Subacute thyroiditis, known as subacute granulomatous thyroiditis, is a self-limiting disease associated with a viral infection, which is common in women. The etiology and pathogenesis of subacute thyroiditis are unknown, but it is generally believed that the cause is a viral infection, often preceded by an upper respiratory tract infection 1-3 weeks before the onset of the disease. The onset of the disease is associated with increased titers of antibodies to certain viruses, including mumps virus, coxsackievirus, influenza virus, echovirus, and adenovirus. The pathologic changes of hyperthyroidism followed by hypothyroidism are the main outcome of the disease. This results in the release of synthesized and stored thyroid hormones and abnormal iodide into the bloodstream, causing an increase in circulating T3 and T4 and the clinical manifestations of hyperthyroidism, with feedback suppression of TSH levels. The iodine uptake capacity of the destroyed thyroid follicles is low at this time. After the stored T3 and T4 are released, T3T4 in the blood circulation gradually decreases to below normal, and TSH begins to rise above normal, promoting the gradual restoration of the structure and function of the thyroid follicular epithelium and follicles, and T3T4 gradually rises to normal, after which TSH gradually decreases to normal. For hyperthyroidism does not require antithyroid drugs and iodine radiotherapy, and is often treated symptomatically with the beta-blocker, Tenexpress. When hypothyroidism occurs, it is not necessary to use thyroid hormone replacement therapy for transient cases. If there are clinical symptoms of hypothyroidism, temporary replacement is possible, but when permanent hypothyroidism occurs, lifelong thyroid hormone replacement is required. Therefore, in general, the prognosis of subthyroiditis is good, the course of the disease is self-limiting, but it can recur, and the induced hyperthyroidism is usually transient, but there is a certain chance that it will turn into lifelong hypothyroidism.