Hashimoto’s disease, also known as Hashimoto’s goiter or chronic lymphocytic thyroiditis, is an autoimmune disease and the most common cause of goiter combined with hypothyroidism. As a result of autoantibody damage, the diseased thyroid tissue is replaced by a large number of lymphocytes, plasma cells and fibrosis. A variety of antibodies such as antithyroglobulin antibodies, antithyroid microsomal antibodies and antithyroid cell surface antibodies can be detected in the serum. Excision of the specimen reveals extensive infiltration of thyroid follicular cells by lymphocytes and plasma cells, and the formation of lymphoid follicles and germinal centers. The disease is most commonly seen in women aged 30-50 years. The main clinical manifestation is a painless diffuse goiter, symmetrical, hard, bullous change on both sides, with smooth or non-smooth surface, mostly accompanied by hypothyroidism, and in larger cases, pressure symptoms such as breath-holding can occur. The disease can be diagnosed by clinical examination that reveals an enlarged thyroid gland, diffuse echogenic inhomogeneity on ultrasound with or without small nodules, poor blood flow, low basal metabolic rate, reduced iodine uptake by the thyroid gland, hypothyroidism in the blood, and increased antibodies. In cases of doubt, a puncture biopsy can be done to help diagnose the disease. Treatment is mainly long-term thyroxine tablets, regular review of thyroid function and antibodies, and ultrasound. If there are symptoms of compression, the pre-tracheal thyroid tissue can be surgically removed to relieve the compression and eliminate the possibility of malignant thyroid lesions.