Chronic lymphocytic thyroiditis (CLT), also known as Hashimoto’s thyroiditis (HT), is a type of autoimmune thyroiditis (AIT). It is 15-20 times more common in women than in men, with a high prevalence in the 30s and 50s, and the prevalence increases with age. The cause of the disease is a combination of genetic and environmental factors, including infections and dietary iodide. Its pathogenesis is an autoimmune disease in which one’s own thyroid tissue is the antigen. HT is the main cause of hypothyroidism (hypothyroidism) in areas of suitable iodine intake. According to the degree of thyroid destruction HT can be divided into 3 stages: occult stage (early stage): normal thyroid function, no goiter or mild goiter, positive thyroid peroxidase antibody (TPOAb), and lymphocytic infiltration in the thyroid gland. Subclinical hypothyroidism: massive lymphocytic infiltration in the thyroid gland and follicular destruction. Clinical hypothyroidism: follicular destruction, thyroid atrophy. HT has an insidious onset, progresses slowly, and the early clinical manifestations are often atypical. The thyroid gland is mostly diffusely enlarged, with tough or rubbery texture and nodular surface. There is often pharyngeal discomfort or mild dysphagia, and sometimes there is a feeling of pressure in the neck. Occasionally there is localized pain and tenderness. Clinical hypothyroidism occurs in the late stage. Patients present with typical signs and symptoms such as chills, bradycardia, constipation, and even mucous edema.HT can coexist with Graves’ disease and is called Hashimoto’s thyrotoxicosis. The symptoms of hyperthyroidism are similar to those of Graves’ disease, and the conscious symptoms may be less severe than those of Graves’ disease alone, which requires regular antithyroid therapy, but hypothyroidism is likely to occur in the course of the therapy; some patients have transient thyrotoxicosis caused by the destruction of thyroid follicles, and the release of thyroid hormones into the blood; patients with HT may also be accompanied by other autoimmune diseases at the same time. Laboratory tests 1, serum thyroid hormone and thyroid stimulating hormone (TSH): early only positive thyroid autoantibodies, thyroid function is normal; later develop into subclinical hypothyroidism [free T4 (FT4) is normal, TSH is elevated, and finally manifested clinical hypothyroidism (FT4 is reduced, TSH is elevated). Some patients may have an alternating course of hyperthyroidism and hypothyroidism. 2. Thyroid autoantibodies: Significantly elevated titers of thyroglobulin antibodies (TgAb) and thyroid peroxidase antibodies (TPOAb) are one of the characteristics of this disease. Especially before the onset of hypothyroidism, antibody positivity is the only basis for the diagnosis of the disease. The literature reports that the TgAb positivity rate of this disease is 80%; and the TPOAb positivity rate is 97%;. However, the antibody positivity rate is lower in young patients. 3.Thyroid ultrasonography: HT shows goiter with uneven echogenicity, which may be accompanied by multiple hypoechoic areas or thyroid nodules. Enlargement of the isthmus can be one of the characteristics of HT. Two-dimensional ultrasound image can be seen on the thin line-like slightly strong echo band, interlaced with each other in a “network” distribution, which is also one of the characteristic images of HT. Fine needle aspiration examination: rarely used in the diagnosis of this disease, but it is of diagnostic value, mainly used to distinguish HT from nodular goiter and other diseases. Microscopic examination of the punctured tissue reveals diffuse infiltration of lymphocytes and plasma cells, and even lymphoid follicles forming the germinal center. Diagnosis HT should be suspected in all cases of diffuse goiter with a tough texture, especially with enlargement of the isthmus conus lobes, regardless of whether thyroid function is altered or not.The diagnosis is established if serum TPOAb and TgAb are positive. A positive serum TPOAb and TgAb will confirm the diagnosis, and clinical hypothyroidism or subclinical hypothyroidism will further support the diagnosis. Fine-needle aspiration is valuable in confirming the diagnosis. Differential diagnosis 1, HT and Graves’ disease, the former thyroid is harder and tougher, the elevated anti-thyroid antibodies in the blood exist for a long time, and the treatment of antithyroid drugs is more sensitive. 2.Nodular goiter: there is a history of regional epidemic, normal thyroid function, negative or low titer of thyroid autoantibodies. Fine-needle aspiration examination is helpful for differentiation. HT can see lymphocyte infiltration; nodular goiter is hyperplasia of follicular epithelial cells without lymphocyte infiltration. Thyroid cancer: The thyroid gland is obviously enlarged and hard with nodules, which needs to be differentiated from thyroid cancer. However, differentiated thyroid cancer often starts with nodules, without goiter, negative antibody, and malignant lesions by fine needle aspiration; it is more difficult to distinguish HT from thyroid lymphoma. Treatment 1, follow-up: if the thyroid function is normal, follow-up is the main measure of HT management. Generally, it is advocated to follow up every six months to one year, mainly to check the thyroid function, and if necessary, thyroid ultrasonography is feasible. 2.Treatment of etiology: There is no treatment method for the etiology of HT. Low iodine diet is advocated. In recent years, there are various new methods to treat this disease from the perspective of immune regulation, which can make the patient’s thyroid autoantibody level drop and the enlarged thyroid shrink. Selenium is an essential trace element in the human body and is an antioxidant. It has important physiological functions such as anti-aging, anti-tumor, cardiovascular protection, and antagonism of heavy metal toxicity. Selenium improves the immune function of the body. Selenium intervention therapy can reduce or inhibit the immune damage of autoimmune thyroiditis. 