Pregnancy is a special period for women, when the synthesis and metabolism of thyroid hormones in the historical organism are altered due to elevated levels of estrogen and chorionic gonadotropin (HCG) in the body. Previous studies have confirmed that, except for subclinical hyperthyroidism during pregnancy, the remaining maternal thyroid function abnormalities: subclinical hypothyroidism, simple maternal hypo-T4emia, clinical hypothyroidism, clinical hyperthyroidism . Subclinical hyperthyroidism. During pregnancy, the most significant maternal change is the increase in estrogen secretion, which causes an increase in thyroid-binding globulin (TBG) synthesis and a decrease in metabolic clearance, resulting in an increase in serum thyroxine levels, which can reach 1.5 times that of non-pregnant women, and the structural similarity between TBS and serum thyrotropin (TSH), which can act on TSH receptors to stimulate an increase in thyroid hormone secretion. Therefore, there are life altering blood T4 and TSH levels in pregnant women. Previously, China and the United Kingdom and the United States established guidelines for thyroid diagnosis and treatment recommending 2.5 miu/L, as the upper limit of normal TSH (30%-50% lower than in the non-pregnant population). Hypothyroidism during pregnancy can affect the development of maternal and fetal obstetric complications, increasing the risk of hyperemesis, miscarriage, preterm delivery, stillbirth and low birth weight babies. Thyroxine has important effects on the entire process of fetal brain development. The mother supplies all the thyroxine needed in the early fetal life. Hypothyroidism during pregnancy is now a recognized cause of neurointellectual impairment in the offspring. Studies in the United States have demonstrated that offspring of mothers with low T4emia are at increased risk for delayed language expression. Hyperthyroidism in pregnancy has significant adverse effects on the mother and the fetus. Treatment of hypothyroidism in pregnancy is mandatory. The etiology is mainly due to autoimmune thyroiditis and hypo-T4emia is often associated with iodine deficiency. L- T4 therapy is preferred for hypothyroidism and must be followed up every 4-6 weeks for the next 5 months. the adjustment of L- T4 dose should be based on normal TSH and T4 values at all stages of pregnancy. the L- T4 dose should be started from 25ug-50ug and L- T4 should be separated from iron, calcium, soy milk and multivitamin preparations. Oral drug therapy is preferred for hyperthyroidism in pregnancy. Propylthiouracil is preferred, as the placental passage rate of this drug is lower than that of methimazole, and should be administered under the guidance of an endocrinologist. Iodine supplementation therapy is mainly for hypo-T4emia and is appropriate to start at 4-6 weeks; if delayed beyond 12 weeks, it increases the risk of delayed neurodevelopment in the offspring.