De Quervain's thyroiditis

Last updated
De Quervain's thyroiditis
Other namesGiant cell thyroiditis, subacute granulomatous thyroiditis
Subacute thyroiditis - intermed mag.jpg
Micrograph showing a granuloma in subacute thyroiditis. H&E stain.
Specialty Endocrinology   OOjs UI icon edit-ltr-progressive.svg

De Quervain's thyroiditis, also known as subacute granulomatous thyroiditis or giant cell thyroiditis, is a self-limiting inflammatory illness of the thyroid gland. [1] De Quervain thyroiditis is characterized by fever, flu-like symptoms, a painful goiter, and neck pain. The disease has a natural history of four phases: thyroid pain, thyrotoxicosis, euthyroid phase, hypothyroid phase, and recovery euthyroid phase.

Contents

De Quervain's thyroiditis has been linked to various diseases, including mumps, adenovirus, and enterovirus. It may have a hereditary component, with two-thirds of patients having positive histocompatibility antigen (HLA) B35 results. Atypical cases have HLA B15/62 positivity, and it is more common in summer or fall months in people who test positive for HLA B67.

De Quervain thyroiditis is diagnosed through clinical and test results, with laboratory features including elevated C-reactive protein and erythrocyte sedimentation rate. Thyroid function testing often shows decreased thyroid stimulating hormone and increased serum levels of triiodothyronine and thyroxine during the acute phase. Thyroid scans show minimal uptake during the acute phase due to disrupted thyroid follicles, but increase during recovery due to the thyroid gland's enhanced iodine trapping capacity. Thyroid ultrasonography typically shows thyroid gland enlargement and hypoechogenicity, while color Doppler ultrasonography may show low or normal vascular flow. Tissue diagnosis is rare, but fine needle aspiration may be helpful in questionable cases to differentiate unilateral involvement from bleeding into a cyst or tumor.

Treatment involves symptomatic medication, glucocorticoid medication for severe cases, and beta-adrenergic blockers for thyrotoxic symptoms. The condition typically resolves within three to six months. However, 20-56% of adult patients experience transient hypothyroidism, which can persist for years. Recurrent hypothyroidism is rare, occurring in about 2% of cases, and usually manifests within a year after diagnosis. Late recurrences have been reported.

Signs and symptoms

Patients typically present with low-grade fever and flu-like symptoms such as sore throat, myalgia, arthralgia, and malaise, which are followed by high-grade fever, a painful, widespread goiter, and neck pain. [2] The neck pain is usually unilateral at first, then spreads to the other side and can radiate to the ipsilateral jaw, ear, occiput, or chest. [3] [4] Other symptoms, such as dysphagia and breathing difficulties caused by airway blockage, are uncommon. [2]

The thyroid gland is extremely painful, rigid, and swollen, which can be symmetrical or asymmetrical. [2] Approximately half of affected adolescents and two-thirds of adults have widespread thyroid gland involvement. [3] [5] Thyroid nodules are seen in one-fourth of adult patients. [6] The surrounding skin is occasionally warm and erythematous. Cervical lymphadenopathy is rare. [2] During the early stages of the condition, almost half of patients experience thyrotoxic symptoms such as anxiety, tachycardia, palpitation, and weight loss. [7] [8]

The typical natural history of de Quervain thyroiditis has four phases, beginning with thyroid discomfort and thyrotoxicosis, followed by a brief euthyroid phase, temporary hypothyroid phase, and recovery euthyroid phase. [7]

Causes

De Quervain's thyroiditis has been linked to a variety of viral illnesses, including mumps, [9] adenovirus, [10] Epstein-Barr virus, [11]  cytomegalovirus, [12] coxsackievirus, [13]  influenza, [10] echovirus, [14] and enterovirus. [15]

Furthermore, the development of de Quervain thyroiditis may have a hereditary component. [2] About two thirds of patients with de Quervain thyroiditis were found to have positive histocompatibility antigen (HLA) B35 results. [16] [17] Furthermore, it was found that identical twins who were heterozygous for the HLA B35 haplotype also developed de Quervain thyroiditis at the same time. [18] Atypical cases of de Quervain thyroiditis have also been documented to have HLA B15/62 positivity, [19] and summer or fall months are when de Quervain thyroiditis is more common in people who test positive for HLA B67. [20]