3, the treatment of hypothyroidism and subclinical hypothyroidism: patients with existing hypothyroidism or obvious subclinical hypothyroidism must be treated with thyroid hormone replacement. The goal of treatment is to restore serum TSH and thyroid hormone levels to the normal range. The therapeutic dose of levothyroxine sodium (L-T4) depends on the patient’s condition, age, weight, and individual differences. The average therapeutic dose for adults is 125 μg/day, or 1.6 to 1.8 μg /(kg・day) by weight. Elderly patients require a lower dose of approximately 1.0 μg / (kg・day). Start with a small dose, especially in elderly patients with cardiovascular disease, long duration of illness, and severe disease. Generally, start with 25-50 μg/day and increase by 25 μg every 1-2 weeks until the goal of complete replacement is reached. For those with heart disease, it is advisable to start with 12.5～25μg per day and increase 12.5～25μg every 2 weeks to avoid triggering and aggravating heart disease. The ideal way to take L I T4 is to take 1 dose in the morning on an empty stomach. The interval between taking it and other drugs should be more than 4h, because some drugs and food will affect its absorption and metabolism. At the beginning of the treatment, the relevant hormone indexes are measured at intervals of 4 to 6 weeks. The dosage is then adjusted according to the results until the treatment goal is reached. After reaching the treatment goal, it is necessary to review the relevant hormone indexes every 6 to 12 months. 4. Treatment of goiter: For people without hypothyroidism, levothyroxine sodium (L-T4) may have the effect of reducing goiter, especially for patients with recent goiter. Thyroid hormone therapy is usually ineffective in patients with long-standing goiters. Glucocorticoids can reduce the size of the enlarged thyroid gland and lower the titer of antithyroid antibodies in the blood; treatment with corticosteroids in patients with rapidly growing thyroid glands and atypical pain can reduce local symptoms. However, due to the side effects of the drug and the possibility of recurrence of the disease after stopping the drug, it is generally not recommended. Surgical resection may be considered for patients with significant, painful goiter and tracheal compression who have not responded to medical treatment. After surgery, hypothyroidism often occurs, and long-term thyroid hormone replacement therapy is needed. 5. The treatment of Hashimoto’s thyroiditis with hypothyroidism is the most controversial. For TSH>;10 mIU/L people generally advocate levothyroxine treatment. In view of the fact that over-treatment will bring a series of adverse effects, such as cardiovascular disease, osteoporosis, etc., most scholars suggest that the TSH in 4.5-10 mIU/L patients can be followed up, especially the elderly patients. Of course, for patients with obvious symptoms, TPOAb-positive patients, pregnant women, as well as children and adolescents, it is necessary to routinely use levothyroxine to treat hypothyroidism. 6, TPOAb-positive pregnant women’s treatment: for women who are known to be TPOAb-positive before pregnancy, thyroid function must be examined to confirm that the thyroid function is normal before pregnancy; for TPOAb-positive with clinical hypothyroidism or subclinical hypothyroidism before pregnancy, thyroid function must be corrected to normal before pregnancy; for TPOAb-positive with normal thyroid function, thyroid function needs to be rechecked regularly during pregnancy, and then the patient should be treated with levothyroxine. For TPOAb-positive pregnant women with normal thyroid function, it is necessary to review the thyroid function on a regular basis during pregnancy. In case of hypothyroidism or hypothyroidism, L-T4 treatment should be given immediately, otherwise it will lead to insufficient supply of thyroid hormone to the fetus, affecting its neurological development. 7, Hashimoto’s disease combined with nodules need to pay attention to determine the nature of the nodules, if the nodules are still small, it is recommended that regular ultrasound review, the first time is a 3-month review. If the patient is concerned, a needle aspiration biopsy with cytologic examination can be performed, and if the diagnosis is not clear, surgical resection can be performed. The incidence of Hashimoto’s thyroiditis combined with thyroid cancer has been on the rise in recent years. Hashimoto’s thyroiditis may be a risk factor for developing thyroid cancer. The long-term prognosis of most autoimmune thyroiditis is favorable and is a benign process. The natural progression of the disease to hypothyroidism is slow. It was previously thought that hypothyroidism caused by autoimmune thyroiditis was permanent. Recent data have shown that some patients with hypothyroidism caused by autoimmune thyroiditis can be temporarily hypothyroid. In about 20% of these patients when replaced with thyroid hormone; there is spontaneous recovery of thyroid function. It has also been observed that a number of enlarged thyroid glands can shrink or disappear, thyroid nodules originally detected disappear or shrink during follow-up, and hard and tough thyroid glands may soften. Factors affecting the prognosis of HT: ① young, obviously enlarged thyroid, family history of the patient, the thyroid function and immune disorders are easy to return to normal. Iodine uptake status, thyroid gland with high iodine uptake rate, low iodine diet patients thyroid function is easy to return to normal. (iii) Biochemical indexes: thyroid stimulating blocking antibody (TSBAb) is negative, TSH is obviously elevated, TRH excitation test is normal, and it is more likely to maintain long-term remission after stopping the drug.