brix TH, Hegedüs L |title=Genetic and environmental factors in the aetiology of simple goitre |journal=Ann. Med. |volume=32 |issue=3 |pages=153–6 |year=2000 |pmid=10821321 |doi= |url=}}</ref><ref name="pmid12588808">{{cite journal |vauthors=Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N |title=The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance |journal=Endocr. Rev. |volume=24 |issue=1 |pages=48–77 |year=2003 |pmid=12588808 |doi=10.1210/er.2001-0029 |url=}}</ref><ref name="TargovnikEsperante2010">{{cite journal|last1=Targovnik|first1=Héctor M.|last2=Esperante|first2=Sebastián A.|last3=Rivolta|first3=Carina M.|title=Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=44–55|issn=03037207|doi=10.1016/j.mce.2010.01.009}}</ref><ref name="SpitzwegMorris2010">{{cite journal|last1=Spitzweg|first1=Christine|last2=Morris|first2=John C.|title=Genetics and phenomics of hypothyroidism and goiter due to NIS mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=56–63|issn=03037207|doi=10.1016/j.mce.2010.02.007}}</ref><ref name="MorenoVisser2010">{{cite journal|last1=Moreno|first1=José C.|last2=Visser|first2=Theo J.|title=Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations|journal=Molecular and Cellular Endocrinology|volume=322|issue=1-2|year=2010|pages=91–98|issn=03037207|doi=10.1016/j.mce.2010.03.010}}</ref><ref name="pmid4980080">{{cite journal |vauthors=Fraser GR |title=The genetics of thyroid disease |journal=Prog Med Genet |volume=6 |issue= |pages=89–115 |year=1969 |pmid=4980080 |doi= |url=}}</ref>
:*Thyroglobulin (Tg) gene
:*[[Thyroglobulin]] (Tg) [[gene]]
:*Thyroid-stimulating hormone receptor (TSHR) gene
:*[[Thyroid-stimulating hormone]] receptor (TSHR) [[gene]]
:*Na+/I- symporter (NIS) gene
:*[[Sodium]]-[[iodine]] (Na+/I-) symporter (NIS) gene <ref name="pmid24311738">{{cite journal| author=Portulano C, Paroder-Belenitsky M, Carrasco N| title=The Na+/I- symporter (NIS): mechanism and medical impact. | journal=Endocr Rev | year= 2014 | volume= 35 | issue= 1 | pages= 106-49 | pmid=24311738 | doi=10.1210/er.2012-1036 | pmc=3895864 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24311738  }} </ref>
*Multinodular goitre marker 1 (MNG1) on chromosome 14 <ref name="pmid10821321">{{cite journal |vauthors=Brix TH, Hegedüs L |title=Genetic and environmental factors in the aetiology of simple goitre |journal=Ann. Med. |volume=32 |issue=3 |pages=153–6 |year=2000 |pmid=10821321 |doi= |url=}}</ref>


==Associated Conditions==
==Associated Conditions==
The following conditions are associated with goiter:<ref name="pmid23148179">{{cite journal |vauthors=Girgis CM, Champion BL, Wall JR |title=Current concepts in graves' disease |journal=Ther Adv Endocrinol Metab |volume=2 |issue=3 |pages=135–44 |year=2011 |pmid=23148179 |pmc=3474632 |doi=10.1177/2042018811408488 |url=}}</ref><ref name="urlHashimoto’s Thyroiditis - Endotext - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK285557/ |title=Hashimoto’s Thyroiditis - Endotext - NCBI Bookshelf |format= |work= |accessdate=}}</ref>
*[[Grave's disease]]
*[[Hashimoto's thyroiditis]]


