The thyroid gland is an important endocrine organ in the body, with the primary role of synthesizing, storing and secreting thyroid hormones and, to a lesser extent, calcitonin. The regulation of thyroid hormones, like that of all other endocrine systems, is regulated through hypothalamus-pituitary-target gland and thus negative feedback (Figure 1). The function of thyroid hormones is to increase the metabolic rate of the body, increase oxygen consumption, promote growth and development, and contribute to the differentiation and maturation of the nervous system. Thyroid hormones play a very important role in the maturation of the cerebral cortex, especially in the development, differentiation and functional perfection of the fetal nervous system. Insufficient thyroid hormones during fetal and neonatal periods can lead to mental retardation, deafness and cretinism; in children, to growth retardation; and in adults, to memory loss and unresponsiveness. Therefore, thyroid function during pregnancy plays a crucial role in the development of the fetus. Compared to T3, T4 is more truly expressive of thyroid function Broadly speaking, thyroid hormones include thyroxine (T4), triiodothyronine (T3), trans-triiodothyronine (rT3), diiodothyronine (T2), and monoiodothyronine (T1). Most of the thyroid hormones are bound to thyroid binding proteins in peripheral blood and exert physiological effects mainly on free T4 (FT4) and free T3 (FT3), which is three to four times more active than T4. All serum T4 is secreted from the thyroid gland, while only a small fraction (10%-20%) of serum T3 is secreted directly from the thyroid gland, and the vast majority (80%-90%) is converted from T4 in the periphery. Strictly speaking, only serum T4 can really show thyroid function, and T3 cannot really show thyroid function. Therefore, the most commonly used thyroid hormone indicators in clinical laboratory tests are T3, T4, FT3 and FT4, with T4 and FT4 having larger units than T3 and FT3. Another important clinical indicator related to thyroid hormones is thyrotropin (TSH). There is a feedback regulation system between TSH and thyroid hormones in the blood, when the thyroid gland secretes insufficient thyroid hormones, it will stimulate the TSH secretion of the pituitary gland, and the elevated TSH stimulates the thyroid gland to secrete more thyroid hormones; when the thyroid gland secretes too much thyroid hormones, it will inhibit the pituitary gland to secrete TSH, and the reduced TSH will reduce the thyroid hormone secretion. Reduced TSH decreases thyroid hormone secretion, which leads to thyroxine regulation and homeostasis. There are no racial differences in thyroid hormones and no major differences between age groups, except for slightly lower T3 levels in the elderly and slightly higher T3 levels in children, which are not of great clinical significance. Notably, the feedback between the hypothalamic-pituitary-thyroid axis is not mature enough in children, and TSH can behave at a high level in children, two to four times higher than in adults. Immune factors can cause thyroid-related disorders, and therefore, clinical diagnosis is aided by testing for thyroid antibodies. Thyroid autoantibodies include thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGA), thyrotropin receptor antibody (TRAb) and thyroid hormone antibody (TAb). TPOAb and TGAb are mainly used for the diagnosis of chronic lymphocytic thyroiditis (also known as Hashimoto’s thyroiditis) and Graves’ hyperthyroidism (also known as toxic diffuse goiter). TRAb is mainly used for the etiologic diagnosis of hyperthyroidism. Other common clinical indicators of thyroid are thyroglobulin (Tg) and thyroxine-binding globulin (TBG). Thyroglobulin is mainly used in the follow-up of papillary thyroid cancer and follicular thyroid cancer. Thyroxine-binding globulin is mainly measured during pregnancy because TBG increases during pregnancy and total serum T3 also increases accordingly, which in combination with FT3 can help to clarify whether hyperthyroidism is combined. FT3 and FT4 are the main indicators to determine whether hyperthyroidism is combined with pregnancy. During pregnancy, the basal metabolic rate of the body increases, the thyroid gland becomes rich in blood transport, the alveoli proliferate and the thyroid gland compensates for hyperplasia, while the increase in blood volume, blood dilution, kidney filtration and iodine excretion cause “iodine starvation”. WHO recommends an iodine intake of 250 μg/day during pregnancy and lactation. During pregnancy, serum chorionic gonadotropin (HCG) has similar subunits to TSH and stimulates the release of TT4 and TT3, resulting in an increase in serum total T4 (TT4) and TT3, with TT4 levels 1.5 to 2 times higher than in non-pregnancy, while liver production of thyrotropin binding protein (TBG) levels are 2 to 3 times higher than in non-pregnancy, so serum FT4 and FT3 levels do not increase. FT3 and FT4 are the main indicators to determine whether the pregnancy is combined with hyperthyroidism. Physiological changes during pregnancy lead to an increased demand for thyroxine in the mother, iodine deficiency and slow onycholysis lead to a relative FT4 deficiency and an increase in TSH, which predisposes to suboptimal hypothyroidism. Maternal TSH cannot pass through the placenta, thyroxine can, and the fetus itself cannot yet synthesize T4 during early pregnancy; therefore, maternal thyroxine is critical to the brain development process of the early embryo. The recommended upper limit of normal serum TSH levels is 2.5 mU/L in early pregnancy and 3.0 mU/L in middle and late pregnancy. The brain development of the embryo during early pregnancy depends on maternal thyroid hormone, and animal tests have shown that pregnant rats with early In human observational studies, it has also been found that mothers with clinical hypothyroidism often have poor pregnancy outcomes, and screening for thyroid function during pregnancy should be given adequate attention.