I. Thyroid hormone changes during pregnancy During pregnancy, thyroid-related hormones and thyroid autoantibodies change accordingly, which makes the occurrence, development and treatment of thyroid disorders during pregnancy have their own physiological characteristics. The increase in serum thyroxine-binding globulin (TBG) increases and clearance decreases during pregnancy; the increase in TBG inevitably leads to an increase in TT4 concentration, so TT4 is not an indicator of the exact level of circulating thyroid hormones during pregnancy; TBG begins to rise on the 20th day after ovulation, peaks at 20-24 weeks, and is maintained until several weeks after delivery; TBG levels are 1.5-2 times higher than during non-pregnancy. Serum TT4 and TT3 increase; serum TT4 level is 1.5-2 times higher than that of non-pregnancy. Placental secretion of chorionic gonadotropin (hCG) increases in early pregnancy, usually peaking at 8-10 weeks. Since hCG causes a subunit similar to TSH, it has a thyroid-stimulating effect, and the increased thyroid hormone partially suppresses TSH secretion, causing serum TSH levels to decrease. Generally, for every 10,000 IU/L increase in hCG, TSH decreases by 0.1 mIU/L. The increase in serum hCG level and decrease in TSH level occur in the 8th-14th weeks of gestation, and the lowest point of decrease is in the 10th-12th weeks of gestation. In addition, placental type II and III deiodinase activity increases. In human placenta, type II and III deiodinases coexist and can complete the T4 to T3 or rT3 transition. When maternal T4 is reduced in hypothyroidism and iodine deficiency states, the activity of type II deiodinase increases in the placenta, thus ensuring the stability of T3 and regulating the need for thyroid hormones during pregnancy. In contrast, the loss of iodine increases during pregnancy due to increased glomerular filtration rate and increased renal clearance of iodine. In mid-gestation, the maternal inorganic iodine pool is transferred to the fetus, and large amounts of iodide and iodinated thyroidogenic acid are transferred to the fetus to ensure hormone production and fetal development. The mandatory maternal iodine loss is exacerbated, with the result that the maternal thyroid gland is further restricted in terms of available iodine and maternal serum inorganic iodine levels are reduced. Therefore, WHO recommends a higher iodine intake in the diet of pregnant women than in the general adult population. In people without autoimmune thyroid disease and without iodine deficiency, elevated estrogen levels in early pregnancy (1-3 months) lead to a nearly 2-fold increase in thyroid binding globulin (TBG) and plateau in mid-pregnancy (4-6 months). In contrast, TT4 concentrations increase rapidly in early pregnancy (1-3 months), rise to 1.5 times the pre-pregnancy level at approximately mid-pregnancy (4-6 months), and reach a steady state. hCG has a stimulatory effect on the thyroid, with hCG levels peaking at 8-10 weeks of gestation, causing TSH suppression, reflecting the fact that TSH is suppressed in early pregnancy. mild elevation of TT4 and FT4 levels rises, after which FT4 levels gradually decrease until the end of pregnancy. The thyroid volume and thyroglobulin are normal on ultrasound during pregnancy. Thyroid hormone levels are significantly altered during pregnancy compared to non-pregnancy. In contrast, in early pregnancy the fetus has no thyroid hormone production and depends entirely on the maternal provision. II. Diagnostic criteria for clinical hypothyroidism in pregnancy The diagnostic criteria for clinical hypothyroidism in pregnancy are: serum TSH > the upper limit of the reference value in pregnancy (97.5 th) and serum FT4 < the lower limit of the reference value in pregnancy (2.5 th). If serum TSH>10mIU/L, regardless of whether FT4 is reduced or not, clinical hypothyroidism is also diagnosed. Third, clinical hypothyroidism in pregnancy must be treated The incidence of clinical hypothyroidism in pregnancy is higher than that in non-pregnant controls. The prevalence reported in China is 1.0%. The most common cause of clinical hypothyroidism is autoimmune thyroiditis, which accounts for about 80% of cases. Other causes include thyroid surgery and 131 iodine therapy. Clinical hypothyroidism in pregnancy impairs the neurointellectual development of the offspring, increases the risk of preterm birth, miscarriage, low birth weight, stillbirth and gestational hypertension, and the evidence is certain that treatment must be given. Clinical hypothyroidism in pregnancy has no effect on the mental development of children after treatment, and no additional monitoring is required. The incidence of subclinical hypothyroidism in pregnancy is significantly