Chronic lymphocytic thyroiditis, also known as Hashimoto’s thyroiditis (HT), is a type of autoimmune thyroiditis (AIT). It is 15-20 times more common in women than in men, with a high prevalence in the 30s and 50s, and the prevalence increases with age. Hashimoto’s thyroiditis is currently thought to be the result of a combination of genetic and environmental factors. The more recognized cause is an autoimmune abnormality. Specific antibodies against thyroid tissue, including thyroglobulin antibodies (TgAb), thyroid peroxidase antibodies (TPOAB), and thyroid stimulation blocking antibodies (TSBAb), appear in the patient’s serum. Iodine intake is an important environmental factor influencing the development of Hashimoto’s thyroiditis, and the incidence of the disease increases significantly with increased iodine intake. Increased iodine intake can promote the development of clinical hypothyroidism in patients with latent Hashimoto’s thyroiditis. There is no treatment for autoimmune thyroiditis that addresses the cause of the disease. Limiting iodine intake to a safe range may help to slow the progression of autoimmune destruction of the thyroid gland. If thyroid function is normal, follow-up is the mainstay of management of Hashimoto’s thyroiditis. Follow-up visits every 6 months to 1 year are generally recommended, mainly to check thyroid function and, if necessary, to perform ultrasonography of the thyroid gland. Patients with pre-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 goiter. Generally start with small doses, 20-40 mg of thyroid tablets daily or 25-50 mcg of L-T4, and gradually increase to maintenance doses to maintain TSH in the normal range. If the thyroid gland enlarges rapidly, or if it is accompanied by pain, or if there are symptoms of pressure, glucocorticoid therapy can be applied for a short time. Hashimoto’s hyperthyroidism should be treated with small doses of antithyroid drugs and propranolol preparations. Iodine 131 and surgery are generally not used to avoid severe hypothyroidism. Hashimoto’s disease combined with nodules requires attention. First, the nature of the nodules should be determined, and if the nodules are still small, regular ultrasound review is recommended, the first time at 3 months. If the patient has concerns, needle aspiration biopsy with cytology can be performed, and if the diagnosis is still unclear, surgical excision can be performed. In recent years, various new methods have emerged to treat this disease from the perspective of immunomodulation, which can lead to a decrease in the patient’s thyroid autoantibody levels, a reduction in the size of the enlarged thyroid gland, and an improvement in the patient’s self-perceived symptoms. It has been suggested that selenium can reduce or inhibit the immune damage of autoimmune thyroiditis (AITD). Selenium is an essential trace element in human body and 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. The thyroid gland is one of the organs with the highest selenium content in the body and contains a variety of selenoproteins, mainly including glutathione peroxidase (GPX) and deiodinase. Selenium deficiency affects the activity of glutathione peroxidase in the thyroid gland, which reduces the clearance of peroxides produced by cellular metabolism and further aggravates goitre. It was found that serum selenium was significantly lower in patients with Hashimoto’s thyroiditis (HT) than in controls, and that clinical symptoms tended to worsen as serum selenium decreased. Selenium combined with levothyroxine in the treatment of AITD can effectively suppress the inflammatory response of the thyroid gland. One investigator administered selenomethionine to 80 sex patients, and after 3 and 6 months of treatment, the thyroid peroxidase antibody TPOAB decreased by 5% and 9%, respectively, where 40 of them continued to take selenium to 12 after TPOAB decreased by 21 compared with the basal value of selenium replacement therapy can reduce the concentration of TPOAB in AITD patients, but the dose of selenium needs more than 100d to exert the maximum antioxidant capacity, and the therapeutic effect of selenium is time-dependent. It has been suggested that selenium replacement therapy in patients with acute or subacute AITD can significantly reduce TPOAB concentrations, while in patients with inactive AITD this change is not significant. For some patients with new onset and concomitant higher concentrations of TPOAB selenium replacement therapy. No significant side effects have been observed in patients currently treated with selenium, except for a very small number with gastric discomfort. Organic forms of selenium such as selenomethionine, selenium yeast are safer and more effective than inorganic selenium therapy.