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{{silent thyroiditis}}


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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an [[autoimmune]] phenomenon. Activated matured [[T-cell|T-cells]] ([[HLA-DR|HLA-DR+]]CD3+), activated [[Helper T cells|helper/inducer T-cells]] ([[HLA-DR|HLA-DR+]]CD4+), activated [[Suppressor T cells|suppressor]], and [[Cytotoxic T cell|cytotoxic T-cells]] ([[HLA-DR|HLA-DR+]]CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of [[T cells|T cells]], especially [[Helper T cells|helper/inducer T cells]], might have an important role in the [[pathogenesis]] of silent thyroiditis. Silent thyroiditis is associated with the [[HLA DR3-DQ2|HLA-DR3]] and [[HLA-DR5|DR5]] genes. [[Lymphocytic]] infiltration of the thyroid gland, the absence of [[Hurthle cells]] and [[Germinal center|germinal centers]] on histological analysis are the microscopic [[histopathological]] findings suggestive of silent thyroiditis.
 
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==
The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.<ref name="pmid25905405">{{cite journal |vauthors=De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Rousset B, Dupuy C, Miot F, Dumont J |title=Thyroid Hormone Synthesis And Secretion |journal= |volume= |issue= |pages= |year= |pmid=25905405 |doi= |url=}}</ref><ref name="pmid11949270">{{cite journal |vauthors=Kirsten D |title=The thyroid gland: physiology and pathophysiology |journal=Neonatal Netw |volume=19 |issue=8 |pages=11–26 |year=2000 |pmid=11949270 |doi=10.1891/0730-0832.19.8.11 |url=}}</ref>
{|
* [[Thyroid hormone|Thyroid hormones (T3 and T4)]] are regulating [[basal metabolic rate]], influence [[oxygen]] consumption by tissues. They are crucial for normal development of the [[brain]] and growth of the body.
|The control, synthesis, and release of the [[thyroid hormone]] is usually controlled by [[hypothalamus]] and [[pituitary gland]].<ref name="pmid25905405">{{cite journal |vauthors=De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Rousset B, Dupuy C, Miot F, Dumont J |title=Thyroid Hormone Synthesis And Secretion |journal= |volume= |issue= |pages= |year= |pmid=25905405 |doi= |url=}}</ref><ref name="pmid11949270">{{cite journal |vauthors=Kirsten D |title=The thyroid gland: physiology and pathophysiology |journal=Neonatal Netw |volume=19 |issue=8 |pages=11–26 |year=2000 |pmid=11949270 |doi=10.1891/0730-0832.19.8.11 |url=}}</ref>
* Secretion of [[thyroid hormones]] follows upper control from the [[hypothalamus]] and the [[pituitary]]. [[Thyrotropin-releasing hormone|Thyroid releasing hormone (TRH)]] acts on [[thyrotropes]] releasing cells in the [[pituitary]] causing them to release [[Thyroid-stimulating hormone|thyroid stimulating hormone (TSH)]].  
* [[Thyroid hormone|Thyroid hormones (T3 and T4)]] regulates the [[basal metabolic rate]] and influences [[oxygen]] consumption by tissues. They are crucial for normal development of the [[brain]] and growth of the body.
* Secretion of [[thyroid hormones]] follows upper control mechanisms from the [[hypothalamus]] and the [[pituitary]]. [[Thyrotropin-releasing hormone|Thyroid releasing hormone (TRH)]] acts on [[thyrotropes]] releasing cells in the [[pituitary]] causing them to release [[Thyroid-stimulating hormone|thyroid stimulating hormone (TSH)]].  
* [[TSH]] acts on [[thyroid gland]] by binding to specific membrane receptors and activating an [[intracellular]] pathway involving [[cAMP]] that ends in the formation and secretion of [[thyroid hormones]].
* [[TSH]] acts on [[thyroid gland]] by binding to specific membrane receptors and activating an [[intracellular]] pathway involving [[cAMP]] that ends in the formation and secretion of [[thyroid hormones]].
* [[Iodine]] is essential for the synthesis of [[thyroid hormones]]. [[Iodide]] is up taken through a special Na/I transporter found in the membrane of [[thyroid]] follicular cell. After the [[iodide]] uptake, it goes through a series of organic reactions ending in the formation of the two forms of [[thyroid hormones]]: [[T3]] and [[T4]]. [[T3]] and [[T4]] remain stored in the [[thyroglobulin]] of the follicles and are released in response to further stimulation by [[TSH]] to the [[Thyroid follicle|thyroid follicles]].
* [[Iodine]] is essential for the synthesis of [[thyroid hormones]]. [[Iodide]] is taken up through a special Na/I transporter found in the membrane of [[thyroid]] follicular cell. After the [[iodide]] uptake, it goes through a series of organic reactions ending in the formation of the two forms of [[thyroid hormones]]: [[T3]] and [[T4]]. [[T3]] and [[T4]] remain stored in the [[thyroglobulin]] within [[Thyroid follicle|thyroid follicles]] and are released in response to further stimulation by [[TSH]] to the [[Thyroid follicle|thyroid follicles]].
* While [[T3]] is 3 to 5 times more potent than [[T4]], it represents only one-fourth of the total hormone secretion. [[T3]] is thought to be the biologically active form of the hormone. Most of the circulating [[T3]] is due to peripheral conversion of [[T4]] in the liver and peripheral tissues while only a small percentage is secreted directly from the [[thyroid gland]] itself.