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*On [[gross pathology]] the following features are observed:<ref name="pmid13263417">{{cite journal| author=MORTENSEN JD, WOOLNER LB, BENNETT WA| title=Gross and microscopic findings in clinically normal thyroid glands. | journal=J Clin Endocrinol Metab | year= 1955 | volume= 15 | issue= 10 | pages= 1270-80 | pmid=13263417 | doi=10.1210/jcem-15-10-1270 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13263417  }} </ref><ref name="pmid25996397">{{cite journal| author=| title=Reorganized text. | journal=JAMA Otolaryngol Head Neck Surg | year= 2015 | volume= 141 | issue= 5 | pages= 428 | pmid=25996397 | doi=10.1001/jamaoto.2015.0540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25996397  }} </ref><ref name="pmid12588812">{{cite journal| author=Hegedüs L, Bonnema SJ, Bennedbaek FN| title=Management of simple nodular goiter: current status and future perspectives. | journal=Endocr Rev | year= 2003 | volume= 24 | issue= 1 | pages= 102-32 | pmid=12588812 | doi=10.1210/er.2002-0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12588812  }} </ref>
**[[Enlarged thyroid gland]]
**Multiple nodules lacking [[fibrous capsule]]
**[[Secondary]] changes such as [[hemorrhage]], [[calcification]] and cystic degeneration are observed
 
[[image:Thyroid_Diffuse_Hyperplasia.jpg|thumb|250px|center|By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons]]


==Microscopic Pathology==
==Microscopic Pathology==
Microscopic studies that aid in the histopathological analysis:
'''Goiter histologic findings:'''
*'''Fine needle aspiration cytology (FNAC)'''
*Simple non-toxic goiters demonstrate:
*'''Open biopsy'''
**[[Hyperplasia]]
**[[Colloid]] accumulation
**Nodularity
 
*Nodular hyperplasia is commonly seen in multinodular goiter. [[Cytological|Cytologic]] findings include:
**Benign appearing [[follicular cells]]
**Abundant [[colloid]], [[macrophages]]
**[[Hurthle cell (patient information)|Hürthle cells]] (occasionally)
 


*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
[[image:THYROID_MICROSCOPIC.jpg|thumb|350px|center|By Ed Uthman from Houston, TX, USA (Diffuse Thyroid Hyperplasia  Uploaded by CFCF) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons]]


==References==
==References==

Latest revision as of 15:21, 18 November 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]

Overview

When the thyrotrophin releasing hormone-thyroid stimulating hormone axis (TRH-TSH thyroid hormone axis) is interfered, it results in structural and functional changes in the thyroid gland. Increased TSH production is trigerred by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process occurs continuously, it leads to goiter.

Pathophysiology

Pathogenesis:[1][2][3][4][5][6][7][8][9][10][11]

  • The effect of primary disease causing goitre:
    • The effect depends on the underlying disease

Genetics

Associated Conditions

The following conditions are associated with goiter:[19][20]

Gross Pathology

By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

Microscopic Pathology

Goiter histologic findings:


By Ed Uthman from Houston, TX, USA (Diffuse Thyroid Hyperplasia Uploaded by CFCF) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

