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 about 7.3-20.5% of thyroid diseases.In 1912, Mr. Tsutomu Hashimoto of Kyushu University, Japan, firstly reported four cases of the disease in a German medical journal, hence the name. Hashimoto’s disease is an organ-specific autoimmune disease, the pathogenesis of which has not been fully elucidated. It may be that on the basis of genetic susceptibility, there is a congenital defect in immunosurveillance, resulting in immune dysfunction and the production of humoral and cellular immune responses against the thyroid gland, resulting in destruction of the follicular epithelium of the thyroid gland and leading to the disease, and the intensity of autoimmune responses is closely related to the disease, and the pathogenesis of which is an autoimmune disease in which one takes one’s own thyroid tissue as the antigen. The pathogenesis of the disease is an autoimmune disease in which the thyroid tissue is the antigen. The cause of the disease is a combination of genetic and environmental factors, often occurring in several generations of the same family, multifactorial inheritance, environmental factors are infections and dietary iodide. Hashimoto’s disease is also common in combination with other forms of autoimmune disease, including pernicious anemia, rheumatoid arthritis, lupus erythematosus, desiccation syndrome, hypoadrenocorticism, hypoparathyroidism, and insulin-dependent diabetes mellitus. Hashimoto’s disease has a tendency to eventually progress to hypothyroidism. Hashimoto’s disease is most common in women between the ages of 30 and 50. The female to male ratio is 20:1 and is also a common cause of sporadic goiter in children. The disease has a slow, insidious onset and a long, slow progression, with most patients asymptomatic at the beginning and the earliest symptom being malaise. It is often diagnosed by accidental detection of goiter and further examination, or detected only when hypothyroidism occurs. The main manifestation is the gradual symmetrical enlargement of the thyroid gland, most of which is diffuse, hard and tough, with clear borders, and some patients may have compression symptoms. Isthmus enlargement is often more obvious, and there may be conical lobe enlargement, painless or mild pain, mild or moderate enlargement, a few may also be nodular enlargement. The tough rubbery texture of the thyroid gland is one of the characteristics of the disease. With the gradual destruction of thyroid tissue, the thyroid gland may gradually shrink. Most patients show hypothyroidism and mucous edema manifestations, generalized weakness, with non-digestive edema, abdominal distension, urination, slow movement, inarticulate, slow response to answers, heart rate is mostly below 60 minutes / times, hoarse voice, thick skin, flaking. The thyroid gland is usually painless and has no adhesion to the surrounding tissues; individual patients may have manifestations similar to subacute thyroiditis such as rapid goiter, pain, and pressure pain. Most of the patients often have pharyngeal discomfort, and a few may have heart enlargement, 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 ignored, so it should attract necessary attention. In the development of Hashimoto’s disease, there may be hyperthyroidism, known as Hashimoto’s hyperthyroidism, the incidence of which accounts for about 20% to 25% of Hashimoto’s disease. The cause of most of the thyroid gland by inflammatory destruction, thyroid hormone release into the blood increased, so the hyperthyroidism is a transient performance; such as by the amount of iodine intake and thyroid inflammation and repair of the impact of the thyroid gland, can be repeated hyperthyroidism or hyperthyroidism and hypothyroidism alternately. A small number of Hashimoto’s hyperthyroidism is due to the combination of Hashimoto’s disease and toxic diffuse goiter, accounting for about 0.3% to 7.6% of Hashimoto’s disease; the patient’s hyperthyroidism may persist for a long time, and may be accompanied by the typical manifestations of toxic diffuse goiter such as protruding eyes and anterior tibial mucus edema, positive blood TSI and TRAb. Patients can have either of the two diseases, or one of the two diseases can be the main clinical manifestation; for example, hyperthyroidism may last for months to years, but due to the continuous destruction of thyroid tissue, it still eventually develops into hypothyroidism. Laboratory tests 1, serum thyroid microsomal antibody (TMAb) and thyroglobulin albumin antibody (TGAb) positive, and most of them are high titer, such as two consecutive ≥ 60% (preferably quantitative testing), even if the symptoms are atypical can be diagnosed. 2.Thyroid puncture biopsy: fine needle puncture to see a large number of lymphocytes, plasma cells, there may be eosinophilic changes in the appearance of follicular cells. 