De Quervain's thyroiditis overview

# Overview
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, EpsteinBarr 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.

# Historical Perspective
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.

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

# Pathophysiology
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.

# Causes
De Quervain's thyroiditis may be caused by viruses such as mumps, adenovirus, EpsteinBarr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus. Genetic factors also predispose an individual towards de Quervain's thyroiditis.

# Differentiating De Quervain's thyroiditis from other Conditions
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.

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

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

# Screening
There is insufficient evidence to recommend routine screening for de Quervain's thyroiditis.

# Natural History, Complications, and Prognosis
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.

# Diagnosis

## Diagnostic Criteria
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.

## History and Symptoms
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.

## Physical Examination
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
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.

## Electrocardiogram
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
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.

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

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

## Echocardiography or Ultrasound
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.

## Other Imaging Findings
24-hour iodine-123 uptake is decreased in de Quervain's thyroiditis.

## Other Diagnostic Studies
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.

# Treatment

## Medical Therapy
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.

## Surgery
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.

## Primary prevention
There are no primary preventive measures available for de Quervain's thyroiditis.

## Secondary Prevention
There are no secondary preventive measures available for de Quervain's thyroiditis.