Pregnancy is a stressful stimulus to the thyroid gland, with a 10-40% increase in thyroid volume and a 50% increase in thyroxine and daily iodine requirements, which can lead to hypothyroidism in the second trimester in iodine-deficient or limited thyroid stores, and postpartum thyroiditis in women at high risk for Hashimoto’s disease who had a normal thyroid function before pregnancy. In the first trimester, 10-20% of pregnant women with normal thyroid function and positive TgAb or TPOAb have a high likelihood of developing PPT. It is now well recognized that clinical hypothyroidism and clinical hyperthyroidism can have adverse effects on pregnancy, and new research is beginning to focus on the potential effects of subclinical hypothyroidism and subclinical hyperthyroidism on maternal and infant health, the association between miscarriage and preterm delivery in women with normal thyroid function and TPOAb and/or TgAb positivity, the prevalence and long term effects of PPT, and the effects of treatment of thyroid disorders on the intelligence of mothers, fetuses and offspring. Thyroid disease is common in pregnant women and may be involved in about 12/1000 pregnancies. Understanding the characteristics of physiological changes in the maternal thyroid gland during pregnancy is important for the correct judgment and treatment of thyroid disorders in pregnancy. I. Physiologic changes in the maternal thyroid gland during pregnancy Four important physiologic changes occur in the maternal thyroid gland during pregnancy, affecting the activity of the thyroid gland. (i) Increase in thyroxine-binding globulin (TBG): Less than 1% of thyroxine (T4) and triiodothyronine (T3) are free in human blood. The rest is mainly bound to TBG. In early pregnancy, estrogen levels increase, the liver’s ability to synthesize TBG is enhanced, and at the same time TBG sialic acid modification is increased, and the half-life of TBG is prolonged from 15 minutes to 3 days.TBG begins to increase at 6-8 weeks of gestation, peaks at the 20th week of gestation (more than 1.5-fold), and persists until labor and delivery, generally increasing 2-3-fold from the basal value.An increase in TBG inevitably brings about an increase in TT3 and TT4 concentrations, and most of the time the blood free TT3 and TT4 concentration increases, and in most cases the blood free TT3 and TT4 concentrations are increased. The increase in TBG inevitably brings about an increase in the concentrations of TT3 and TT4, while in most cases there is no change in blood free T3 (FT3) and free T4 (FT4), so TT4 does not reflect the true level of thyroid hormones in the blood circulation during pregnancy. In order to maintain sufficient FT3 and FT4 for maternal metabolism and fetal development, the mother must synthesize more T3 and T4. Serum FT4 levels are 10%-15% higher in early pregnancy than in non-pregnancy. (ii) Iodine deficiency: There is a dynamic balance between the thyroid and kidney in the extra-thyroidal pool of iodine. The increase in renal function during pregnancy increases the glomerular filtration rate and renal clearance of iodine. In iodine-deficient areas of the world, this may cause a decrease in circulating iodine concentration, possibly increasing the proportion of circulating iodine uptake and causing goiter. Even in iodine-sufficient areas such as the United States, the thyroid volume in women increases by 15% (10% to 20%) during pregnancy. Iodine deficiency is exacerbated by iodine transport to the embryo as early as mid-gestation, when the maternal thyroid pumping mechanism takes precedence over fetal needs despite the inadequate supply of iodine to the embryo. Fetal demand for iodine increases in the second half of gestation as thyroid hormone synthesis by the fetal thyroid gland increases. Iodine is transported through the placenta, and as the placenta enlarges, deiodination of iodinated thyrotropine in the placenta increases the amount of iodine transported to the fetus for fetal iodine requirements. However, excessive iodide ions can inhibit the function of the thyroid gland in synthesizing hormones in the fetus. (iii) Increase in human chorionic gonadotropin: Placental secretion of human chorionic gonadotropin (hCG) increases in the early stages of pregnancy, and usually reaches a peak at 8-10 weeks, with a concentration of 30,000-100,000 IU/L. hCG shares the same α-subunit and similar