References

  1. ↑ Rapoport, Basil (1991). "Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism". Annual Review of Medicine. 42 (1): 91–96. doi:10.1146/annurev.me.42.020191.000515. ISSN 0066-4219.
  2. ↑ Larsen, P.R. (1972). "Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man". Metabolism. 21 (11): 1073–1092. doi:10.1016/0026-0495(72)90038-8. ISSN 0026-0495.
  3. ↑ Gaitan, Eduardo; Wahner, Heinz W.; Cuello, Carlos; Correa, Pelayo; Jubiz, William; Gaitan, Jorge E. (1969). "Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1". The Journal of Clinical Endocrinology & Metabolism. 29 (5): 675–683. doi:10.1210/jcem-29-5-675. ISSN 0021-972X.
  4. ↑ Elte JW, Bussemaker JK, Haak A (1990). "The natural history of euthyroid multinodular goitre". Postgrad Med J. 66 (773): 186–90. PMC 2429462. PMID 2114018.
  5. ↑ Berghout A, Wiersinga WM, Smits NJ, Touber JL (1990). "Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter". Am. J. Med. 89 (5): 602–8. PMID 2239979.
  6. ↑ Soto, Roberto J.; Imas, Berta; Brunengo, Ana M.; Goldberg, David; Burian, Rosa; Gnocchi, Luisa (1967). "Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena". The Journal of Clinical Endocrinology & Metabolism. 27 (11): 1581–1587. doi:10.1210/jcem-27-11-1581. ISSN 0021-972X.
  7. ↑ Gärtner R, Dugrillon A (1998). "[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter]". Internist (Berl) (in German). 39 (6): 566–73. PMID 9677510.
  8. ↑ Peteiro-Gonzalez, D.; Lee, J.; Rodriguez-Fontan, J.; Castro-Piedras, I.; Cameselle-Teijeiro, J.; Beiras, A.; Bravo, S. B.; Alvarez, C. V.; Hardy, D. M.; Targovnik, H. M.; Arvan, P.; Lado-Abeal, J. (2010). "New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter". The Journal of Clinical Endocrinology & Metabolism. 95 (7): 3522–3526. doi:10.1210/jc.2009-2109. ISSN 0021-972X.
  9. ↑ Capen, C.C. (1992). "Pathophysiology of chemical injury of the thyroid gland". Toxicology Letters. 64-65: 381–388. doi:10.1016/0378-4274(92)90211-2. ISSN 0378-4274.
  10. ↑ Maceri, Dennis R.; Sullivan, Michael J.; McClatchney, Kenneth D. (1986). "AUTOIMMUNE THYROIDITIS". The Laryngoscope. 96 (1): 82???86. doi:10.1288/00005537-198601000-00015. ISSN 0023-852X.
  11. ↑ Neumann, Susanne; Willgerodt, Helmut; Ackermann, Frank; Reske, Andreas; Jung, Martin; Reis, André; Paschke, Ralf (1999). "Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1". The Journal of Clinical Endocrinology & Metabolism. 84 (10): 3750–3756. doi:10.1210/jcem.84.10.6023. ISSN 0021-972X.
  12. ↑ Brix TH, Hegedüs L (2000). "Genetic and environmental factors in the aetiology of simple goitre". Ann. Med. 32 (3): 153–6. PMID 10821321.
  13. ↑ Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N (2003). "The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance". Endocr. Rev. 24 (1): 48–77. doi:10.1210/er.2001-0029. PMID 12588808.
  14. ↑ Targovnik, Héctor M.; Esperante, Sebastián A.; Rivolta, Carina M. (2010). "Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations". Molecular and Cellular Endocrinology. 322 (1–2): 44–55. doi:10.1016/j.mce.2010.01.009. ISSN 0303-7207.
  15. ↑ Spitzweg, Christine; Morris, John C. (2010). "Genetics and phenomics of hypothyroidism and goiter due to NIS mutations". Molecular and Cellular Endocrinology. 322 (1–2): 56–63. doi:10.1016/j.mce.2010.02.007. ISSN 0303-7207.
  16. ↑ Moreno, José C.; Visser, Theo J. (2010). "Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations". Molecular and Cellular Endocrinology. 322 (1–2): 91–98. doi:10.1016/j.mce.2010.03.010. ISSN 0303-7207.
  17. ↑ Fraser GR (1969). "The genetics of thyroid disease". Prog Med Genet. 6: 89–115. PMID 4980080.
  18. ↑ Portulano C, Paroder-Belenitsky M, Carrasco N (2014). "The Na+/I- symporter (NIS): mechanism and medical impact". Endocr Rev. 35 (1): 106–49. doi:10.1210/er.2012-1036. PMC 3895864. PMID 24311738.
  19. ↑ Girgis CM, Champion BL, Wall JR (2011). "Current concepts in graves' disease". Ther Adv Endocrinol Metab. 2 (3): 135–44. doi:10.1177/2042018811408488. PMC 3474632. PMID 23148179.
  20. ↑ "Hashimoto's Thyroiditis - Endotext - NCBI Bookshelf".
  21. ↑ MORTENSEN JD, WOOLNER LB, BENNETT WA (1955). "Gross and microscopic findings in clinically normal thyroid glands". J Clin Endocrinol Metab. 15 (10): 1270–80. doi:10.1210/jcem-15-10-1270. PMID 13263417.
  22. ↑ "Reorganized text". JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  23. ↑ Hegedüs L, Bonnema SJ, Bennedbaek FN (2003). "Management of simple nodular goiter: current status and future perspectives". Endocr Rev. 24 (1): 102–32. doi:10.1210/er.2002-0016. PMID 12588812.

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