Mechanism

It's still unclear exactly what causes de Quervain thyroiditis. According to available data, it is not an autoimmune illness. Still, the most likely cause is a viral infection. [2] One theory for the pathophysiology of virus-associated thyroiditis is that thyroid follicular cell destruction results from cytotoxic T cell identification of viral and cell antigens presented as a complex. [15] [21]

Diagnosis

The most common methods for diagnosing de Quervain thyroiditis are clinical and test results. [2] Elevations of C-reactive protein and erythrocyte sedimentation rate are laboratory features of the condition. [3] While typically normal, the blood leukocyte count may be slightly increased. There may be anemia that is normochromic and normocytic. Thyroid function testing frequently reveals decreased thyroid stimulating hormone (TSH) and increased serum levels of triiodothyronine (T3) and thyroxine (T4) during the acute phase of the disease. [2] The intrathyroidal T3 and T4 levels are often reflected by the T3 to T4 ratio, which is typically less than 20 (ng/dL divided by μg/dL). [22] Nearly all patients have increased serum thyroglobulin, which is consistent with follicular destruction. [23]

Thyroid scans using technetium (99mTc) pertechnetate or RAIU usually show minimal uptake during the acute phase. This happens when thyroid follicles are disrupted, which impairs iodine trapping. [2] Thyroid scan uptake increases throughout the recovery phase due to the thyroid gland's enhanced capacity to trap iodine, which eventually returns to normal after full recovery. [7]

Thyroid gland enlargement and a region of hypoechogenicity that correlates to the inflammatory area are typically seen on thyroid ultrasonography. [24] Low or normal vascular flow may be shown by color Doppler ultrasonography. [25]

Rarely is tissue diagnosis required. Fine needle aspiration may be helpful in questionable cases, such as the area of pain restricted to a single nodule or confined area, to differentiate unilateral involvement from bleeding into a cyst or tumor. [26]

Treatment

The goals of treatment are to lessen hyperthyroid symptoms and relieve discomfort. Pain control only necessitates symptomatic treatment with non-steroidal anti-inflammatory medications or aspirin. [2] Severely sick individuals may benefit from glucocorticoid medication, which often produces a substantial response in 24 to 48 hours. [4] Thyrotoxic symptoms are managed with beta-adrenergic blockers such atenolol and propranolol. [2]

Outlook

De Quervain thyroiditis is a self-limiting condition that often goes away without any problems in three to six months. [3] [5] Regardless of the severity of the disease or the type of treatment used, 20–56% of adult patients experienced transient hypothyroidism a few weeks after the hyperthyroid period. [27] Though it only happens in 5–15% of cases, persistent hypothyroidism can develop years after the diagnosis. [6] [28] Recurrent de Quervain thyroiditis is rare, occurring in about 2% of cases, and usually manifests again within a year after diagnosis. But there have also been reports of late recurrences after several years. [6] [29] [30]

Epidemiology

Subacute or De Quervain thyroiditis is an unusual diagnosis, occurring in 12.1 out of 100,000 people annually. [31] Children are rarely affected by the De Quervain thyroiditis. With a female-to-male ratio of 4–7:1, females are more likely to be impacted than males. [2]

History

De Quervain thyroiditis was originally reported in 1895 by Mygind. [32] Fritz de Quervain distinguished this illness from other types of thyroiditis in 1904 based on a histological discovery, [33] and de Quervain and Giordanengo confirmed the diagnosis in 1936. [34]

Related Research Articles

<span class="mw-page-title-main">Hyperthyroidism</span> Clinical syndrome caused by excessive thyroid hormone

Hyperthyroidism is the condition that occurs due to excessive production of thyroid hormones by the thyroid gland. Thyrotoxicosis is the condition that occurs due to excessive thyroid hormone of any cause and therefore includes hyperthyroidism. Some, however, use the terms interchangeably. Signs and symptoms vary between people and may include irritability, muscle weakness, sleeping problems, a fast heartbeat, heat intolerance, diarrhea, enlargement of the thyroid, hand tremor, and weight loss. Symptoms are typically less severe in the elderly and during pregnancy. An uncommon but life-threatening complication is thyroid storm in which an event such as an infection results in worsening symptoms such as confusion and a high temperature; this often results in death. The opposite is hypothyroidism, when the thyroid gland does not make enough thyroid hormone.

