Chronic lymphocytic thyroiditis (CLT), also known as Hashimoto’s thyroiditis (HT), is a type of autoimmune thyroiditis (AIT). The incidence is 15-20 times higher in women than in men, with a high incidence at the age of 30-50 years, and the prevalence increases with age. Its etiology is the result of a combination of genetic qualities and environmental factors, which are infections and dietary iodide. Its pathogenesis is an autoimmune disease with its own thyroid tissue as antigen. HT is the main cause of hypothyroidism (hypothyroidism) in areas suitable for iodine intake. According to the degree of thyroid destruction HT can be divided into 3 stages: recessive stage (early stage): normal thyroid function, no goiter or mild goiter, positive TPOAb and lymphocyte infiltration in the thyroid gland. Subclinical hypothyroidism stage: large number of lymphocytes infiltrating in the thyroid gland and follicular destruction. Clinical hypothyroidism: follicular destruction and thyroid atrophy. The onset of HT is insidious and progresses slowly, and the early clinical manifestations are often atypical. The thyroid gland is diffusely enlarged, firm or rubbery in texture, with a nodular surface. There is often pharyngeal discomfort or mild dysphagia, and sometimes there is a feeling of pressure in the neck. Occasionally, there is localized pain and tenderness. Clinical hypothyroidism appears in late stages. HT can coexist with Graves’ disease and is called Hashimoto’s thyrotoxicosis. The symptoms of hyperthyroidism are similar to those of Graves’ disease, but the symptoms may be milder than those of Graves’ disease alone, requiring regular antithyroid therapy, but hypothyroidism may occur during treatment.