Subacute thyroiditis is a destructive thyroid tissue injury caused by a systemic inflammatory response to a viral infection or post-viral infection of the thyroid gland, and is classified as subacute granulomatous thyroiditis, non-infectious thyroiditis, migrating thyroiditis, and De Quervain’s thyroiditis. Subacute thyroiditis is a self-limiting disease that can cause permanent hypothyroidism in 5-15% of cases. Viral infections, non-viral diseases, genetic and autoimmune factors have been found to be involved in the development of subacute thyroiditis. The clinical presentation is characterized by gradual or sudden onset of pain in the thyroid area, which may radiate to the ear and throat, and may worsen with neck turning and swallowing movements. Physical examination reveals diffuse or asymmetric mild/moderate goiter with or without nodules and a hard thyroid gland. Laboratory tests often show a significant increase in sedimentation (ESR), a bidirectional separation of elevated serum thyroid hormone concentrations and decreased thyroid iodine uptake, increased C-reactive protein, negative or low TgAb and TPOAb levels, significantly increased serum thyroglobulin (Tg) levels, and abnormal early thyroid fine needle aspiration cytology (FNAC). The current clinical treatment of subacute thyroiditis is mainly based on symptom relief, glucocorticoid application (analgesia, symptomatic treatment – treating the symptoms) and relieving the cause (removal of antigens – treating the root cause). However, there are controversies in the specific management. Patients with metritis are first given pain relief, and non-steroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid, indomethacin and cyclooxygenase-2 inhibitors are preferred in patients with milder symptoms. Patients with subarachnoiditis who exhibit a hyperthyroid state should be given beta-blockers (e.g., Tretinoin) to lower their heart rate. The 2008 Chinese guidelines for the management of subacute thyroiditis state that the use of antithyroid drugs is not recommended because thyroid hormones are not overproduced, and the 2010 American Thyroid Association (ATA) guidelines do not mention the use of antithyroid drugs in the treatment of subacute thyroiditis. L-T4 may be used in small doses for a short period of time in patients with significant hypothyroidism, and may be withdrawn only after 3-6 months of normalization of thyroid function as confirmed by thyroid function tests. Permanent hypothyroidism requires long-term replacement therapy. There is clinical controversy as to whether or not to use glucocorticoids to treat subacute thyroiditis. Subacute thyroiditis causes 3 states of thyroid tissue due to the invasive destruction of the virus and the metaplasia it causes, the destroyed part, the damaged unbroken part, and the normal unaffected part. Glucocorticoids have the function of suppressing inflammation, reducing immune response, and stabilizing glandular cell membrane structure, thus reducing further destruction of thyroid follicles by metaplasia and effectively relieving pain; accelerating the repair of damaged but not yet broken cells, shortening the course of the disease, and reducing the risk of slipping into hypothyroidism. In contrast to the chronic small amount of breakage in Hashimoto’s nail infection, subthyroiditis is painful due to the large number of broken parts. Therefore, hormones need to be used early when NSAIDs are not effective in controlling the pain symptoms. (If pain can be controlled, it means that there are not many breaks and hormones can be dispensed with). Its compared with NSAID drugs, hormones can relieve pain faster. Shortening the course of the disease. 2010 American Thyroid Association (ATA) guidelines recommend glucocorticoid therapy for patients who have failed NSAID therapy or for patients with subacute thyroiditis with moderate to severe symptoms. Prednisone 40 mg/day is recommended, maintained for 1-2 weeks and then tapered for 2-4 weeks or longer depending on clinical symptoms. The 2008 Chinese guidelines for the diagnosis and treatment of subacute thyroiditis recommend an initial prednisone of 20-40 mg/day, maintained for 1-2 weeks, with a slow taper for a total course of not less than 6-8 weeks. In recent years, intramuscular injections of long-acting glucocorticoids such as betamethasone (Depo-Provera) have also received attention. For the indication of discontinuation of hormone therapy, it is recommended that glucocorticosteroids should be discontinued only after the iodine uptake rate returns to normal, which is better than the discontinuation criterion of normalization of blood sedimentation, and the cure rate is improved and the recurrence rate is reduced. If the iodine uptake rate continues to decrease after the application of glucocorticosteroids, which indicates that the inflammatory response continues, the use of glucocorticosteroids should be prolonged; if the use of glucocorticosteroids is repeated during discontinuation or reduction, the use of glucocorticosteroids can continue. Viral infection is the main cause of subacute thyroiditis, and there is still clinical controversy about whether to treat it with antiviral drugs. However, based on the fact that antigen removal is the key and basis for treating immune diseases, we advocate the use of anti-inflammatory and antiviral drugs for subacute thyroiditis (subacute thyroiditis is mainly a viral infection, but there are also a small number of bacterial infections, and the decision to use anti-inflammatory drugs can be made based on blood work). Although there are no definitive effective antiviral drugs, there are reports in the literature that ribavirin combined with half a dose of prednisone is more effective than a full dose of prednisone alone. Other treatments include herbal remedies to clear heat and detoxify the toxin (e.g. Qing Kai Ling capsule, Shuang Huang Lian oral solution, etc.), vitamin C (to improve one’s resistance), etc. Blood sedimentation and routine blood tests should be reviewed regularly. The whole course of subacute thyroiditis treatment is about 6-12 months. Usually, after 6-12 months, thyroid function returns to normal in 95% of patients, hypothyroidism occurs in 5% of patients, and relapse can occur in 2% of patients. After treatment, the damaged but undamaged part of the thyroid gland is repaired and the patient’s nail function returns to normal, so subthyroiditis is self-limiting. However, if too much of the damaged part is destroyed, even if the damaged part is restored, it is not enough to compensate, and permanent hypothyroidism occurs. In this sense, it also supports the early use of hormones to reduce the immune metamorphosis, reduce the damaged part of the thyroid gland, accelerate the repair of the damaged part, and prevent the development of permanent hypothyroidism. Of course hormones have their adverse effects and contraindications. Therefore, it is necessary to prevent their side effects during application, such as using antacid preparations to protect the stomach, adding calcium tablets and vitamin D to prevent osteoporosis, etc. For those who have contraindications to hormones, such as allergy to glucocorticoids, history of severe psychiatric disease, epilepsy, active peptic ulcer, post-operative gastrointestinal anastomosis, fracture, trauma repair, herpes simplex or ulcerative keratoconjunctivitis, severe hypertension, severe diabetes, uncontrolled infection (such as chickenpox, fungal, tuberculosis infection), early pregnancy and puerperium, common psoriasis, etc., they should be used cautiously or with caution when actively treating the original disease. Hormones should be used with caution or prohibited when actively treating the primary disease.