<span class="mw-page-title-main">Hypothyroidism</span> Insufficient production of thyroid hormones by the thyroid gland

Hypothyroidism is a disorder of the endocrine system in which the thyroid gland does not produce enough thyroid hormones. It can cause a number of symptoms, such as poor ability to tolerate cold, extreme fatigue, muscle aches, constipation, slow heart rate, depression, and weight gain. Occasionally there may be swelling of the front part of the neck due to goitre. Untreated cases of hypothyroidism during pregnancy can lead to delays in growth and intellectual development in the baby or congenital iodine deficiency syndrome.

<span class="mw-page-title-main">Gigantism</span> Human growth disorder

Gigantism, also known as giantism, is a condition characterized by excessive growth and height significantly above average. In humans, this condition is caused by over-production of growth hormone in childhood.

Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid.

<span class="mw-page-title-main">Hashimoto's thyroiditis</span> Autoimmune disease

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimoto's disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. A slightly broader term is autoimmune thyroiditis, identical other than that it is also used to describe a similar condition without a goiter.

Ord's thyroiditis is an atrophic form of chronic thyroiditis, an autoimmune disease where the body's own antibodies fight the cells of the thyroid.

<span class="mw-page-title-main">Thyroid disease</span> Medical condition

Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.

<span class="mw-page-title-main">Thyroiditis</span> Medical condition

Thyroiditis is the inflammation of the thyroid gland. The thyroid gland is located on the front of the neck below the laryngeal prominence, and makes hormones that control metabolism.

<span class="mw-page-title-main">McCune–Albright syndrome</span> Mosaic genetic disorder affecting the bone, skin and endocrine systems

McCune–Albright syndrome is a complex genetic disorder affecting the bone, skin and endocrine systems. It is a mosaic disease arising from somatic activating mutations in GNAS, which encodes the alpha-subunit of the Gs heterotrimeric G protein.

<span class="mw-page-title-main">Adrenocorticotropic hormone deficiency</span> Medical condition

Adrenocorticotropic hormone deficiency is a rare disorder characterized by secondary adrenal insufficiency with minimal or no cortisol production and normal pituitary hormone secretion apart from ACTH. ACTH deficiency may be congenital or acquired, and its symptoms are clinically similar to those of glucocorticoid deficiency. Symptoms consist of weight loss, diminished appetite, muscle weakness, nausea, vomiting, and hypotension. Low blood sugar and hyponatremia are possible; however, blood potassium levels typically remain normal because affected patients are deficient in glucocorticoids rather than mineralocorticoids because of their intact renin-angiotensin-aldosterone system. ACTH may be undetectable in blood tests, and cortisol is abnormally low. Glucocorticoid replacement therapy is required. With the exception of stressful situations, some patients with mild or nearly asymptomatic disease may not require glucocorticoid replacement therapy. As of 2008 about two hundred cases have been described in the literature.

Desiccated thyroid, also known as thyroid extract, is thyroid gland that has been dried and powdered for medical use. It is used to treat hypothyroidism., but less preferred than levothyroxine. It is taken by mouth. Maximal effects may take up to three weeks to occur.

<span class="mw-page-title-main">Subacute thyroiditis</span> Medical condition

Subacute thyroiditis refers to a temporal classification of the different forms of thyroiditis based on onset of symptoms. The temporal classification of thyroiditis includes presentation of symptoms in an acute, subacute, or chronic manner. There are also other classification systems for thyroiditis based on factors such as clinical symptoms and underlying etiology.

<span class="mw-page-title-main">Endocrine disease</span> Disorders of the endocrine system

Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology.

Postpartum thyroiditis refers to thyroid dysfunction occurring in the first 12 months after pregnancy and may involve hyperthyroidism, hypothyroidism or the two sequentially. According to the National Institute of Health, postpartum thyroiditis affects about 8% of pregnancies. There are, however, different rates reported globally. This is likely due to the differing amounts of average postpartum follow times around the world, and due to humans' own innate differences. For example, in Bangkok, Thailand the rate is 1.1%, but in Brazil it is 13.3%. The first phase is typically hyperthyroidism. Then, the thyroid either returns to normal or a woman develops hypothyroidism. Of those women who experience hypothyroidism associated with postpartum thyroiditis, one in five will develop permanent hypothyroidism requiring lifelong treatment.

