The etiology and pathogenesis of hyperthyroidism have not yet been fully elucidated. However, TSH is often low or even undetectable in this disease as determined by radioimmunoassay, and does not respond to TRH excitation tests. The fact that the pituitary thyroid axis is functioning normally in this disease, but TSH secretion has not increased, is not the cause of the disease. In the last two or three decades, it has been proven that the onset of the disease is mainly due to the autoimmune response induced by stress factors such as mental stimulation on a genetic basis. As early as 1956, Adams and Purves discovered a substance in the serum of patients with the disease that, when injected into guinea pigs, stimulates iodine uptake by the thyroid gland, synthesizes and releases hormones, and hyperplasia of the gland. Since then, a large body of research has proven that this disease is an autoimmune disease. Indirect evidence includes: ① A large number of lymphocytes and packed cells infiltrate in the enlarged thyroid gland and the posterior tissues of the eye. The absolute value and % of lymphocytes in the peripheral blood circulation were increased with hyperplasia of lymph nodes, thymus and visceral lymphoid tissue. The patient and his family members often have other autoimmune diseases of the thyroid gland, such as pontine thyroiditis, mucinous edema, infiltrative proptosis, etc. ③ The patient himself or his decompensated family members often have other autoimmune diseases, such as myasthenia gravis, type I diabetes mellitus, your anemia, atrophic gastritis, etc. ⑤ The rate of positive anti-thyroid and gastric antibodies in the blood circulation of the patient and his family members and their full pricing are often (3) IgA IgM deposits in the thyroid gland. The direct evidence that this disease is an autoimmune disease includes: ① In terms of humoral immunity, it is known that many antibodies against thyroid cell components, including thyroid-stimulating antibodies, or thyroid-stimulating immunoglobulin (TSI) or TSH receptor antibodies (TRAb), can be detected in the sera of 95% of patients and have the ability to inhibit TSH and bind to receptors or related tissues. This activates adenylyl cyclase and enhances thyroid cell function. This antibody can cause neonatal hyperthyroidism through the placenta. The persistence of positive antibodies after discontinuation of hyperthyroidism treatment may lead to relapse. As for cellular immunity, in addition to the aforementioned sexual evidence, it has been confirmed that this antibody system is produced by B lymphocytes. There is no doubt that this disease is an autoimmune disease, but its pathogenesis is still speculative, especially because the cause of the initiation is unknown. It is currently believed that the disease may be due to a genetic defect in the immune guardianship and regulation of the Ts cells of the patient, and when stress such as mental stimulation or infection occurs, the immune stability in the body is disrupted and the “forbidden” cells are out of control, which results in the proliferation of TSI-producing B cells and the secretion of a large number of autoantibodies to TSI with the assistance of Th cells. The result is the proliferation of TSI-producing B cells, which secrete large amounts of autoantibodies to TSI with the help of Th cells and cause disease.