* While [[T3]] is 3 to 5 times more potent than [[T4]], it represents only one-fourth of the total hormone secretion. [[T3]] is thought to be the biologically active form of the hormone. Most of the circulating [[T3]] is due to peripheral conversion of [[T4]] in the [[liver]] and peripheral tissues while only a small percentage is secreted directly from the [[thyroid gland]] itself.
* [[T3]] and [[T4]] act on nuclear receptors ([[DNA]] binding [[proteins]]) and cause the regulate the [[transcription]] of many [[proteins]] to regulate the [[metabolic rate]] of the body.
* [[T3]] and [[T4]] act on nuclear receptors ([[DNA]] binding [[proteins]]) and cause the regulate the [[transcription]] of many [[proteins]] to regulate the [[metabolic rate]] of the body.
* The higher regulation of [[thyroxine]] secretion follows the [[negative feedback]] role, meaning that high levels of [[T3]] and [[T4]] will suppress [[TRH]] and [[TSH]] secretion and vice versa (Low levels of [[Thyroxin|thyroxine]] will stimulate [[TRH]] and [[TSH]] secretion). This is useful in diagnosing the cause of hyperthyroidism.
* The higher regulation of [[thyroxine]] secretion follows the [[negative feedback]] role, meaning that high levels of [[T3]] and [[T4]] will suppress [[TRH]] and [[TSH]] secretion and vice versa (Low levels of [[Thyroxin|thyroxine]] will stimulate [[TRH]] and [[TSH]] secretion). This is useful in diagnosing the cause of [[hyperthyroidism]].
* [[TSH]] will be low in primary hyperthyroidism where the gland is the source of the excess hormones. In secondary hyperthyroidism,  [[TSH]] will be high as the [[pituitary]] or the [[hypothalamus]] are the sources of the disease.
* [[TSH]] will be low in [[hyperthyroidism|primary hyperthyroidism]] where the gland is the source of the excess [[hormones]]. In secondary [[hyperthyroidism]],  [[TSH]] will be high as the [[pituitary]] or the [[hypothalamus]] are the sources of the disease.
|
[[Image: Regulation der Schilddrüsenfunktion .jpg|right|300px|thumb|'''Regulation of thyroid hormone secretion.''' <small>Source:By CFCF; slightly modified by Geo-Science-International - This file was derived from Thyroid vector.svg:, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=47043638</small>]]
|}
===Pathogenesis===
===Pathogenesis===
*The exact pathogenesis of [disease name] is not fully understood.
*The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an [[autoimmune]] phenomenon. The following features are suggestive of an [[autoimmune]] pathogenesis of silent thyroiditis:<ref name="pmid3415401">{{cite journal |vauthors=Volpé R |title=Is silent thyroiditis an autoimmune disease? |journal=Arch. Intern. Med. |volume=148 |issue=9 |pages=1907–8 |year=1988 |pmid=3415401 |doi= |url=}}</ref><ref name="pmid22443972">{{cite journal |vauthors=Samuels MH |title=Subacute, silent, and postpartum thyroiditis |journal=Med. Clin. North Am. |volume=96 |issue=2 |pages=223–33 |year=2012 |pmid=22443972 |doi=10.1016/j.mcna.2012.01.003 |url=}}</ref><ref name="pmid6606505">{{cite journal |vauthors=Farid NR, Hawe BS, Walfish PG |title=Increased frequency of HLA-DR3 and 5 in the syndromes of painless thyroiditis with transient thyrotoxicosis: evidence for an autoimmune aetiology |journal=Clin. Endocrinol. (Oxf) |volume=19 |issue=6 |pages=699–704 |year=1983 |pmid=6606505 |doi= |url=}}</ref><ref name="pmid3488044">{{cite journal |vauthors=Tajiri J, Higashi K, Morita M, Ohishi S, Umeda T, Sato T |title=Elevation of anti-DNA antibody titer during thyrotoxic phase of silent thyroiditis |journal=Arch. Intern. Med. |volume=146 |issue=8 |pages=1623–4 |year=1986 |pmid=3488044 |doi= |url=}}</ref>
OR
**[[Lymphocytic]] infiltration of the thyroid gland
*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].
**Presence of [[Antithyroid microsomal antibodies|antithyroid antibodies]]
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
**Association with [[HLA-DR3]] and [[HLA-DR5|DR5]]
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
**Presence of [[Antinuclear antibodies|anti-DNA antibodies]]
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
*The progression to [disease name] usually involves the [molecular pathway].
*Activated matured [[T-cell|T-cells]] ([[HLA-DR|HLA-DR+]]CD3+), activated [[Helper T cells|helper/inducer T-cells]] ([[HLA-DR|HLA-DR+]]CD4+), activated [[Suppressor T cells|suppressor]], and [[Cytotoxic T cell|cytotoxic T-cells]] ([[HLA-DR|HLA-DR+]]CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of [[T-cell|T-cells]], especially of [[Helper T cells|helper/inducer T cells]], might have an important role in the pathogenesis of silent thyroiditis.<ref name="pmid7704090">{{cite journal |vauthors=Kushima K, Ban Y, Taniyama M, Itoh K |title=Circulating activated T lymphocyte subsets in patients with silent thyroiditis |journal=Endocr. J. |volume=41 |issue=6 |pages=663–9 |year=1994 |pmid=7704090 |doi= |url=}}</ref>
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
Silent thyroiditis is associated with the following [[HLA]] genes:<ref name="pmid6606505">{{cite journal |vauthors=Farid NR, Hawe BS, Walfish PG |title=Increased frequency of HLA-DR3 and 5 in the syndromes of painless thyroiditis with transient thyrotoxicosis: evidence for an autoimmune aetiology |journal=Clin. Endocrinol. (Oxf) |volume=19 |issue=6 |pages=699–704 |year=1983 |pmid=6606505 |doi= |url=}}</ref>
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*[[HLA-DR3]]  
*The development of [disease name] is the result of multiple genetic mutations.
*[[HLA-DR5]]
 
