Many patients have elevated thyroid peroxidase antibodies (TPOAb) and diffuse thyroid lesions. According to the current diagnostic guidelines, Hashimoto’s thyroiditis can be diagnosed based on physical examination, ultrasound and blood tests in the following cases 1. Diffuse thyroid lesions, enlarged, tough, sometimes with large or asymmetrical isthmus, or nodules 2. Hashimoto’s thyroiditis can be diagnosed in patients with these typical manifestations as long as the blood is positive for thyroglobulin antibodies (TGAb) or thyroid peroxidase antibodies (TPOAb) The diagnosis of Hashimoto’s thyroiditis can be made if the blood is positive for thyroglobulin (TGAb) or thyroid peroxidase antibodies (TPOAb). 3. Hashimoto’s thyroiditis can be diagnosed in those who have atypical manifestations and who have high titers of antithyroid antibodies, i.e., if the results of two consecutive determinations of both antibodies are greater than or equal to 60% when measured by the immunoassay method. 4. Hashimoto’s thyroiditis can be diagnosed in those who also have hyperthyroidism and who have high titers of these antibodies for more than six months. It is an autoimmune disease. It has a tendency to develop into hypothyroidism and is more common in clinical practice. Hashimoto’s thyroiditis was first reported and described in 1912 by a Japanese man named Czer Hashimoto, hence the name Hashimoto’s disease or Hashimoto’s thyroiditis. The thyroid tissue of patients with this disease has lymphocytic infiltration, fibrosis, interstitial atrophy and eosinophilic changes of the glandular follicle cells, also known as chronic lymphocytic thyroiditis. Hashimoto’s thyroiditis is an organ-specific autoimmune disease, the pathogenesis of which has not yet been fully elucidated. It may be based on a 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 the disease. The process is similar to that of subacute thyroiditis, but is not accompanied by pain or fever, so it is called painless thyroiditis. However, when the thyroid gland is destroyed to a certain extent, many patients gradually develop hypothyroidism, and a few show mucinous edema. The course of the disease is long, from a few months to several years. After treatment of mild or early cases, the thyroid gland can shrink significantly or return to normal size, symptoms are relieved, signs disappear, and thyroid function returns to normal. However, there are no specific drugs available. Some patients need long-term treatment with thyroid tablets due to long duration of the disease or severe thyroid lesions, which result in hypothyroidism due to the replacement of thyroid tissue by extensive fibrous tissue. The incidence of carcinoma in this disease is 0.5%-22.5%, with most reports ranging from 5%-17.7%, and excess iodine is prone to its carcinogenesis. Therefore, vigilance is necessary.