Increased maternal/fetal demand for thyroxine (TH) during pregnancy may worsen hypothyroidism. This can lead to an increase in hypothyroidism or to the development of subclinical hypothyroidism into clinical hypothyroidism. There is also a trend toward hypothyroidism in those with positive peroxidase antibodies (TPOAb). Maternal hypothyroidism during pregnancy is associated with spontaneous abortion, gestational hypertension, placental abruption, fetal distress, preterm delivery, and the occurrence of low birth weight infants. Fetal brain development in early gestation is completely dependent on maternal supply of thyroid hormones. Maternal clinical hypothyroidism is known to cause incomplete differentiation and development of the parts of the fetal cerebral cortex responsible for speech, hearing, and intelligence. Maternal subclinical hypothyroidism during pregnancy may also result in mild impairment of mental and motor abilities in the offspring. The diagnosis of clinical hypothyroidism and subclinical hypothyroidism in pregnancy is the same as in the general population. Clinical hypothyroidism has clinical manifestations such as edema, fear of cold, weight gain, drowsiness, unresponsiveness, and increased serum TSH and decreased FT4 and TT4 in laboratory tests. Subclinical hypothyroidism has no obvious clinical symptoms, and laboratory tests show increased serum TSH and normal FT4 and TT4. It should be emphasized that due to the physiological changes of pregnancy, the reference range of thyroid function indicators during pregnancy changes and a pregnancy-specific reference range needs to be adopted. TSH 2.5 mlU/L is currently recommended as a conservative upper limit in early pregnancy, beyond which the diagnosis of hypothyroidism in pregnancy can be considered. TT4 concentration increases during pregnancy and is approximately 1.5 times the normal value in non-pregnancy. If TSH is normal during pregnancy (0.3 to 2.5 mIU/L) and only TT4 is below 100 nmoL (7.8 μg/dl), hypothyroidism can be diagnosed. Once hypothyroidism is diagnosed, exogenous thyroxine (L-T4) should be supplemented in a timely and adequate manner. The earlier treatment is initiated, the better, preferably at the beginning of pregnancy to achieve the standard of serum TSH < 2.5 mIU/L; serum FT4 is maintained at the upper 1/3 level of the normal range for non-pregnant adults; serum TT4 is maintained at 1.5 times the level of the normal value for non-pregnant adults. To ensure adequate supply of thyroid hormone during the first period of rapid fetal brain development, i.e., the 4th to 6th months of gestation. Usually the LT4 dose is increased by 30% to 50% during pregnancy compared to the non-pregnant requirement. The amount of increase in dose depends on the degree of TSH increase and the cause of maternal hypothyroidism. For autoimmune thyroid disease, the dose should be increased by 35%-40%; for hypothyroidism after thyroid surgery and 131I treatment, the dose should be increased by 70%-75%. With appropriate thyroxine replacement therapy in pregnant women with hypothyroidism, the mental development of the child will not be affected. The treatment strategy for women with autoimmune thyroid disease but normal thyroid function before pregnancy is either to give a small amount of L-T4 so that the pregnant woman's TSH is less than 2.5 mIU/L or to monitor TSH. If the dose of L-T4 is adjusted, TSH should be measured every 4-6 weeks. after delivery, the dosage of thyroxine can be slowly reduced to the pre-pregnancy level, and TSH monitoring is also required during the dose reduction. concomitant intake of L-T4 with iron-containing and calcium-containing preparations and soy foods should be avoided, and the interval should be at least 4 hours. Thyroid hormone preparations applied during pregnancy and lactation do not have any toxic effects on the fetus or cause malformations as long as they are taken in appropriate doses. Maternal subclinical hypothyroidism, hypo-T4emia and positive TPOAb can have adverse effects on fetal brain development. The principles of hypothyroidism treatment in pregnancy are early initiation, attainment of targets as soon as possible, and maintenance throughout pregnancy. Some patients with clinical hypothyroidism may be diagnosed later in early gestation, when their fetuses are likely to have irreversible impairment of mental and cognitive abilities. In such cases, the American College of Endocrinology recommends that the pregnancy be maintained and that thyroid replacement therapy be initiated immediately to rapidly normalize thyroid hormone levels. Pre-pregnancy screening should be done for those at high risk of developing hypothyroidism. People at high risk for hypothyroidism include: 1) those with hyperthyroidism, hypothyroidism or lobectomy. ② Family history of thyroid disease. (iii) Goiter. ④ Positive autoantibodies to the thyroid gland. ⑤ Clinical indication of high or low thyroid function, including anemia, hyponatremia, hypercholesterolemia. ⑥Type 1 diabetes mellitus. ⑦Other autoimmune diseases. ⑧Check for infertility with TSH measurement. ⑨History of head and neck radiation therapy. ⑩History of miscarriage and preterm delivery. Once the diagnosis of clinical hypothyroidism is made, L-T4 treatment is given; if the thyroid function is normal, regular follow-up observation is recommended. Pregnant women with Hashimoto's thyroiditis should be monitored more closely after delivery. Usually after six months, the thyroid gland becomes enlarged again or even larger than during pregnancy, and anti-thyroid antibodies are significantly elevated. Those with pre-pregnancy hypothyroidism have a greater chance of developing hypothyroidism again after delivery. Therefore, postpartum treatment and follow-up are necessary. Newborns born to women with Hashimoto's thyroiditis may have hyperthyroidism or hypothyroidism and should be checked for thyroid function. There is a genetic predisposition to thyroid disease, but it does not mean that the offspring will definitely develop thyroid disease, i.e., the offspring will have a greater chance of developing thyroid disease than the normal offspring.