De Quervain's thyroiditis pathophysiology
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De Quervain's thyroiditis Microchapters |
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Differentiating De Quervain's thyroiditis from other Diseases |
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Diagnosis |
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Treatment |
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 de Quervain's thyroiditis is unclear. It is proposed that cytotoxic T cell recognition of complex viral and cell antigens presentation leads to the thyroid follicular cell damage which is responsible for the pathogenesis of de Quervain's thyroiditis. De Quervain's thyroiditis is usually preceded by a viral prodrome and also have a genetic predisposition. HLA B35 and HLA B15/62 are associated with de Quervain's 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 de Quervain's thyroiditis is unclear, but autoimmunity mechanism is proposed.[3][4][5]
- De Quervain's thyroiditis is usually preceded by a viral prodrome. Various viral infections are associated with the de Quervain's thyroiditis including mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus.
- De Quervain's thyroiditis is associated with HLA BB35. It is postulated that the antigen triggers the activation of HLA B35 positive inflammatory cells which in turn activates the cytotoxic T-lymphocytes.
- Cytotoxic T cell recognition of viral and cell antigens presented in a complex leads to the thyroid follicular cell damage.
- The autoimmune process leads to inflammatory cells infiltration of the gland. The changes may lead to granulomatous or non-granulomatous lesions.
- Granulomatous lesion
- Granulomatous lesion comprises of colloid, small lymphocytes, neutrophils, macrophages with or without epithelioid features, and multinucleated giant cells of foreign body type. In the granulomatous lesion, the giant cells are usually CD68+, thyroglobulin– and cytokeratin–. Small lymphocytes in the granulomas are CD3+, CD8+, CD45RO+ cytotoxic T-cells. Numerous plasmacytoid monocytes were also closely associated with the granulomas.
- Non-granulomatous lesion
- Follicles in the non-granulomatous lesion are infiltrated by CD8+ T-lymphocytes, plasmacytoid monocytes, and histiocytes, resulting in disrupted basement membrane and rupture of the follicles.
- Granulomatous lesion
Genetics
- De Quervain's thyroiditis is associated with:[6][7]
- The human leukocyte antigen (HLA B35
- HLA B15/62 (in rare cases)
Associated conditions
The following conditions may be associated with De Quervain's thyroiditis:[8]
Gross Pathology
On gross pathology, subacute thyroiditis frequently resembles thyroid malignancy. Subacute thyroiditis usually has the following features:[9]
- Firm to dense consistency
- Pale white color
- Poorly defined margins
- Involvement of adjacent normal thyroid
Microscopic pathology
The primary pathology of de Quervain's thyroiditis is:[3][9]
- Infiltration with polymorphonuclear leukocytes initially
- Predominance of lymphocytes and macrophages in advanced form
- Destruction of the follicular epithelium
- Parenchymal destruction and scar tissue
- Loss of the follicular integrity
Gallery
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De Quervain's thyroiditis (By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491382)
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De Quervain's thyroiditis (By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491421)
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De Quervain's thyroiditis (By Nephron - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491421)
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 Kojima M, Nakamura S, Oyama T, Sugihara S, Sakata N, Masawa N (2002). "Cellular composition of subacute thyroiditis. an immunohistochemical study of six cases". Pathol. Res. Pract. 198 (12): 833–7. doi:10.1078/0344-0338-00344. PMID 12608662.
- ↑ Erdem N, Erdogan M, Ozbek M, Karadeniz M, Cetinkalp S, Ozgen AG, Saygili F, Yilmaz C, Tuzun M, Kabalak T (2007). "Demographic and clinical features of patients with subacute thyroiditis: results of 169 patients from a single university center in Turkey". J. Endocrinol. Invest. 30 (7): 546–50. PMID 17848836.
- ↑ Desailloud R, Hober D (2009). "Viruses and thyroiditis: an update". Virol. J. 6: 5. doi:10.1186/1743-422X-6-5. PMC 2654877. PMID 19138419.
- ↑ Nyulassy S, Hnilica P, Buc M, Guman M, Hirschová V, Stefanovic J (1977). "Subacute (de Quervain's) thyroiditis: association with HLA-Bw35 antigen and abnormalities of the complement system, immunoglobulins and other serum proteins". J. Clin. Endocrinol. Metab. 45 (2): 270–4. doi:10.1210/jcem-45-2-270. PMID 885992.
- ↑ de Bruin TW, Riekhoff FP, de Boer JJ (1990). "An outbreak of thyrotoxicosis due to atypical subacute thyroiditis". J. Clin. Endocrinol. Metab. 70 (2): 396–402. doi:10.1210/jcem-70-2-396. PMID 2298855.
- ↑ Fatourechi V, Aniszewski JP, Fatourechi GZ, Atkinson EJ, Jacobsen SJ (2003). "Clinical features and outcome of subacute thyroiditis in an incidence cohort: Olmsted County, Minnesota, study". J. Clin. Endocrinol. Metab. 88 (5): 2100–5. doi:10.1210/jc.2002-021799. PMID 12727961.
- ↑ 9.0 9.1 Shrestha RT, Hennessey J. Acute and Subacute, and Riedel’s Thyroiditis.