==Associated Conditions==
==Associated Conditions==
The following conditions are associated with silent thyroiditis:<ref name="pmid1551281">{{cite journal |vauthors=Magaro M, Zoli A, Altomonte L, Mirone L, La Sala L, Barini A, Scuderi F |title=The association of silent thyroiditis with active systemic lupus erythematosus |journal=Clin. Exp. Rheumatol. |volume=10 |issue=1 |pages=67–70 |year=1992 |pmid=1551281 |doi= |url=}}</ref><ref name="pmid8393255">{{cite journal |vauthors=Ozawa Y, Shishiba Y |title=Recovery from lymphocytic hypophysitis associated with painless thyroiditis: clinical implications of circulating antipituitary antibodies |journal=Acta Endocrinol. |volume=128 |issue=6 |pages=493–8 |year=1993 |pmid=8393255 |doi= |url=}}</ref><ref name="pmid3250857">{{cite journal |vauthors=Nagai K, Sakata S, Takuno H, Tanabashi S, Kametani M, Tokimitsu N, Miura K |title=A case of silent thyroiditis associated with idiopathic thrombocytopenic purpura |journal=Endocrinol. Jpn. |volume=35 |issue=6 |pages=791–4 |year=1988 |pmid=3250857 |doi= |url=}}</ref><ref name="pmid11554636">{{cite journal |vauthors=Wilkins M, Moe MM |title=Acute painless thyroiditis with transient thyrotoxicosis during external beam irradiation to non-Hodgkin's lymphoma of the thyroid gland |journal=Clin Oncol (R Coll Radiol) |volume=13 |issue=4 |pages=311 |year=2001 |pmid=11554636 |doi= |url=}}</ref<nowiki><ref name="pmid8484389"></nowiki>{{cite journal |vauthors=Yamakita N, Sakata S, Hayashi H, Maekawa H, Miura K |title=Case report: silent thyroiditis after adrenalectomy in a patient with Cushing's syndrome |journal=Am. J. Med. Sci. |volume=305 |issue=5 |pages=304–6 |year=1993 |pmid=8484389 |doi= |url=}}</ref>
*[[SLE]]
*[[Lymphocytic hypophysitis]]
*[[Idiopathic thrombocytopenic purpura|Immune thrombocytopenic purpura]] (ITP)
*[[Cushing's syndrome]] (post [[adrenalectomy]] and [[steroid]] therapy cessation)
*[[Hodgkin's lymphoma]] (post-irradiation)