3.The result of thyroid function test depends on the stage of the disease. A few patients may have transient hyperthyroidism in the early stage of the disease, and the blood T3, T4, FT3, FT4 may be increased. In most patients, thyroid function may be completely normal in the early stage. Later, T3 and T4 may be normal, but thyrotropin (TSH) is elevated, or thyrotropin-releasing hormone (TRH) excitatory test TSH is highly reactive, at this time, the thyroid iodine-131 uptake rate can also be elevated, but can be inhibited by the T3 inhibition test, which can be differentiated from Graves’ disease. When hypothyroidism occurs in the later stages of the disease, FT4, T4, FT3, and T3 are decreased, TSH is elevated, and the thyroid iodine-131 uptake rate is decreased. In laboratory tests, most patients have markedly elevated blood titers (or concentrations) of thyroglobulin antibodies (TGAb) and antimicrosomal antibodies (TMAb) or thyroid peroxidase antibodies (TOPAb), increased sedimentation rate, elevated globulin, and decreased albumin. Patients suspected of having Hashimoto’s disease may undergo thyroid function, TGAb (thyroglobulin antibody), TPOAb (thyroid peroxidase antibody), thyroid iodine-131 uptake, thyroid ECT, and thyroid biopsy if necessary. Typical Hashimoto’s disease is not difficult to diagnose. However, most of the patients are atypical, so it is often easy to misdiagnose clinically: I. Misdiagnosis of thyroid adenoma, such as only based on the hardness of the thyroid gland on palpation, or based on ultrasound alone to find nodules and diagnosed as thyroid adenomas, and without further examination, then applied to the surgical treatment. This adds insult to injury to the thyroid tissue, which is already potentially hypothyroid, and the patient has to rely on thyroxine replacement therapy for the rest of his/her life. Some years ago, a legal publication published a case in which a hospital in the south treated Hashimoto’s disease as a thyroid tumor surgery, resulting in the patient’s lifelong hypothyroidism and was sentenced to pay more than 1 million dollars. Second, misdiagnosed as hyperthyroidism Some patients with Hashimoto’s disease at the beginning of the disease due to autoimmunity to increase the release of thyroid hormones and hyperthyroidism, if only based on the thyroid enlargement and clinical hyperthyroidism and long-term, high-dose use of antithyroid medication, there will be a rapid and serious hypothyroidism. Every year, our department encounters several cases of Hashimoto’s disease as hyperthyroidism treatment for many years, ready to do iodine-131 treatment and the thyroid gland iodine-131 uptake rate is low. Misdiagnosed as “abnormal pharyngeal sensation” Some patients do not have obvious goiter or other symptoms of thyroid function, but only complain of pharyngeal discomfort. Misdiagnosis of heart disease A few patients with Hashimoto’s disease have atypical thyroid symptoms, but due to pericardial effusion in hypothyroidism, resulting in panic, palpitations, shortness of breath and T-wave changes on electrocardiogram, which can be easily misdiagnosed as heart disease. E. Misdiagnosis of simple goiter In recent years, the incidence of Hashimoto’s disease in children has increased rapidly, which makes the conclusion that “it is extremely rare in children” become history. Peking Union Medical College Hospital from 1980 to 1982, the number of children with Hashimoto’s disease is equivalent to four times the total number of cases in the past 30 years. A considerable number of children with Hashimoto’s disease were diagnosed as simple goiter for a long time, and some were misdiagnosed as hyperthyroidism. Sixth, misdiagnosed as menopausal syndrome After the disease in women around 50 years old, often complain of fatigue, lethargy, irritability, bouts of sweating, insomnia, mild swelling, etc., so it is easy to be misdiagnosed as menopausal syndrome. Since the 1980s, with the development of serum antithyroid autoantibody measurement technology and the application of fine needle aspiration cytology of the thyroid, the diagnosis rate of the disease has been gradually improved, and misdiagnosis has been gradually reduced. Treatment Principles Mildly enlarged and asymptomatic thyroid gland can be left untreated and should be followed up for observation. When the thyroid gland is obviously enlarged or there is hypothyroidism, even if there is only an increase in serum TSH, thyroid preparations should be given. Generally start with a small dose of thyroxine (T4) 20-40 mg daily or levothyroxine (L-T4) 25-50 mcg, gradually increasing to a maintenance dose to keep TSH in the normal range. If the thyroid gland is rapidly enlarged, or accompanied by pain, or with pressure symptoms, glucocorticoid therapy can be applied for a short period of time. Hashimoto’s hyperthyroidism should be treated with small doses of antithyroid drugs and propranolol preparations, and surgery is generally not necessary to avoid accelerating the possibility of lifelong hypothyroidism. For iodine-131 treatment, the Chinese Medical Association in 2005 compiled and published the “Clinical Technical Code of Practice Nuclear Medicine Branch” to Graves’ hyperthyroidism combined with chronic lymphocytic thyroiditis (Hashimoto’s disease) iodine-131 uptake rate increased patients as one of the indications for the use of iodine-131 treatment. If Hashimoto’s disease is combined with hyperthyroidism, the effect of medical treatment is poor, in order to reduce the harm of hyperthyroidism for a long time for the patient, the early use of iodine-131 treatment, even if hypothyroidism appeared earlier, is much more favorable than hyperthyroidism for many years without healing. Because hypothyroidism correctly using thyroxine to replace the thyroid function, can make the patient to maintain a normal life and work.