<unk>  is also known as subacute thyroiditis. In 1895, Mygind first<unk> scribed<unk> . In 1904, Fritz<unk><unk>  differentiated this disease from other forms of thyroiditis on the basis of the pathological findings.<unk>  can be classified according to the<unk> velopment of symptoms into the prodromal stage, hyperthyroid stage, euthyroid stage, and hypothyroid stage. The exact pathogenesis of<unk>  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<unk> .<unk>  is usually preceded by a viral prodrome and also have a genetic predisposition. Human leukocyte antigen B35 and B15/62 are associated with<unk> .<unk>  may be caused by viruses such as mumps, adenovirus, Epstein–Barr virus, coxsackievirus, cytomegalovirus, influenza, echovirus, and enterovirus.<unk>  must be differentiated from other causes of thyroiditis, such as Hashimoto's thyroiditis, Riedel's thyroiditis, and suppurative thyroiditis. Common risk factors in the<unk> velopment of<unk>  are viral illness, family history, and female gender.<unk> <unk> velops 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<unk>  is hyperthyroidism with the neck pain. A positive history of viral illness and family history of<unk>  are suggestive of<unk> . The most common symptoms of<unk>  are neck pain, palpitations, tachycardia, nervousness, and tremors. Patients with<unk>  usually appear fatigued and restless. Physical examination of patients with<unk>  is usually remarkable for neck tenderness, tachycardia, and palpitations. In the recovery phase of<unk>  patient may<unk> velop hypothyroidism. Laboratory findings consistent with the diagnosis of<unk>  usually include increased ESR, free T3, and free T4 and<unk> creased thyroid stimulating hormone. Anti-thyroid peroxidase antibody is usually low or absent. The most common EKG finding associated with the thyrotoxicosis in<unk>  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<unk>  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<unk>  to assess the esophageal or tracheal compression. In<unk> , T1-weighted MRI shows mild and T2-weighted image shows a more pronounced hyperintensity in the thyroid gland. Ultrasound findings associated with<unk>  are hypoechoic areas, glandular irregularities, and nonhomogeneous echotexture. The histological analysis in<unk>  may show the<unk> struction 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<unk>  is aspirin or non-steroidal anti-inflammatory drugs for pain control. Beta-adrenergic blockers are recommended for the patients who<unk> velop thyrotoxic symptoms. Corticosteroids are usually used in severely ill patients. Surgical intervention is not usually recommended for the management of<unk> . Thyroidectomy is considered only when there are repeated relapses<unk> spite appropriate treatment.
De Quervain's thyroiditis
Riedel's thyroiditis
Hashimoto's thyroiditis
Silent thyroiditis
Primary thyroid lymphoma
Postpartum thyroiditis
Follicular thyroid cancer
Anaplastic thyroid cancer