<span class="mw-page-title-main">Sodium/iodide cotransporter</span> Mammalian protein found in Homo sapiens

The sodium/iodide cotransporter, also known as the sodium/iodide symporter (NIS), is a protein that in humans is encoded by the SLC5A5 gene. It is a transmembrane glycoprotein with a molecular weight of 87 kDa and 13 transmembrane domains, which transports two sodium cations (Na+) for each iodide anion (I−) into the cell. NIS mediated uptake of iodide into follicular cells of the thyroid gland is the first step in the synthesis of thyroid hormone.

<span class="mw-page-title-main">Thyroid hormones</span> Hormones produced by the thyroid gland

Thyroid hormones are any hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine, derived from food. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre.

<span class="mw-page-title-main">Autoimmune polyendocrine syndrome type 2</span> Medical condition

Autoimmune polyendocrine syndrome type 2, a form of autoimmune polyendocrine syndrome also known as APS-II, or PAS II, is the most common form of the polyglandular failure syndromes. PAS II is defined as the association between autoimmune Addison's disease and either autoimmune thyroid disease, type 1 diabetes, or both. It is heterogeneous and has not been linked to one gene. Rather, individuals are at a higher risk when they carry a particular human leukocyte antigen. APS-II affects women to a greater degree than men.

Thyroid disease in pregnancy can affect the health of the mother as well as the child before and after delivery. Thyroid disorders are prevalent in women of child-bearing age and for this reason commonly present as a pre-existing disease in pregnancy, or after childbirth. Uncorrected thyroid dysfunction in pregnancy has adverse effects on fetal and maternal well-being. The deleterious effects of thyroid dysfunction can also extend beyond pregnancy and delivery to affect neurointellectual development in the early life of the child. Due to an increase in thyroxine binding globulin, an increase in placental type 3 deioidinase and the placental transfer of maternal thyroxine to the fetus, the demand for thyroid hormones is increased during pregnancy. The necessary increase in thyroid hormone production is facilitated by high human chorionic gonadotropin (hCG) concentrations, which bind the TSH receptor and stimulate the maternal thyroid to increase maternal thyroid hormone concentrations by roughly 50%. If the necessary increase in thyroid function cannot be met, this may cause a previously unnoticed (mild) thyroid disorder to worsen and become evident as gestational thyroid disease. Currently, there is not enough evidence to suggest that screening for thyroid dysfunction is beneficial, especially since treatment thyroid hormone supplementation may come with a risk of overtreatment. After women give birth, about 5% develop postpartum thyroiditis which can occur up to nine months afterwards. This is characterized by a short period of hyperthyroidism followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.

Autoimmune polyendocrine syndrome, type 3 is a condition characterized by the coexistence of autoimmune thyroiditis and at least one other autoimmune disease. Based on other organ-specific autoimmune involvement, there are multiple subtypes that are classified: type 3a shows thyroid autoimmune disease in conjunction with type 1 diabetes, type 3b shows thyroid autoimmune disease in conjunction with pernicious anemia (PA), and type 3c shows thyroid autoimmune disease in conjunction with alopecia, vitiligo, or other organ-specific autoimmune disease.

<span class="mw-page-title-main">Jostel's TSH index</span>

Jostel's TSH index, also referred to as Jostel's thyrotropin index or Thyroid Function index (TFI), is a method for estimating the thyrotropic function of the anterior pituitary lobe in a quantitative way. The equation has been derived from the logarithmic standard model of thyroid homeostasis. In a paper from 2014 further study was suggested to show if it is useful, but the 2018 guideline by the European Thyroid Association for the diagnosis of uncertain cases of central hypothyroidism regarded it as beneficial. It is also recommended for purposes of differential diagnosis in the sociomedical expert assessment.

