Under normal circumstances, the normal tissues and organs of the body are protected from destruction by immune function. In patients with chronic lymphatic thyroiditis, the body produces substances that destroy thyroid tissue due to immune dysfunction. These substances include thyroid autoantibodies such as thyroglobulin antibodies and thyroid peroxidase antibodies. Higher antibodies suggest that the autoimmunity may be more intense and that the thyroid gland is in a destructive stage. Hashimoto’s thyroiditis is a form of chronic lymphocytic thyroiditis in which an enlarged thyroid gland is the most prominent clinical manifestation. It is usually painless and develops slowly, but may also have light pressure pain; nodules may be present on the surface. In middle-aged women with diffuse goiter, especially when accompanied by conus lobe enlargement, the disease should be suspected regardless of thyroid function. Patients with Hashimoto’s thyroiditis may have hyperthyroidism, normal thyroid function, or may present with hypofunction. Hashimoto’s thyroiditis is the first consideration when there is a change from hyperthyroidism to hypothyroidism without medication. The majority of Hashimoto’s cases end in hypothyroidism, but hypothyroidism does not always occur and can occur early or late; serum thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TgAb) levels are one of the gold indicators for detecting Hashimoto’s thyroiditis, especially if serum TSH levels are elevated. However, some patients require multiple tests to detect increased antibody titers, while others have consistently low titers of anti-thyroid antibodies. Therefore, fine-needle aspiration or surgical biopsy for pathological examination should be considered if necessary. Antibodies do not increase in subacute thyroiditis. There is no treatment for autoimmune thyroiditis that addresses the cause. Infection and iodide in the diet are two environmental factors in the development of the disease. Take care not to get infected and not to consume more iodide in general. Limiting iodine intake to a safe range (urinary iodine at 100-200 μg/L) may help to slow down the progression of thyroid autoimmune destruction. If thyroid function is normal, follow-up is the main measure in the management of thyroiditis. Follow-up visits every 6 months to 1 year are generally recommended, mainly to check thyroid function and, if necessary, to perform thyroid ultrasonography. Patients with existing hypothyroidism or significant subclinical hypothyroidism must be treated with thyroid hormone replacement therapy. The goal of treatment is to restore serum TSH and thyroid hormone levels to normal ranges. Adequate amounts of thyroid preparations are effective in suppressing TSH and regressing goiters. Goiter combined with hyperthyroidism is treated with propranolol in mild cases and low-dose antithyroid agents in moderate and severe cases. The dose should not be large and the duration should be shortened as appropriate to prevent hypothyroidism from occurring as a result of treatment. When Hashimoto’s thyroiditis causes rapid enlargement of the thyroid gland with symptoms of compression, pharmacological doses of glucocorticoids are effective. In this case, glucocorticosteroids should only be used for a short period of time, and the side effects of long-term use may outweigh the effectiveness. Hashimoto’s disease combined with nodules requires attention to determine the nature of the nodule, and if the nodule is still small, regular ultrasound review is recommended, the first time at 3 months. If the patient has concerns, a needle aspiration biopsy with cytology can be performed, and if the diagnosis is still unclear, surgical excision can be performed. The incidence of Hashimoto’s thyroiditis combined with thyroid cancer, especially papillary thyroid cancer, has been on the rise in recent years. Hashimoto’s thyroiditis may be one of the high-risk factors for the development of thyroid cancer. For women with known positive TPOAb before pregnancy, thyroid function must be checked to confirm normal thyroid function before pregnancy; thyroid function should be reviewed regularly during pregnancy and L-T4 treatment should be given immediately in case of hypothyroidism or low T4emia, otherwise it will lead to insufficient supply of thyroid hormones to the fetus and affect its neurodevelopment. In women with positive TPOAb with clinical hypothyroidism or subclinical hypothyroidism before pregnancy, thyroid function must be corrected to normal before pregnancy can occur. It should be emphasized that there are no effective drugs to reduce TPOAb, and the rise and fall of autoantibodies can only be regulated almost by oneself. In recent years, various new methods have emerged to treat the disease from the perspective of immunomodulation, which can lead to a decrease in the level of autoantibodies in the thyroid gland, a reduction in the size of the enlarged thyroid gland, and an improvement in the patient’s self-perceived symptoms. The use of immune agents to treat autoimmune thyroiditis often requires prolonged medication with side effects, and experience needs to be accumulated. It has been suggested that taking selenium can reduce or inhibit the immune damage of autoimmune thyroiditis. Selenium is an essential trace element in the body and is an antioxidant. It has important physiological functions such as anti-aging, anti-tumor, cardiovascular protection, and antagonism to heavy metal toxicity. Selenium can improve the immune function of human body. In 2003, the U.S. Food and Drug Administration (FDA) confirmed that selenium is a cancer inhibitor, and selenium supplementation can reduce the mortality rate of tumors by half, and high-dose selenium supplementation can reduce the toxicity of chemotherapy drug treatment and significantly improve the effect of radiotherapy and chemotherapy treatment. The long-term prognosis of most autoimmune thyroiditis is good and is a benign process. The natural progression of the disease to hypothyroidism is slow. It was previously thought that hypothyroidism caused by autoimmune thyroiditis was permanent. Recent data suggest that some patients with hypothyroidism caused by autoimmune thyroiditis can be temporarily hypothyroid. These patients have spontaneous recovery of thyroid function in approximately 20% of cases when replaced with thyroid hormone. Factors affecting the prognosis of HT: 1. Patients with mild, significant goiter and a family history of thyroid function and immune disorders can easily return to normal. 2. Iodine status, high iodine uptake by the thyroid gland and easy recovery of thyroid function in patients on a low iodine diet. 3. Chemical indicators, negative thyroid stimulating blocking antibody (TSBAb), markedly elevated TSH, normal TRH excitation test, and greater possibility of maintaining long-term remission after discontinuation of medication.