There are many reasons for hyperthyroidism, and the specific factors are as follows: 1. Genetic factors Clinically, familial hyperthyroidism is not uncommon, with up to 30% to 60% of identical twins suffering from hyperthyroidism, and only 3% to 9% of heterozygotes. In addition to hyperthyroidism, family history surveys can also suffer from other kinds of thyroid diseases such as hypothyroidism, or TSI positivity in family relatives, which indicates that hyperthyroidism has a family genetic tendency. This mode of inheritance may be autosomal recessive, autosomal dominant, or polygenic. In 1956, Adams et al. discovered that long-acting thyroid stimulating hormone (LATS), an immunoglobulin (IgG) produced by B lymphocytes, is an autoantibody against the thyroid gland that binds to thyroid subcellular components and excites the thyroid follicular epithelium to secrete thyroid hormone, causing hyperthyroidism. LATS is increased in 60% to 90% of hyperthyroid patients. LATS-P substance, also an IgG, has since been found to excite only human thyroid tissue and is also known as human thyroid stimulating immunoglobulin (HTSI), which is positive in over 90% of hyperthyroid patients. Direct evidence of immune mechanisms in the pathogenesis of hyperthyroidism include: ① In humoral immunity it is known that there are a variety of antibodies against thyroid cell components, such as thyroid-stimulating antibodies (TISI) against TSH receptors, or TSH receptor antibodies (TRAb), which bind to TSH receptors or their associated tissues to further activate cAMP and enhance thyroid function, and such antibodies can pass through the placental tissue and cause neonatal hyperthyroidism, or incomplete treatment of hyperthyroidism with persistent positive antibodies, leading to recurrence of hyperthyroidism; ② in cellular immunity, it was confirmed that these antibodies are produced due to B lymphocytes. The presence of sensitized T lymphocytes against thyroid antigens in the blood of hyperthyroid patients and the activation of phytohemagglutinin (PHA) by lymphocytes in hyperthyroidism can produce LATS, which excites T lymphocytes and then stimulates B lymphocytes, resulting in the production of immunoglobulins that excite the thyroid gland, such as TSI, and triggering hyperthyroidism. Organ-specific autoimmune diseases are all caused by immune dysregulation due to defective function of suppressor T lymphocytes (Ts), therefore, the immune response is a complex result involving the interaction of T and B lymphocytes and phagocytes. It is now believed that it is mainly associated with genetic defects related to reduced suppressor T lymphocyte function, and that defective Ts function can lead to T cell sensitization, causing B cells to produce TRAb and cause hyperthyroidism. Indirect evidence includes: (1) a large number of lymphocytes and plasma cells infiltrating the thyroid gland and behind the eyes; (2) an increase in the number of lymphocytes in the peripheral blood circulation, which may be accompanied by hyperplasia of lymph nodes, reticuloendothelial tissue in the liver and spleen; (3) the occurrence of other autoimmune diseases in the patient and his relatives simultaneously or sequentially; (4) positive blood anti-thyroid antibodies, TRAb, anti-gastric wall cell antibodies and anti-cardiac antibodies in the patient and his relatives; ⑤ Elevated IgG, IgA and IgM in the thyroid gland and blood. It is believed that the cause of hyperthyroidism is due to the genetic defect in the immune guardianship and regulation of Ts cells, and when there are factors such as external trauma or infections, the immunity in the body is destroyed and the “forbidden” cells are out of control. The disease is caused by the secretion of large amounts of TSI autoantibodies by Ts cells. The disease is caused by the secretion of a large number of TSI autoantibodies by Ts cells. In recent years, it has been found that HLA-B8 is 2 times higher than normal in Caucasians, HLA-BW35 is higher in Asian Japanese, and HIA-BW46 positive susceptibility is higher in foreign Chinese, and B13 and B40 are more obvious, which have attracted attention. 3, other causes of pathogenesis (1) exogenous iodine increase causes hyperthyroidism, called iodine hyperthyroidism. (2) Ectopic endocrine tumors can cause hyperthyroidism, such as ovarian tumors, choriocarcinoma, digestive system tumors, respiratory system tumors and breast cancer, etc. The secretion of thyroid stimulating hormones can cause clinical hyperthyroidism; (3) Albright syndrome in (4) familial hyperglobulinemia (TBG) can cause hyperthyroidism, which can be due to familial genetic defects or related to medication; (5) hyperfunctioning nodular goiter or adenoma, which was not considered to be an autoimmune disease in the past because IgG, TSI, IATS and other immune adjuvants were not detected in the blood. In 1988, it was reported that serum thyroglobulin and microsomal antibodies were detected in single nodules with a positive rate of 16.9% (62/383) and 54.7% (104/190) in multiple nodules. The hyperplastic thyroid tissue in these nodules is not regulated by TSI and becomes autonomously hyperactive or hyperfunctioning thyroid nodules or adenomas. Currently, thyroid adenoma and carcinoma development are also thought to be due to oncogenes; (6) increased TSH secretion by pituitary tumors, causing pituitary hyperthyroidism, such as hyperthyroidism associated with TSH-secreting tumors or acromegaly; (7) subacute thyroiditis, chronic lymphocytic thyroiditis, and painless thyroiditis can all be associated with hyperthyroidism.