Goiter is an enlargement of the thyroid gland formed by the proliferation of benign thyroid epithelial cells. Simple goiter, also known as non-toxic goiter, is a goiter caused by non-inflammatory or non-neoplastic causes and is not associated with abnormal thyroid function (hypo- or hyperthyroidism). The incidence is 5% of the population and the disease is disseminated, with the incidence in women being 3-5 times higher than in men. I. Etiology and pathogenesis of simple goiter has complex causes. Exogenous factors include: food iodide deficiency (WHO recommends a daily iodine intake of 150μg for adults, urinary iodine below 150μg/L indicates iodine deficiency), goiter-causing substances and drugs. Endogenous causes: congenital disorders of thyroid hormone synthesis, such as iodine transport disorders in the thyroid gland, TPO activity deficiency, iodinated tyrosine coupling disorders, abnormal Tg formation, Tg hydrolysis disorders, deiodinase deficiency, etc. These disorders lead to a decrease in thyroid hormone synthesis, a relative shortage of serum T3 and T4, and a feedback increase in TSH secretion, which stimulates thyroid follicular hyperplasia and leads to goiter. Second, clinical manifestations are generally without obvious symptoms. The thyroid gland is often mildly or moderately enlarged, with a smooth surface and a soft texture. A severely enlarged thyroid gland can cause pressure symptoms, coughing, shortness of breath, difficulty swallowing or hoarseness. A retrosternal goiter can block venous return to the head, neck and upper extremities, manifesting as facial bruising and dilated superficial veins in the neck and chest. In long-standing cases, nodules may form in the thyroid gland. Diagnosis, differential diagnosis and graded diagnosis are mainly based on the patient’s enlarged thyroid gland, normal serum T3 and T4, increased TT4/TT3 values, normal TSH, and increased serum thyroglobulin (Tg) levels, with the degree of increase positively correlated with the volume of the goiter. Simple goiter should be differentiated from autoimmune presenting thyroiditis, as the latter may also present as goiter in the early stages. However, thyroglobulin antibodies and thyroid peroxidase antibodies are often significantly increased in the long term and can be differentiated. When nodules are present, especially if they are bleeding, rapidly enlarging, and show “cold” nodules on a thyroid nuclear scan, attention should be paid to differentiating them from thyroid cancer, and a fine needle biopsy of the thyroid gland may be performed if necessary. Goiter can be divided into three degrees: degree I is when there is no goiter in appearance but the thyroid gland can be palpated; degree II is when the goiter can be seen and palpated but the goiter does not exceed the outer edge of the sternocleidomastoid muscle; degree III is when the goiter exceeds the outer edge of the sternocleidomastoid muscle. Ultrasonography is the main test to determine goiter. IV. Treatment is generally not required. Treatment with levothyroxine (L-T4) can be tried for those with significant goiter, but the therapeutic effect is not significant. serum TSH must be monitored during L-T4 treatment and should not be used when serum TSH is below normal or at the lower limit of normal. L-T4 therapy should also not be used if there are areas of autonomic function present on thyroid nuclear scan. Those with significant goiter and symptoms of compression should be treated with primary surgery.