Thyroid dysfunction can affect women at all stages from conception to delivery and can be harmful to both the mother and the fetus. The fetal thyroid gland begins to develop by the end of the third trimester, and the fetal hypothalamic-pituitary-thyroid axis does not mature until late in gestation. Therefore, maternal thyroxine (T4) levels play an important role in fetal brain development. The prevalence of hypothyroidism in women of childbearing age is about 2% to 4%. Autoimmune thyroid disease (AITD) is the most common autoimmune disease in women and is the most common cause of abnormal thyroid function. The increased demand for thyroxine by mother/fetus during pregnancy can lead to hypothyroidism. Hypothyroidism can be aggravated during pregnancy. It may lead to the development of subclinical hypothyroidism into clinical hypothyroidism. TPOAb positive patients also have a tendency to develop hypothyroidism. This means that AITD patients have a high rate of miscarriage due to a relative shortage of thyroxine (TH) production during pregnancy that does not meet the needs of the pregnancy. In patients with infertility or recurrent miscarriage, thyroid dysfunction needs to be alerted, diagnosed promptly, and treated with thyroid hormone supplementation as soon as possible. The diagnosis of clinical hypothyroidism and subclinical hypothyroidism during pregnancy is the same as that of the general population. Clinical hypothyroidism has clinical manifestations such as edema, fear of cold, weight gain, drowsiness, unresponsiveness, etc. Laboratory tests show an increase in serum TSH and a decrease in F4 and TT4. Subclinical hypothyroidism has no obvious clinical symptoms, and laboratory tests show increased serum TSH and normal F4 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. A TSH of 2.5 mlU/L is currently recommended as a conservative upper limit for early pregnancy, beyond which the diagnosis of hypothyroidism in pregnancy can be considered. The goal of treatment is to ensure an adequate supply of thyroid hormones during the first period of rapid fetal brain development, i.e., the fourth to sixth months of gestation, so treatment must be initiated before the fourth month of pregnancy. The earlier treatment is initiated, the better, preferably at the beginning of pregnancy when serum TSH