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Gross pathology findings in silent thyroiditis include:<ref name="urlPathology Outlines - Silent thyroiditis">{{cite web |url=http://www.pathologyoutlines.com/topic/thyroidsilentthyroiditis.html |title=Pathology Outlines - Silent thyroiditis |format= |work= |accessdate=}}</ref>
*Diffuse goiter
*Slightly enlarged thyroid gland


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*Microscopic [[histopathological]] findings in silent thyroiditis include:<ref name="pmid3415401">{{cite journal |vauthors=Volpé R |title=Is silent thyroiditis an autoimmune disease? |journal=Arch. Intern. Med. |volume=148 |issue=9 |pages=1907–8 |year=1988 |pmid=3415401 |doi= |url=}}</ref><ref name="pmid17696838">{{cite journal |vauthors=Mittra ES, McDougall IR |title=Recurrent silent thyroiditis: a report of four patients and review of the literature |journal=Thyroid |volume=17 |issue=7 |pages=671–5 |year=2007 |pmid=17696838 |doi=10.1089/thy.2006.0335 |url=}}</ref>
 
**Diffuse [[lymphocytic]] infiltrate
 
**Lack of [[Hurthle cells]] (Askanazy cells) and [[germinal centers]]
**Lack of [[fibrosis]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}


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

Overview

The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. Activated matured T-cells (HLA-DR+CD3+), activated helper/inducer T-cells (HLA-DR+CD4+), activated suppressor, and cytotoxic T-cells (HLA-DR+CD8+) were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T cells, especially helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis. Silent thyroiditis is associated with the HLA-DR3 and DR5 genes. Lymphocytic infiltration of the thyroid gland, the absence of Hurthle cells and germinal centers on histological analysis are the microscopic histopathological findings suggestive of silent thyroiditis.