References

  1. ↑ Engkakul, Pontipa; Mahachoklertwattana, Pat; Poomthavorn, Preamrudee (2011). "de Quervain thyroiditis in a young boy following hand–foot–mouth disease". European Journal of Pediatrics. 170 (4): 527–529. doi:10.1007/s00431-010-1305-5. ISSN   0340-6199. PMID   20886354.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 Engkakul, Pontipa; Mahachoklertwattana, Pat; Poomthavorn, Preamrudee (2011). "Eponym: de Quervain thyroiditis". European Journal of Pediatrics. 170 (4): 427–431. doi:10.1007/s00431-010-1306-4. ISSN   0340-6199. PMID   20886353.
  3. 1 2 3 4 Greene, James N. (1971). "Subacute thyroiditis". The American Journal of Medicine. 51 (1). Elsevier BV: 97–108. doi:10.1016/0002-9343(71)90327-5. ISSN   0002-9343. PMID   4936649.
  4. 1 2 Volpé, Robert (1993). "The Management of Subacute (DeQuervain's) Thyroiditis". Thyroid. 3 (3): 253–255. doi:10.1089/thy.1993.3.253. ISSN   1050-7256. PMID   8257868.
  5. 1 2 Ogawa, E.; Katsushima, Y.; Fujiwara, I.; Iinuma, K. (2003). "Subacute Thyroiditis in Children: Patient Report and Review of the Literature". Journal of Pediatric Endocrinology and Metabolism. 16 (6). Walter de Gruyter GmbH: 897–900. doi:10.1515/jpem.2003.16.6.897 (inactive 2024-07-03). ISSN   2191-0251. PMID   12948304.{{cite journal}}: CS1 maint: DOI inactive as of July 2024 (link)
  6. 1 2 3 Fatourechi, Vahab; Aniszewski, Jaroslaw P.; Fatourechi, Guiti Z. Eghbali; Atkinson, Elizabeth J.; Jacobsen, Steven J. (2003-05-01). "Clinical Features and Outcome of Subacute Thyroiditis in an Incidence Cohort: Olmsted County, Minnesota, Study". The Journal of Clinical Endocrinology & Metabolism. 88 (5): 2100–2105. doi:10.1210/jc.2002-021799. ISSN   0021-972X. PMID   12727961.
  7. 1 2 3 Bindra, Archana; Braunstein, Glenn D. (2006-05-15). "Thyroiditis". American Family Physician. 73 (10): 1769–1776. ISSN   0002-838X. PMID   16734054.
  8. ↑ Pearce, Elizabeth N.; Farwell, Alan P.; Braverman, Lewis E. (2003-06-26). "Thyroiditis". New England Journal of Medicine. 348 (26). Massachusetts Medical Society: 2646–2655. doi:10.1056/nejmra021194. ISSN   0028-4793. PMID   12826640.
  9. ↑ Eylan, E.; Zmucky, R.; Sheba, Ch. (1957). "Mumps Virus and Subacute Thyroiditis". The Lancet. 269 (6978): 1062–1063. doi:10.1016/S0140-6736(57)91438-1. PMID   13429875.
  10. 1 2 BUCHTA, RICHARD M. (1980-11-01). "Subacute Thyroiditis in a 4½-Year-Old Girl". Archives of Pediatrics & Adolescent Medicine. 134 (11). American Medical Association (AMA): 1090–1091. doi:10.1001/archpedi.1980.02130230068019. ISSN   1072-4710. PMID   7435469.
  11. ↑ Volta, Cecilia; Carano, Nicola; Street, Maria Elisabeth; Bernasconi, Sergio (2005). "Atypical Subacute Thyroiditis Caused by Epstein-Barr Virus Infection in a Three-Year-Old Girl". Thyroid. 15 (10): 1189–1191. doi:10.1089/thy.2005.15.1189. hdl: 11381/1444490 . ISSN   1050-7256.
  12. ↑ Al Maawali, A.; Al Yaarubi, S.; Al Futaisi, A. (2008). "An Infant with Cytomegalovirus-induced Subacute Thyroiditis". Journal of Pediatric Endocrinology and Metabolism. 21 (2). Walter de Gruyter GmbH. doi:10.1515/jpem.2008.21.2.191 (inactive 2024-07-03). ISSN   2191-0251.{{cite journal}}: CS1 maint: DOI inactive as of July 2024 (link)
