Silent thyroiditis pathophysiology: Difference between revisions
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==Overview== | ==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-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. | 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. | ||
==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> | {| | ||
|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)]] 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. | * [[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)]]. | * 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 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 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 [[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. | * [[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. | ||
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[[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>]] | |||
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===Pathogenesis=== | ===Pathogenesis=== | ||
*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> | *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> | ||
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==Genetics== | ==Genetics== | ||
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> | 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> | ||
*[[HLA-DR3]] | *[[HLA-DR3]] | ||
*[[HLA-DR5]] | *[[HLA-DR5]] | ||
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*[[Lymphocytic hypophysitis]] | *[[Lymphocytic hypophysitis]] | ||
*[[Idiopathic thrombocytopenic purpura|Immune thrombocytopenic purpura]] (ITP) | *[[Idiopathic thrombocytopenic purpura|Immune thrombocytopenic purpura]] (ITP) | ||
*[[Cushing's syndrome]] (post [[adrenalectomy]] and steroid therapy cessation) | *[[Cushing's syndrome]] (post [[adrenalectomy]] and [[steroid]] therapy cessation) | ||
*[[Hodgkin's lymphoma]] (post-irradiation) | *[[Hodgkin's lymphoma]] (post-irradiation) | ||
==Gross Pathology== | |||
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== | ||
*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> | *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 | **Diffuse [[lymphocytic]] infiltrate | ||
**Lack of Hurthle cells (Askanazy cells) and [[germinal centers]] | **Lack of [[Hurthle cells]] (Askanazy cells) and [[germinal centers]] | ||
**Lack of [[fibrosis]] | **Lack of [[fibrosis]] | ||
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{{Reflist|2}} | {{Reflist|2}} | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
[[Category:Medicine]] | |||
[[Category:Endocrinology]] | |||
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Latest revision as of 00:11, 30 July 2020
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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]
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 |
Pathogenesis
- 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:[3][4][5][6]
- Lymphocytic infiltration of the thyroid gland
- Presence of antithyroid antibodies
- Association with HLA-DR3 and DR5
- Presence of anti-DNA antibodies
- 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 of helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis.[7]
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]
- SLE
- Lymphocytic hypophysitis
- Immune thrombocytopenic purpura (ITP)
- Cushing's syndrome (post adrenalectomy and steroid therapy cessation)
- Hodgkin's lymphoma (post-irradiation)
Gross Pathology
Gross pathology findings in silent thyroiditis include:[12]
- Diffuse goiter
- Slightly enlarged thyroid gland
Microscopic Pathology
- Microscopic histopathological findings in silent thyroiditis include:[3][13]
- Diffuse lymphocytic infiltrate
- Lack of Hurthle cells (Askanazy cells) and germinal centers
- Lack of fibrosis
References
- ↑ 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.
- ↑ 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.
- ↑ 3.0 3.1 Volpé R (1988). "Is silent thyroiditis an autoimmune disease?". Arch. Intern. Med. 148 (9): 1907–8. PMID 3415401.
- ↑ 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.
- ↑ 5.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Pathology Outlines - Silent thyroiditis".
- ↑ 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.