Chronic lymphocytic thyroiditis is a relatively common autoimmune disease of the thyroid gland, also known as autoimmune thyroiditis. It was first described by Japanese surgeon Hakaru Hashimoto in 1912 while working in Berlin, Germany, and is therefore also known as Hashimoto’s thyroiditis (HT) or Hashimoto’s disease. The etiology of Hashimoto’s thyroiditis is thought to be the result of an interaction of genetic factors and multiple internal and external environmental factors. The disease is often found to occur in several generations of the same family. Hashimoto’s thyroiditis is the most common type of thyroiditis, with an increasing trend in recent years. 90% of the cases are in women, and the age of onset is later in men than in women. There is a high incidence in women between the ages of 30 and 50, and other age groups have also developed the disease. There is often a family history of thyroid disease, sometimes combined with other autoimmune diseases. The onset of the disease is insidious and often goes undetected. It is sometimes detected incidentally during physical examination or when symptoms of hypothyroidism are present. The typical clinical manifestations are: middle-aged and elderly women, slow onset and long duration of the disease, diffuse enlargement of the thyroid gland, hard and tough, painless or light pressure pain, smooth surface, nodules may be present, local pressure and systemic symptoms are not obvious, occasional throat discomfort, normal or abnormal thyroid function. A long period of time often elapses from onset to the appearance of abnormal thyroid function. Hypothyroidism can occur, as well as hyperfunction, and sometimes manifestations resembling subacute thyroid inflammation, but eventually progressing to hypothyroidism. The rate of progression of Hashimoto’s disease to hypothyroidism is related to many factors, with women progressing five times faster than men, and those with high initial thyroid antibodies and elevated initial TSH progressing faster after age 45. In a 20-year follow-up study, the rate of progression to hypothyroidism was 2.6% per year in antibody-positive individuals, with a 33% incidence of hypothyroidism at the end of follow-up, and 2.1% per year in those with elevated TSH, with a 27% incidence of hypothyroidism. Hashimoto’s pseudohyperthyroidism (transient hyperthyroidism) is caused by thyroid gland destruction and thyroid hormone release. It is generally less symptomatic and easier to control, and the iodine uptake rate of the thyroid gland is reduced. 2. Laboratory tests Thyroid function is normal or low. Thyroid function is related to different periods of Hashimoto’s disease development. Most thyroid function is normal, but it may be reduced in those with long disease duration. Sometimes the thyroid function is hyperactive and the duration is variable. Thyroglobulin antibodies (TGA) and thyroid microsomal antibodies (TMA) are significantly elevated and can persist for a long time, up to 80% for several years, or even more than 10 years. Both antibodies have special significance for the diagnosis of this disease. TMA is better than TGA for the diagnosis of Hashimoto’s disease, and 50% of the cases can be diagnosed by TMA alone. The iodine uptake rate of the thyroid gland may be normal, increased or decreased. Nuclear scans are unevenly distributed, with irregular sparse and concentrated areas with poorly defined borders or cold nodules. Ultrasound of the thyroid gland shows diffuse enlargement with thickened light spots and diffuse echogenic hypoechogenicity with uneven distribution. Thyroid puncture biopsy has lymphocytes, lymphoid follicle formation, may have eosinophils, and fibrosis. Treatment There is no reliable treatment to eliminate the disease, but symptomatic treatment is available for thyroid size and thyroid function abnormalities. If the thyroid function is normal, the thyroid gland is small and has no obvious symptoms of compression can be followed up and observed; if the enlarged thyroid gland compresses the neighboring organs or affects the appearance, some people propose to take thyroid hormone to shrink the thyroid gland, and most cases end up with hypothyroidism, and early medication is better than final. Those who develop hypothyroidism in Hashimoto’s disease are replaced with thyroid hormone, L-T4 is better than thyroid tablets, starting in small amounts and gradually increasing until the gland shrinks and sensitive TSH is reduced to normal. When hyperthyroidism occurs in Hashimoto’s disease if it is transient, beta-blockers can be used. Even if anti-thyroid drugs are used, small doses and short duration applications should be chosen. 4, prognosis Most of the prognosis is good, the natural progression to hypothyroidism trend (76%), previously considered permanent, but some have spontaneous recovery of nail function after replacement.