  13. ↑ Brouqui, P.; Raoult, D.; Conte-Devolx, B. (1991-06-15). "Coxsackie Thyroiditis". Annals of Internal Medicine. 114 (12). American College of Physicians: 1063–1064. doi:10.7326/0003-4819-114-12-1063_2. ISSN   0003-4819. PMID   1851403.
  14. ↑ Volpé, Robert; Row, Vas V.; Ezrin, Calvin (1967). "Circulating Viral and Thyroid Antibodies in Subacute Thyroiditis 1". The Journal of Clinical Endocrinology & Metabolism. 27 (9): 1275–1284. doi:10.1210/jcem-27-9-1275. ISSN   0021-972X. PMID   4292248.
  15. 1 2 Desailloud, Rachel; Hober, Didier (2009). "Viruses and thyroiditis: an update". Virology Journal. 6 (1): 5. doi: 10.1186/1743-422X-6-5 . ISSN   1743-422X. PMC   2654877 . PMID   19138419.
  16. ↑ Bech, Karine; Lumholtz, Bo; Nerup, Jørn; Thomsen, Mogens; Platz, Per; Ryder, Lars P.; Svejgaard, Arne; Siersbæk-Nielsen, Kaj; Hansen, Jens Mølholm; Larsen, Jørgen Hannover (1977). "HLA Antigens in Graves' Disease". Acta Endocrinologica. 86 (3): 510–516. doi:10.1530/acta.0.0860510. ISSN   0804-4643. PMID   72471.
  17. ↑ NYULASSY, ŠTEFAN; HNILICA, PETER; BUC, MILAN; GUMAN, MILAN; HIRSCHOVÁ, VIERA; JÁN, ŠTEFANOVIC (1977). "Subacute (de Quervain's) Thyroiditis: Association with HLA-Bw35 Antigen and Abnormalities of the Complement System, Immunoglobulins and Other Serum Proteins". The Journal of Clinical Endocrinology & Metabolism. 45 (2). The Endocrine Society: 270–274. doi:10.1210/jcem-45-2-270. ISSN   0021-972X. PMID   885992.
  18. ↑ RUBIN, ROBERT A.; GUAY, ANDRÉ T. (1991). "Susceptibility to Subacute Thyroiditis Is Genetically Influenced: Familial Occurrence in Identical Twins". Thyroid. 1 (2). Mary Ann Liebert Inc: 157–161. doi:10.1089/thy.1991.1.157. ISSN   1050-7256. PMID   1822362.
  19. ↑ DE BRUIN, TJERK W. A.; RIEKHOFF, FRANS P. M.; DE BOER, JOHANNES J. (1990). "An Outbreak of Thyrotoxicosis due to Atypical Subacute Thyroiditis*". The Journal of Clinical Endocrinology & Metabolism. 70 (2). The Endocrine Society: 396–402. doi:10.1210/jcem-70-2-396. ISSN   0021-972X. PMID   2298855.
  20. ↑ Ohsako, N; Tamai, H; Sudo, T; Mukuta, T; Tanaka, H; Kuma, K; Kimura, A; Sasazuki, T (1995). "Clinical characteristics of subacute thyroiditis classified according to human leukocyte antigen typing". The Journal of Clinical Endocrinology & Metabolism. 80 (12). The Endocrine Society: 3653–3656. doi:10.1210/jcem.80.12.8530615. ISSN   0021-972X. PMID   8530615.
  21. ↑ Kojima, Masaru; Nakamura, Shigeo; Oyama, Tetsunari; Sugihara, Shiro; Sakata, Noriyuki; Masawa, Nobuhide (2002). "Cellular Composition of Subacute Thyroiditis. An Immunohistochemical Study of Six Cases". Pathology — Research and Practice. 198 (12). Elsevier BV: 833–837. doi:10.1078/0344-0338-00344. ISSN   0344-0338. PMID   12608662.
  22. ↑ AMINO, NOBUYUKI; YABU, YUKIKO; MIKI, TETSURO; MORIMOTO, SHIGETO; KUMAHARA, YUICHI; MORI, HIDEMITSU; IWATANI, YOSHINORI; NISHI, KEIKO; NAKATANI, KIYOMI; MIYAI, KIYOSHI (1981). "Serum Ratio of Triiodothyronine to Thyroxine, and Thyroxine-Binding Globulin and Calcitonin Concentrations in Graves' Disease and Destruction- Induced Thyrotoxicosis*". The Journal of Clinical Endocrinology & Metabolism. 53 (1). The Endocrine Society: 113–116. doi:10.1210/jcem-53-1-113. ISSN   0021-972X. PMID   6165731.
