Subacute thyrolditiB, also known by various names such as subacute sarcoid thyroiditis and De Quervain’s thyroiditis. The disease is self-limiting and is the most common painful thyroid disorder. The incidence of persistent hypothyroidism is generally reported to be less than 10%, with a peak incidence in women aged 30 to 50. A variety of viruses such as coxsackievirus, mumps virus, influenza virus, and adenovirus infections are associated with the disease, and can also occur after non-viral infections (e.g., Q fever or malaria). Genetic factors may be involved in the pathogenesis, and an association with HLA-B35 has been reported. Various antithyroid autoantibodies can be present during active disease and may be secondary to antigen release following thyroid follicular destruction. Clinical presentation Onset is often 1-3 weeks after viral infection, and some studies have found a trend toward seasonal onset of the disease (summer and fall. There is a tendency for the disease to develop seasonally (summer and autumn, in line with the peak of enterovirus incidence) and to cluster in different geographical areas. The form of onset and the degree of disease vary. 1. The prodromal symptoms of upper respiratory tract infection: muscle pain, fatigue, lethargy, sore throat, etc., with varying degrees of temperature increase, peaking in 3-4 days of onset. It may be accompanied by enlarged lymph nodes in the neck. 2. Characteristic pain in the thyroid area: gradual or sudden, with varying degrees. It may be aggravated by neck turning and swallowing movements, and often radiates to the ipsilateral ear, throat, mandibular angle, chin, occiput, chest and back. A small number of patients have hoarseness and difficulty swallowing. 3. Enlarged thyroid gland: diffuse or asymmetric mild or moderate enlargement, mostly with nodules, hard texture, obvious tenderness, no tremor or murmur. Goiter often involves one lobe first and then extends to the other lobe. 4. Clinical manifestations associated with changes in thyroid function: (1) thyrotoxic phase: about 50%-75% of patients have weight loss, fear of heat, tachycardia, etc. at the beginning of the disease, which lasts about 3-8 weeks; (2) hypothyroid phase: about 25% of patients enter the hypothyroid phase before the synthesis of thyroid hormones is restored, with edema, fear of cold, constipation and other symptoms; (3) hypothyroid phase: about 25% of patients enter the hypofunction phase before the synthesis of thyroid hormones is restored, with symptoms such as edema, fear of cold, constipation, etc. (3) thyroid function recovery stage: most patients recover normal function for a short period of time (weeks to months), and only a few become permanently hypothyroid. The whole course of the disease is about 6-12 months. Some cases have recurrent exacerbations that last from a few months to 2 years. About 2-4% relapse and very few recurrent episodes. The diagnosis is based on acute onset, fever and other systemic symptoms, painful, enlarged and hard thyroid gland, combined with a significant increase in ESR and a bidirectional separation of elevated serum thyroid hormone concentration and reduced iodine uptake by the thyroid gland. Treatment Early treatment is aimed at reducing the inflammatory response and relieving pain. Acetylsalicylic acid (1-3 e/d in divided doses), nonsteroidal anti-inflammatory drugs (e.g., indomethacin 75-150 mg/d in divided doses), or cyclooxygenase-2 inhibitors are used in mild cases. Glucocorticosteroids are indicated for those with severe pain, persistent and significantly elevated body temperature, and ineffective treatment with salicylic acid or other NSAIDs for rapid pain relief and reduction of symptoms of thyrotoxicosis. Initially, prednisone should be administered at 20 plus one me/d for 1-2 weeks, and the dose should be slowly reduced according to the changes in symptoms, signs and ESR for a total duration of 6-8 weeks or more. The total course of treatment is more than 6-8 weeks. Too rapid dose reduction and premature discontinuation may cause recurrence of the disease and should be avoided. In case of recurrence during drug discontinuation or dose reduction, glucocorticoids can still be used, and the same good results can be obtained. For those with significant thyrotoxicosis, B-monoceptor blockers can be used. Since there is no overproduction of thyroid hormone in this disease, it is not treated with antithyroid drugs. Thyroid hormones are used for those with significant and prolonged hypothyroidism; however, short-term, small amounts are appropriate because lower TSH is detrimental to thyroid cell recovery; permanent hypothyroidism requires long-term replacement therapy.