Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, lymphoid goiter, also known as Hashimoto’s thyroiditis, is one of the most common types of thyroiditis, accounting for 7.3-20.5% of thyroid disorders. 1912, Mr. Hashimoto Ce, Kyushu University, Japan, first reported four cases of this disease in the German Medical Journal, hence the name. Hashimoto’s disease is an organ-specific autoimmune disease, the pathogenesis of which has not yet been fully elucidated. It may be based on genetic susceptibility and an innate immune surveillance defect, resulting in immune dysfunction and humoral and cellular immune responses against the thyroid gland, resulting in destruction of the thyroid follicular epithelium and causing disease. The intensity of the autoimmune response is closely related to the disease. The etiology is the result of a combination of genetic and environmental factors, often occurring in several generations of the same family, with multifactorial inheritance and environmental factors such as infections and dietary iodide. Combinations of Hashimoto’s disease with other forms of autoimmune disease are also common, including pernicious anemia, rheumatoid arthritis, lupus erythematosus, dry syndrome, hyperaldosteronism, hypoparathyroidism, and insulin-dependent diabetes mellitus. Hashimoto’s disease eventually has a tendency to develop into hypothyroidism. Hashimoto’s disease is most often seen in women between the ages of 30 and 50. The ratio of women to men is 20:1, and it is also a common cause of sporadic goiter in children. The disease has a slow, insidious onset and a long, slow progression. Most patients are asymptomatic at the beginning, with the earliest symptom being malaise. It is often diagnosed by accidental detection of an enlarged thyroid gland and further examination, or when hypothyroidism develops. The main manifestation is a gradual and symmetrical enlargement of the thyroid gland, mostly diffuse, with a hard texture and clear borders, and some patients may have symptoms of pressure. The enlargement of the isthmus is often obvious, and there may be conus enlargement, painless or mild pain, mild or moderate enlargement, and in some cases, nodular enlargement. The tough, rubbery texture of the thyroid gland is one of the features of the disease. As the thyroid tissue is gradually destroyed, the thyroid gland may gradually shrink. Most patients present with hypothyroidism and mucinous edema, generalized weakness, non-finger puffiness, abdominal distention, low urinary output, slow movement, non-speaking, slow response to replies, heart rate below 60 min/time, hoarseness, thick skin, and flaking. The thyroid gland is generally painless and has no adhesions to surrounding tissues; individual patients may have manifestations similar to those of subacute thyroiditis such as rapid thyroid swelling, pain, and pressure pain. Most patients often have pharyngeal discomfort, and a few may have enlarged heart, pericardial effusion, or coronary artery disease. In recent years, many female high school students have been found to suffer from this disease, but it is easy to be neglected and therefore should be given the necessary attention. During the development of Hashimoto’s disease there can be hyperthyroidism, called Hashimoto’s hyperthyroidism, the incidence of about 20% to 25% of Hashimoto’s disease. Most of them are caused by inflammatory destruction of the thyroid gland and increased release of thyroid hormones into the blood, so the hyperthyroidism is transient; if affected by iodine intake and thyroid inflammation and repair, hyperthyroidism or alternating hyperthyroidism and hypothyroidism can occur repeatedly. A minority of Hashimoto’s hyperthyroidism is due to Hashimoto’s disease combined with toxic diffuse goiter, accounting for 0.3% to 7.6% of Hashimoto’s disease; hyperthyroidism may persist for a longer period of time and may be accompanied by typical toxic diffuse goiter manifestations such as proptosis and anterior tibial mucinous edema, and positive blood TSI and TRAb. Patients may have either of the two diseases and the clinical manifestations of either disease may predominate; for example, hyperthyroidism may persist for months to years, but eventually develop into hypothyroidism due to the continuous destruction of the thyroid tissue.