higher than in non-pregnant controls, especially in early pregnancy. Subclinical hypothyroidism increases the risk of adverse pregnancy outcomes and impairment of neurointellectual development in offspring; L-T4 attainment treatment significantly improves the intelligence of offspring of pregnant women with subclinical hypothyroidism. The diagnostic criteria for subclinical hypothyroidism in pregnancy are: serum TSH > the upper limit of the pregnancy-specific reference value (97.5 th) and serum FT4 within the reference value range (2.5 th-97.5 th). V. Treatment of clinical hypothyroidism in pregnancy The treatment targets of serum TSH for clinical hypothyroidism in pregnancy are: 0.1-2.5 mIU/L in T1, 0.2-3.0 mIU/L in T2 and 0.3-3.0 mIU/L in T3. Once clinical hypothyroidism is identified, treatment should be started immediately to achieve the above treatment targets as early as possible. Choose levothyroxine (L-T4) therapy for clinical hypothyroidism in pregnancy. Those with subclinical hypothyroidism in pregnancy with positive TPOAb should also receive L-T4 therapy. However, subclinical hypothyroidism with a negative TPOAb may be left untreated. The complete replacement dose for clinical hypothyroidism in pregnancy is higher than the complete replacement dose for non-clinical hypothyroidism in pregnancy. The starting dose of L-T4 is 50-100 μg/day, and the dose is increased according to the patient’s tolerance level to reach the standard as soon as possible. In patients with severe clinical hypothyroidism, a twofold replacement dose is given within a few days of starting treatment to normalize the extra-thyroidal T4 pool as soon as possible. Slowly increasing doses are required in those with co-morbid cardiac disease. Treatment, treatment goals and monitoring frequency for subclinical hypothyroidism in pregnancy are the same as for clinical hypothyroidism, and the dose of L-T4 may be less than for clinical hypothyroidism. The starting dose of L-T4 can be selected according to the degree of TSH elevation: 50 μg/day for TSH > the upper pregnancy-specific reference value, 75 μg/day for TSH > 8.0 mIU/L, and 100 μg/day for TSH > 10 mIU/L. 100 μg/day. Adjust the dose of L-T4 according to the therapeutic target of TSH. The demand for thyroid hormones by the mother and fetus increases during pregnancy. Healthy pregnant women increase the production and secretion of endogenous thyroid hormones through self-regulation of the hypothalamic-pituitary-thyroid axis. The increase in maternal demand for thyroid hormone occurs between the 4th and 6th weeks of gestation and gradually rises until a steady state is reached at the 20th week of gestation, which is maintained until delivery. Therefore, the dose of L-T4 needs to be increased by approximately 30-50% after pregnancy in women with ongoing treatment for hypothyroidism. Clinical hypothyroidism due to thyroidectomy and 131 iodine ablation may require a higher dose. Patients who have been treated for GD or goiter have a much higher dose requirement for L-T4 than other subgroups of the population. Increasing the dose of L-T4 immediately once a hypothyroid woman becomes pregnant is significantly effective in reducing TSH levels in early pregnancy. Patients were randomized to increase the L-T4 dose (2-fold or 3-fold) once they became pregnant. L-T4 replacement doses need to be increased by approximately 25-30% in clinically hypothyroid women after pregnancy. Adjust the dose in a timely manner according to the serum TSH therapeutic goals described above. Clinically hypothyroid women planning to become pregnant need to restore thyroid hormone levels to normal with L-T4 replacement therapy. Although there is no difference in pregnancy outcome between these two control levels, the risk of mild hypothyroidism in early pregnancy is further reduced in the latter. Women with established clinical hypothyroidism who are planning a pregnancy need to control serum TSH at levels of 0.1-2.5 mIU/L before becoming pregnant. The increased demand for thyroid hormones in clinical hypothyroidism during pregnancy is a result of the pregnancy itself. Therefore, maternal serum TSH levels should decrease to pre-pregnancy levels 6 weeks after delivery, and the increased L-T4 dose should be reduced accordingly. The postpartum L-T4 dose should be restored to pre-pregnancy levels in clinically hypothyroid pregnant women. According to China’s national situation, this guideline supports the screening of thyroid disease for women in early pregnancy in hospitals and maternal and child health care departments in China with conditions; the screening indicators are serum TSH, FT4 and TPOAb; the timing of screening is chosen before 8 weeks of gestation, preferably before pregnancy.