De Quervain's thyroiditis

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

De Quervain’s thyroiditis is also known as subacute thyroiditis. In 1895, Mygind first described de Quervain’s thyroiditis. In 1904, Fritz de Quervain differentiated this disease from other forms of thyroiditis on the basis of the pathological findings. De Quervain’s thyroiditis can be classified according to the development of symptoms into the prodromal stage, hyperthyroid stage, euthyroid stage, and hypothyroid stage. The exact pathogenesis of de Quervain’s thyroiditis is unclear. It is proposed that cytotoxic T cell recognition of viral and cell antigens, presented in a complex, 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. Human leukocyte antigen B35 and B15/62 are associated with de Quervain’s thyroiditis. De Quervain’s thyroiditis may be caused by viruses such as mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus. De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Common risk factors in the development of de Quervain’s thyroiditis are viral illness, family history, and female gender. De Quervain’s thyroiditis develops after a viral prodrome and presents as painful thyroid gland with symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications include hypothyroidism and rarely, esophageal or tracheal compression. The hallmark of de Quervain’s thyroiditis is hyperthyroidism with the neck pain. A positive history of viral illness and family history of de Quervain’s thyroiditis are suggestive of de Quervain’s thyroiditis. The most common symptoms of de Quervain’s thyroiditis are neck pain, palpitations, tachycardia, nervousness, and tremors. Patients with de Quervain’s thyroiditis usually appear fatigued and restless. Physical examination of patients with de Quervain’s thyroiditis is usually remarkable for neck tenderness, tachycardia, and palpitations. In the recovery phase of de Quervain’s thyroiditis patient may develop hypothyroidism. Laboratory findings consistent with the diagnosis of de Quervain’s thyroiditis usually include increased ESR, free T3, and free T4 and decreased thyroid stimulating hormone. Anti-thyroid peroxidase antibody is usually low or absent. The most common EKG finding associated with the thyrotoxicosis in de Quervain’s thyroiditis is sinus tachycardia. Rarely signs of myocardial damage including ST-segment elevation and arrhythmias can also be seen in thyrotoxicosis. Chest X-ray findings in de Quervain’s thyroiditis are usually not significant, but if there is concomitant myocarditis or heart failure, cardiomegaly and pulmonary edema are probable. Non-contrast CT may be used in de Quervain’s thyroiditis to assess the esophageal or tracheal compression. In de Quervain’s thyroiditis, T1-weighted MRI shows mild and T2-weighted image shows a more pronounced hyperintensity in the thyroid gland. Ultrasound findings associated with de Quervain’s thyroiditis are hypoechoic areas, glandular irregularities, and nonhomogeneous echotexture. The histological analysis in de Quervain’s thyroiditis may show the destruction of the follicular epithelium, loss of the follicular integrity and infiltration of inflammatory cells. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules. The mainstay of therapy for de Quervain’s thyroiditis is aspirin or non-steroidal anti-inflammatory drugs for pain control. Beta-adrenergic blockers are recommended for the patients who develop thyrotoxic symptoms. Corticosteroids are usually used in severely ill patients. Surgical intervention is not usually recommended for the management of de Quervain’s thyroiditis. Thyroidectomy is considered only when there are repeated relapses despite appropriate treatment.

In 1895, Mygind first described de Quervain’s thyroiditis. In 1904, Fritz de Quervain differentiated this disease from other forms of thyroiditis on the basis of the pathological findings.

De Quervain’s thyroiditis can be classified according to the development of symptoms into the prodromal stage, hyperthyroid stage, euthyroid stage, and hypothyroid stage.

The exact pathogenesis of de Quervain’s thyroiditis is unclear. It is proposed that cytotoxic T cell recognition of viral and cell antigens, presented in a complex, 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.

De Quervain’s thyroiditis may be caused by viruses such as mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus. Genetic factors also predispose an individual towards de Quervain’s thyroiditis.

De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. De Quervain’s thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As de Quervain’s thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

De Quervain’s thyroiditis is particularly common in middle-aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide.

Common risk factors in the development of de Quervain’s thyroiditis are viral illness, family history, and female gender.

There is insufficient evidence to recommend routine screening for de Quervain’s thyroiditis.

De Quervain’s thyroiditis develops after a viral prodrome and presents as painful thyroid gland with symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications include hypothyroidism and rarely, esophageal or tracheal compression.

There are no established criteria for the diagnosis of de Quervain’s thyroiditis but painful thyroid mass, decreased radioactive iodine uptake, elevated ESR, serum T3, and T4 are helpful in diagnosing de Quervain’s thyroiditis.