Pathophysiology

The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.[1][2]
Regulation of thyroid hormone secretion. Source:By CFCF; slightly modified by Geo-Science-International - This file was derived from Thyroid vector.svg:, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=47043638

Pathogenesis

Genetics

Silent thyroiditis is associated with the following HLA genes:[5]

Associated Conditions

The following conditions are associated with silent thyroiditis:[8][9][10][11]

Gross Pathology

Gross pathology findings in silent thyroiditis include:[12]

  • Diffuse goiter
  • Slightly enlarged thyroid gland

Microscopic Pathology

References

  1. ↑ De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Rousset B, Dupuy C, Miot F, Dumont J. "Thyroid Hormone Synthesis And Secretion". PMID 25905405.
  2. ↑ Kirsten D (2000). "The thyroid gland: physiology and pathophysiology". Neonatal Netw. 19 (8): 11–26. doi:10.1891/0730-0832.19.8.11. PMID 11949270.
  3. ↑ 3.0 3.1 Volpé R (1988). "Is silent thyroiditis an autoimmune disease?". Arch. Intern. Med. 148 (9): 1907–8. PMID 3415401.
  4. ↑ Samuels MH (2012). "Subacute, silent, and postpartum thyroiditis". Med. Clin. North Am. 96 (2): 223–33. doi:10.1016/j.mcna.2012.01.003. PMID 22443972.
  5. ↑ 5.0 5.1 Farid NR, Hawe BS, Walfish PG (1983). "Increased frequency of HLA-DR3 and 5 in the syndromes of painless thyroiditis with transient thyrotoxicosis: evidence for an autoimmune aetiology". Clin. Endocrinol. (Oxf). 19 (6): 699–704. PMID 6606505.
  6. ↑ Tajiri J, Higashi K, Morita M, Ohishi S, Umeda T, Sato T (1986). "Elevation of anti-DNA antibody titer during thyrotoxic phase of silent thyroiditis". Arch. Intern. Med. 146 (8): 1623–4. PMID 3488044.
  7. ↑ Kushima K, Ban Y, Taniyama M, Itoh K (1994). "Circulating activated T lymphocyte subsets in patients with silent thyroiditis". Endocr. J. 41 (6): 663–9. PMID 7704090.
  8. ↑ Magaro M, Zoli A, Altomonte L, Mirone L, La Sala L, Barini A, Scuderi F (1992). "The association of silent thyroiditis with active systemic lupus erythematosus". Clin. Exp. Rheumatol. 10 (1): 67–70. PMID 1551281.
  9. ↑ Ozawa Y, Shishiba Y (1993). "Recovery from lymphocytic hypophysitis associated with painless thyroiditis: clinical implications of circulating antipituitary antibodies". Acta Endocrinol. 128 (6): 493–8. PMID 8393255.
  10. ↑ Nagai K, Sakata S, Takuno H, Tanabashi S, Kametani M, Tokimitsu N, Miura K (1988). "A case of silent thyroiditis associated with idiopathic thrombocytopenic purpura". Endocrinol. Jpn. 35 (6): 791–4. PMID 3250857.
  11. ↑ Wilkins M, Moe MM (2001). "Acute painless thyroiditis with transient thyrotoxicosis during external beam irradiation to non-Hodgkin's lymphoma of the thyroid gland". Clin Oncol (R Coll Radiol). 13 (4): 311. PMID 11554636.</ref<ref name="pmid8484389">Yamakita N, Sakata S, Hayashi H, Maekawa H, Miura K (1993). "Case report: silent thyroiditis after adrenalectomy in a patient with Cushing's syndrome". Am. J. Med. Sci. 305 (5): 304–6. PMID 8484389.
  12. ↑ "Pathology Outlines - Silent thyroiditis".
  13. ↑ Mittra ES, McDougall IR (2007). "Recurrent silent thyroiditis: a report of four patients and review of the literature". Thyroid. 17 (7): 671–5. doi:10.1089/thy.2006.0335. PMID 17696838.

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