β-subunit and receptor as thyroid-stimulating hormone (TSH), and hCG has a mild stimulating effect on the TSH receptor of the thyroid cell hCG has a mild stimulatory effect on the TSH receptor in thyroid cells, which increases the secretion of thyroid hormones, and the increased thyroid hormones partially inhibit the secretion of TSH, which reduces the serum TSH level by 20% to 30%, and lowers the lower limit of the TSH level by an average of 0.4 mIU/L compared with non-pregnant women, and can be reduced to less than 0.1 mIU/L in 20% of the pregnant women.The decrease of the TSH level occurs in the pregnancy between 8 and 14 weeks, and the decrease is at the lowest point from the pregnancy between 10 and 12 weeks. High levels of hCG in early pregnancy stimulate the TSH receptor hormone “spillover” syndrome, especially in pregnancies complicated by high levels of hCG or an increase in the proportion of variant hCG (which enhances thyroid stimulating activity), such as in hyperemesis gravidarum or associated with severe vomiting of pregnancy. These may cause transient biochemical changes similar to hyperthyroidism in early pregnancy. Maternal blood hCG and TSH levels show a mirror image relationship during pregnancy. For every 10 000 IU/L increase in serum hCG concentration, serum T4 concentration increases by 0.6 pmol/L, while serum TSH concentration decreases by 0.1 mlU/L. In early pregnancy, about 15% of normal pregnant women have a lower than normal serum TSH level; in mid-pregnancy (April-June), 10% of the serum TSH level is lower than normal; and in late pregnancy (July-October), 5% of the serum TSH level is lower than normal. In late pregnancy (7-10 months), 5% of serum TSH levels are below normal. However, serum hCG reaches levels of 50,000 to 70,000 IU/L and needs to be maintained for a period of time to cause clinical hyperthyroidism. In most pregnant women, the peak in serum hCG lasts only a few days and therefore does not lead to hyperthyroidism. Only 1.5% of pregnant women develop transient hyperthyroidism of pregnancy due to the stimulatory effect of hCG on the thyroid gland. (d) Deiodination of thyroid hormones: Blood T3 is more active than T4 with a shorter half-life, especially for intracellular function, and is a more important hormone in biology. Three types of deiodinases that activate and inactivate T4 and T3 have been identified in target tissues and are thus able to ensure a stable supply of T3 at critical sites. type II deiodinases promote the conversion of T4 to T3, especially when intracellular and when there is an inadequate supply of thyroid hormones, and are found in the placenta. Type III deiodinase, which inactivates T4 and T3 (by deiodination), is also found in the placenta and increases with gestation; this may explain the decrease in hormone levels and the decrease in T4 transport to the fetus in late pregnancy, but enhances iodine transport from the placenta to the fetus. Second, changes in thyroid antibodies during pregnancy during pregnancy because of maternal immunological tolerance to the fetus, thyroid autoantibodies gradually decline in titer after pregnancy, 20-30 weeks of gestation to the lowest titer, a decrease of about 50%. After delivery, the titer of thyroid antibodies rebounded and returned to the pre-pregnancy level at 6 months postpartum. In conclusion, the increase of maternal TBG during pregnancy leads to the increase of blood total T4 and total T3; the increase of hCG leads to the transient decrease of TSH; the increase of renal iodine clearance and the increase of placental iodine transport leads to the decrease of serum iodine concentration is the characteristic of maternal thyroid changes during pregnancy. Third, the assessment of serum thyroid indexes during pregnancy, the aforementioned changes in the thyroid gland during pregnancy will inevitably affect the changes in the reference value of serum thyroid indexes, so each region and hospital should establish their own reference value of TSH in pregnant women, in the absence of their own reference value of the region and hospitals, China’s “Guidelines for the diagnosis and treatment of pregnancy and postpartum thyroid disorders,” suggests that the reference value of TSH for the early stages of pregnancy (T1 stage, 1 to 12 weeks) 0.1 to 2.5; mid-pregnancy (T2 stage, 13 to 27 weeks) 0.2 to 3.0; late pregnancy (T3 stage, 28 to 40 weeks) 0.3 to 3.0.