The hallmark of de Quervain’s thyroiditis is hyperthyroidism with the neck pain. A positive history of viral illness and a positive family history are suggestive of de Quervain’s thyroiditis. The most common symptoms of de Quervain’s thyroiditis are neck pain, palpitations, tachycardia, nervousness, and tremors.

Patients with de Quervain’s thyroiditis usually appear fatigued and restless. Physical examination of patients with de Quervain’s thyroiditis is usually remarkable for neck tenderness, tachycardia, and palpitations. In the recovery phase of de Quervain’s thyroiditis patient may develop hypothyroidism.

Laboratory findings consistent with the diagnosis of de Quervain’s thyroiditis usually include increased ESR, CRP, free T3, and free T4 and decreased thyroid stimulating hormone. Anti-thyroid peroxidase antibody is usually low or absent.

The most common EKG finding associated with the thyrotoxicosis in de Quervain’s thyroiditis is sinus tachycardia. Rarely signs of myocardial damage, including ST-segment elevation and arrhythmias, can also be seen in thyrotoxicosis.

Chest X-ray findings in de Quervain’s thyroiditis are usually not significant but may show cardiomegaly and pulmonary edema, if there is concomitant myocarditis or heart failure.

Non-contrast CT may be used in de Quervain’s thyroiditis to assess the tracheal or esophageal compression.

In de Quervain’s thyroiditis, T1-weighted MRI shows mild and T2-weighted image shows a more pronounced hyperintensity in the thyroid gland.

There are no echocardiographic findings related to de Quervain’s thyroiditis. Ultrasound findings associated with de Quervain’s thyroiditis are hypoechoic areas, glandular irregularities, and non-homogeneous echo-texture.

24-hour iodine-123 uptake is decreased in de Quervain’s thyroiditis.

The histological analysis in de Quervain’s thyroiditis may show the destruction of the follicular epithelium, loss of the follicular integrity and infiltration of inflammatory cells. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules.

The mainstay of therapy for de Quervain’s thyroiditis is aspirin or non-steroidal anti-inflammatory drugs for pain control. Beta-adrenergic blockers are recommended for the patients who develop thyrotoxic symptoms. Corticosteroids are usually used in severely ill patients. Levothyroxine is required if the patient develops hypothyroidism following the resolution of the hyperthyroid state.

Surgical intervention is not usually recommended for the management of de Quervain’s thyroiditis. Thyroidectomy is considered only when there are repeated relapses despite appropriate treatment.

There are no primary preventive measures available for de Quervain’s thyroiditis.

There are no secondary preventive measures available for de Quervain’s thyroiditis.

​

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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]

In 1895, Mygind first described de Quervain’s thyroiditis. In 1904, Fritz de Quervain differentiated this disease from other forms of thyroiditis on the basis of the pathological findings.

De Quervain’s thyroiditis is named after Fritz de Quervain who differentiated de Quervain’s thyroiditis clearly from other forms of thyroiditis. The most prominent historical events related to de Quervain’s thyroiditis include:^[1][2][3]

• In 1895, Mygind first described de Quervain’s thyroiditis. Mygind presented 18 cases of thyroiditis akuta simplex (the thyroiditis which affected the previously normal gland without abscess formation).
• In 1904, Fritz de Quervain differentiated de Quervain’s thyroiditis clearly from other forms of thyroiditis based on pathological findings.
• In 1936, de Quervain’s thyroiditis was reaffirmed by de Quervain and Giordanengo.

​

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

De Quervain’s thyroiditis can be classified according to the development of symptoms into the prodromal stage, hyperthyroid stage, euthyroid stage, and hypothyroid stage.

De Quervain’s thyroiditis can be classified according to the development of symptoms into the following stages:^[1][2][3]

The prodromal stage includes low-grade fever and viral flu-like symptoms, such as sore throat, myalgia, arthralgia, and malaise.

It follows the prodromal stage and includes the symptoms of thyrotoxicosis.

Thyroid hormones are within the normal range and there are no specific symptoms.

Thyroid hormones are decreased as a result of glandular damage.

​

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

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.

The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.[1][2] 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. Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH) acts on thyrotropes releasing cells in the pituitary causing them to release 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. Iodine is essential for the synthesis of thyroid hormones. Iodide is uptaken 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 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. 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 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.

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.