  23. ↑ Madeddu, G.; Casu, A. R.; Costanza, C.; Marras, G.; Arras, M. L.; Marrosu, A.; Langer, M. (1985). "Serum thyroglobulin levels in the diagnosis and follow-up of subacute 'painful' thyroiditis. A sequential study". Archives of Internal Medicine. 145 (2): 243–247. doi:10.1001/archinte.1985.00360020063012. ISSN   0003-9926. PMID   3977482.
  24. ↑ OMORI, Nariko; OMORI, Kazue; TAKANO, Kazue (2008). "Association of the Ultrasonographic Findings of Subacute Thyroiditis with Thyroid Pain and Laboratory Findings". Endocrine Journal. 55 (3). Japan Endocrine Society: 583–588. doi:10.1507/endocrj.k07e-163. ISSN   0918-8959. PMID   18490832.
  25. ↑ HIROMATSU, YUJI; ISHIBASHI, MASATOSHI; MIYAKE, IKUYO; SOYEJIMA, ERI; YAMASHITA, KIMIKO; KOIKE, NORIMASA; NONAKA, KYOHEI (1999). "Color Doppler Ultrasonography in Patients with Subacute Thyroiditis". Thyroid. 9 (12). Mary Ann Liebert Inc: 1189–1193. doi:10.1089/thy.1999.9.1189. ISSN   1050-7256. PMID   10646657.
  26. ↑ Walfish, P. G. (1997). "Thyroiditis". Current Therapy in Endocrinology and Metabolism. 6: 117–122. ISSN   0831-652X. PMID   9174718.
  27. ↑ Benbassat, C. A.; Olchovsky, D.; Tsvetov, G.; Shimon, I. (2007). "Subacute thyroiditis: Clinical characteristics and treatment outcome in fifty-six consecutive patients diagnosed between 1999 and 2005". Journal of Endocrinological Investigation. 30 (8). Springer Science and Business Media LLC: 631–635. doi:10.1007/bf03347442. ISSN   0391-4097. PMID   17923793.
  28. ↑ Lio, Serafino; Pontecorvi, Alfredo; Caruso, Michela; Monaco, Fabrizio; D'Armiento, Massimo (1984). "Transitory subclinical and permanent hypothyroidism in the course of subacute thyroiditis (de Quervain)". Acta Endocrinologica. 106 (1). Oxford University Press (OUP): 67–70. doi:10.1530/acta.0.1060067. ISSN   0804-4643. PMID   6428116.
  29. ↑ Nishihara, Eijun; Ohye, Hidemi; Amino, Nobuyuki; Takata, Kazuna; Arishima, Takeshi; Kudo, Takumi; Ito, Mitsuru; Kubota, Sumihisa; Fukata, Shuji; Miyauchi, Akira (2008). "Clinical Characteristics of 852 Patients with Subacute Thyroiditis before Treatment". Internal Medicine. 47 (8). Japanese Society of Internal Medicine: 725–729. doi:10.2169/internalmedicine.47.0740. ISSN   0918-2918. PMID   18421188.
  30. ↑ Iitaka, M; Momotani, N; Ishii, J; Ito, K (1996). "Incidence of subacute thyroiditis recurrences after a prolonged latency: 24-year survey". The Journal of Clinical Endocrinology & Metabolism. 81 (2). The Endocrine Society: 466–469. doi: 10.1210/jcem.81.2.8636251 . ISSN   0021-972X. PMID   8636251.
  31. ↑ Frates, Mary C.; Marqusee, Ellen; Benson, Carol B.; Alexander, Erik K. (2013). "Subacute Granulomatous (de Quervain) Thyroiditis: Grayscale and Color Doppler Sonographic Characteristics". Journal of Ultrasound in Medicine. 32 (3): 505–511. doi:10.7863/jum.2013.32.3.505. PMID   23443191.
  32. ↑ Mygind, Holger (1895). "Thyroiditis Acuta Simplex". The Journal of Laryngology, Rhinology, and Otology. 9 (3). Cambridge University Press (CUP): 181–193. doi:10.1017/s1755146300152771. ISSN   1755-1463.
  33. ↑ Quervain, F. de (2024-07-02). "Die akute, nicht eiterige Thyreoiditis : und die Beteiligung der Schilddrüse an akuten Intoxikationen und Infektionen überhaupt". (No Title) (in Latin). Retrieved 2024-07-03.
  34. ↑ Quervain, F; Giordanengo, G (1936). "Die akute und subakute nicht eiterige Thyreoiditis". Mitt Grenzgeb Med Chir. 44: 538–590.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.