Goiter is an enlargement of the thyroid gland formed by the proliferation of benign thyroid epithelial cells. A simple goiter, also known as a non-toxic goiter, is a goiter of non-inflammatory and non-neoplastic origin that is not associated with clinical thyroid function abnormalities. Patients with goiter simplex account for about 5% of the population, the disease is disseminated, and the incidence is 3 to 5 times higher in women than in men. If the prevalence of simple goiter among children in a region exceeds 10%, it is called endemic goiter. (a) Endemic goiter The most common cause of endemic goiter is iodine deficiency disease. It is mostly found in mountainous areas and areas far from the sea. Iodine is one of the important raw materials for the thyroid gland to synthesize thyroid hormone. Insufficient synthesis of thyroid hormone when iodine is deficient causes the pituitary gland to secrete excessive tsh, which stimulates hypertrophy of the thyroid gland. Areas of hyperplasia or atrophy, hemorrhage, fibrosis and calcification of the thyroid gland, as well as autonomic hyperfunction and toxic nodular goiter, occur in response to long-term tsh stimulation. The Who recommended daily intake of iodine for adults is 150 micrograms. Urinary iodine is an accepted indicator of iodine nutrition levels, and a median urinary iodine (mui) of 100-200 micrograms/liter is the most appropriate iodine nutritional status. Urinary iodine values of school-age children are generally used to reflect the iodine nutritional status of the area; mui <100~80ug/L for mild iodine deficiency, MUI <80~50ug/L for moderate iodine deficiency, and MUI <50ug/L for severe iodine deficiency. The prevalence of goiter and thyroid volume increased with the degree of iodine deficiency, and the prevalence of goiter decreased significantly with iodine supplementation. Some people in areas of mild iodine deficiency may develop goiter in the presence of increased iodine needs of the organism, such as during pregnancy, lactation, and adolescence. Iodine and the prevalence of goiter show a U-shaped curve. In other words, when iodine is deficient, the prevalence of goiter increases, which is called "low iodine goiter". As iodine intake increases, the prevalence of goiter gradually decreases and reaches less than 5% (i.e., the bottom end of the U). If iodine intake continues to increase, the prevalence of goiter increases, and some scholars call this type of goiter "high iodine goiter". (B) Sporadic goiter The causes of sporadic goiter are complex. Exogenous factors include iodide in food, goitre-causing substances and medications. Endogenous factors include congenital disorders of thyroid hormone synthesis in children, such as impaired iodine transport in the thyroid gland, lack of peroxidase activity, impaired iodinated tyrosine coupling, abnormal thyroglobulin formation, impaired thyroglobulin hydrolysis, and deficiency of deiodinase. The above disorders lead to a decrease in thyroid hormone synthesis and a feedback increase in TSH secretion, resulting in goiter. In severe cases, hypothyroidism can occur. Pathology】 The thyroid gland is diffusely or nodularly enlarged, with weight ranging from 60 to 1000 g. Nodules, fibrosis, hemorrhage and calcification can be seen on the cut surface. At the beginning of the lesion, the entire gland is follicularly hyperplastic and vascular; as the lesion progresses, the area of the follicles changes, with some follicles degenerating and others enlarging and enriched with gelatin, and these follicles are separated by fibrous tissue. Clinical manifestations】 Clinically, there are usually no obvious symptoms. The thyroid gland is often mildly to moderately enlarged, with a smooth surface and a soft texture. A severely enlarged thyroid gland may cause pressure symptoms, coughing, shortness of breath, difficulty in swallowing or hoarseness. A retrosternal goiter may obstruct venous return to the head, neck and upper extremities. Diagnosis and differential diagnosis] Serum TT4 and TT3 are normal, and the ratio of TT4/TT3 is often increased. Serum thyroglobulin (Tg) levels are increased, and the degree of increase is positively correlated with the size of the goiter. Serum TSH levels are generally normal. Early autoimmune thyroiditis manifests mainly as goiter. Longer periods may be without changes in thyroid function or may manifest as subclinical hypothyroidism or (and) positive serum autoantibodies to the thyroid gland. Goiter can be classified into three degrees: I degree if it is not enlarged in appearance but is palpable; II degree if it is both visible and palpable but not enlarged beyond the outer edge of the sternocleidomastoid muscle; and III degree if it is enlarged beyond the outer edge of the sternocleidomastoid muscle. ultrasound is the main test to determine goiter. (1) Prevention of endemic goiter Since 1996, China has introduced legislation for universal salt iodization to prevent and control peng deficiency disease, and in 2002, China revised the national standard for salt iodization from not less than 40 mg/kg to (35 to 15) mg/kg. salt iodization should be implemented differently according to the natural iodine environment of the region, and the urinary iodine level of residents should be monitored regularly. In 2001, the World Health Organization (WHO) and other international authorities proposed that iodine intake should be limited to a median urinary iodine level (MUI) of 100 to 200ug/L and a goiter prevalence of less than 5%. They suggest that excess iodine (MUI>300 Mg) can lead to an increased prevalence of autoimmune thyroiditis and hyperthyroidism. (b) Treatment of goiter Generally, no treatment is required. L-T4 can be tried in patients with significant goiter, but the therapeutic effect is not significant. serum TSH levels must be monitored during L-T4 therapy and should not be applied when serum TSH is low or at the lower limit of normal; L-T4 therapy should also not be applied to those whose thyroid nuclear scan confirms the presence of autonomously functioning areas; L-T4 should be given in small doses to avoid inducing and aggravate coronary artery disease. Surgery should be used for those with significant goiter and symptoms of compression.