• De Quervain’s thyroiditis is associated with:^[6][7]
  • The human leukocyte antigen (HLA B35
  • HLA B15/62 (in rare cases)

The following conditions may be associated with De Quervain’s thyroiditis:^[8]

• Rheumatoid arthritis
• Sjogren syndrome
• Ulcerative colitis
• Urticaria
• Thyroid malignancy

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

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

• 
  De Quervain’s thyroiditis (By Nephron – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491382)
• 
  De Quervain’s thyroiditis (By Nephron – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491421)
• 
  De Quervain’s thyroiditis (By Nephron – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=18491421)

​

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

De Quervain’s thyroiditis may be caused by viruses such as mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus. Genetic factors also predispose an individual towards de Quervain’s thyroiditis.

De Quervain’s thyroiditis is caused by:^[1][2][3][4]

• Viruses:
  • Mumps
  • Adenovirus
  • Epstein–Barr virus
  • Coxsackievirus
  • Cytomegalovirus
  • Influenza
  • Echovirus
  • Enterovirus
• Genetic factors:
  • HLA-B35
  • HLA-B15/62

​

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

De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. De Quervain’s thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As de Quervain’s thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

• De Quervain’s thyroiditis must be differentiated from other causes of thyroiditis, such as Hashimoto’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis.^[1]

• De Quervain’s thyroiditis must be differentiated from other causes of hypothyroidism on the basis of history and symptoms and laboratory findings:^{[2][3][1][4][5][6]}

(†)T3RU; Triiodothyronine Resin uptake. (^)TPOAb; Thyroid peroxidase antibodies. (*)TSH may be decreased transiently in the thyrotoxicosis. (**)TPOAb may be present in drug-induced hypo/hyperthyroidism such as Interferon-alpha, interleukin-2, and lithium.

• De Quervain’s thyroiditis can initially present with thyrotoxicosis which must be differentiated from other causes of thyrotoxicosis.^{[2][3][1][4][5][6][7][8][9]}

(†)T3RU; Triiodothyronine Resin uptake. (^)TPOAb; Thyroid peroxidase antibodies.

​

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

De Quervain’s thyroiditis is particularly common in middle-aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide.

De Quervain’s thyroiditis is the most common cause of painful thyroid disease in adults which may account for up to 0.027 per 6496 of adult thyroid diseases. The prevalence is estimated to be 0.41 per 100,000 adult population.^[1][2]

The prevalence is estimated to be 0.41 per 100,000 adult population.^[1]

The overall incidence of endogenous de Quervain’s thyroiditis is approximately 4.9 cases per 100,000 per year.^[3]

De Quervain’s thyroiditis is more common in fourth and fifth decades of life.^[1][3]

De Quervain’s thyroiditis is more common in females.The female to male ratio ranges between 2:1 to 6:1.^[1][4]

There is no evidence of racial predilection in de Quervain’s thyroiditis.

There is no regional predilection reported towards de Quervain’s thyroiditis but it was the cause in 1.8% of hypothyroid cases in a study done in Denmark.^[5]

​

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

Common risk factors in the development of de Quervain’s thyroiditis are viral illness, family history, and female gender.

The risk factors for de Quervain’s thyroiditis are:^{[1][2][3][4][5][6]}

• Viral illness
• Family history
• Female gender
• Human leukocyte antigen (HLA) B35

• HLA-B15/62

​

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

There is insufficient evidence to recommend routine screening for de Quervain’s thyroiditis.

There is insufficient evidence to recommend routine screening for de Quervain’s thyroiditis.

​

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

De Quervain’s thyroiditis develops after a viral prodrome and presents as painful thyroid gland with symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease. Complications include hypothyroidism and rarely, esophageal or tracheal compression.

De Quervain’s thyroiditis develops after a viral prodrome and presents as painful thyroid gland with symptoms of thyrotoxicosis. It further leads to a euthyroid phase and eventually hypothyroid phase before the complete resolution of the disease.^[1][2][3]

It includes:

• Low-grade fever and viral flu-like symptoms, such as sore throat, myalgia, arthralgia, and malaise.
• High-grade fever and neck pain with a tender and diffuse thyroid gland enlargement follow flu-like symptoms.

It follows the prodromal stage and includes the symptoms of thyrotoxicosis such as:

• Tachycardia and tremors
• Irritability and nervousness

Thyrotoxic stage is followed by a 1–3-week period of euthyroid phase.

The transient hypothyroid stage lasts for 6-12 months.

• Rarely, the hypothyroid stage may persist for a longer duration.

Complications that can develop as a result of de Quervain’s thyroiditis are:^[1][2][3]

• Hypothyroidism
• Tracheal compression
• Esophageal compression

Prognosis of de Quervain’s thyroiditis is usually good.