Thyroid disorders are more common in women, especially in women of childbearing age. Abnormal thyroid function can affect menstruation and conception, and if thyroid function is abnormal during pregnancy, it may have an impact on the pregnancy process, the survival of the fetus, and even the physical and mental development of the child. Therefore, thyroid disease in women of childbearing age deserves attention. 1. Physiological changes in the thyroid gland during normal pregnancy: (1) Increased clearance of iodine by the kidneys, which can lead to goiter in pregnancy in iodine-deficient areas. (2) Increased thyroid binding globulin (TBG) in the blood, resulting in increased serum total thyroxine (TT4) and total triiodothyronine (TT3), but normal free thyroxine (FT4) and free triiodothyronine (FT3). (3) During the first 3 months of pregnancy, human chorionic gonadotropin increases, FT4 in maternal blood is mildly elevated, and thyrotropin (TSH) is correspondingly decreased. Fetal thyroid tissue appears at 10 weeks of gestation, and the hypothalamus begins to function at approximately 12 weeks of gestation. The placental barrier allows the passage of small amounts of thyroid hormones. In addition, iodine, thyroid-stimulating immunoglobulin (TSI) and antithyroid drugs can also pass through the placenta. Pregnancy itself also has an effect on hyperthyroidism. Many patients with hyperthyroidism in remission or in remission have their disease reappear or worsen after pregnancy; due to the reduced immune activity of the mother during pregnancy, a small number of patients may have their existing hyperthyroidism reduce or improve naturally during pregnancy, but after delivery, their hyperthyroidism worsens or reappears. Pregnancy and hyperthyroidism: It is sometimes difficult to diagnose hyperthyroidism during pregnancy, and some physiological changes during pregnancy can be easily confused with symptoms of hyperthyroidism. During pregnancy, thyroid binding globulin increases significantly, resulting in a 30% to 50% increase in total serum T4. Hyperthyroidism should be considered if the weight does not increase with the number of months of pregnancy, if the proximal extremities are thin, and if the heart rate at rest is above 100 beats/min. If the serum TSH is reduced and FT3 or FT4 is increased, hyperthyroidism can be diagnosed. Graves’ disease may be diagnosed if it is accompanied by infiltrative proptosis, diffuse goiter, tremor or vascular murmur in the thyroid area, and positive serum TRAb or TsAb. Uncontrolled hyperthyroidism increases the incidence of miscarriage, preterm delivery, pre-eclampsia, and placental abruption in pregnant women, and increases the risk of preterm birth, intrauterine growth retardation, and full-term small sample babies. Maternal TSAb can stimulate the fetal thyroid gland through the placenta to cause fetal or neonatal hyperthyroidism. Therefore, if the patient’s hyperthyroidism is not controlled, it is recommended not to get pregnant; if the patient is receiving ATD treatment and the serum TT3 or FT3, TT4 or FT4 reaches the normal range, stop ATD or apply the minimum dose of ATD and get pregnant, if the patient is found to have hyperthyroidism during pregnancy, ATD treatment is preferred if the patient chooses to continue the pregnancy, or surgery during the 4th to 6th month of pregnancy Treatment. The main anti-thyroid drugs (ATD) are methimazole (MMI) and propylthiouracil (PTU). The goal of ATD treatment for hyperthyroidism in pregnancy is to achieve and maintain the upper limit of normal serum FT4 in the shortest possible time using the least effective dose, and to avoid ATD from affecting fetal brain development through the placenta. The starting dose of PTU 50-100mg/dose orally 3 times a day or MMll0-20mg once a day: monitor thyroid function and reduce the drug dose in time. The thyroid function should be checked every 2-4 weeks at the beginning of treatment and extended to 4-6 weeks later. If ATD therapy is not effective, if you are allergic to ATD, or if you have an enlarged thyroid gland, you can consider surgery if you need to control hyperthyroidism with high doses of ATD. The timing of surgery is usually chosen in the fourth to sixth month of pregnancy. Beta-blockers such as pranolol are associated with spontaneous abortion and may cause complications such as intrauterine growth retardation, prolonged labor, and neonatal bradycardia, so they should be used with caution. Studies over the past 20 years have shown that ATD is safe for offspring during lactation, and that the use of PTU 150 mg/d or MMI 10m/d has no significant effect on infant brain development, but the infant’s thyroid function should be monitored; the mother should take ATD after breastfeeding, followed by an interval of 3 to 4 hours before the next breastfeeding. PTU should be the first choice for the treatment of hyperthyroidism during lactation. I-131 is contraindicated for the treatment of hyperthyroidism in women during pregnancy and lactation. Women of childbearing age must be certain that they are not pregnant prior to I-131 treatment. If I-131 treatment is chosen, pregnancy should be avoided for 6 months after treatment. 3. Pregnancy and hypothyroidism: Patients with clinical hypothyroidism have reduced fertility. Maternal hypothyroidism during pregnancy is associated with gestational hypertension, placental abruption, spontaneous miscarriage, fetal distress, preterm delivery, and the occurrence of low birth weight infants. The impact of maternal subclinical hypothyroidism in early pregnancy on the first stage of fetal brain development is of great concern. Until fetal thyroid function is fully established (i.e., before 20 weeks of gestation), the main source of thyroid hormones required for fetal brain development is the mother, and maternal thyroid hormone deficiency can lead to impaired mental development in the offspring. The reference ranges of TSH and thyroid hormones during pregnancy are different from those of the general population due to a variety of factors. It is generally believed that the reference range of TSH in early pregnancy should be 30% to 50% lower than that of the non-pregnant population. Currently, some international scholars have proposed 2.5 mIU/L as the upper limit of the normal range of TSH in early pregnancy, and exceeding this limit can be diagnosed as hypothyroidism in pregnancy. Due to the large fluctuation of FT4 during pregnancy, the international recommendation has applied TT4 to assess the thyroid function of pregnant women. TT4 concentration increases during pregnancy and is approximately 1.5 times the normal value in non-pregnancy. Hypothyroidism that has been diagnosed before pregnancy requires adjustment of the L I T4 dose to bring serum TSH within the normal range before pregnancy is considered. During pregnancy, the L-T4 replacement dose is usually increased by 30% to 50% compared to the non-pregnant state. If you have no previous history of hypothyroidism and you are diagnosed with hypothyroidism during pregnancy, you should be treated with L-I T4 immediately, with the aim of bringing serum TSH to the pregnancy-specific normal range as soon as possible. The earlier the target is reached, the better (preferably within 8 weeks of gestation). After the TSH standard is reached, TSH, FT4 and TT4 should be monitored every 6-8 weeks. The American College of Clinical Endocrinologists advocates routine screening of pregnant women for TSH in order to detect and treat clinical and subclinical hypothyroidism in a timely manner. The prevalence of subclinical hypothyroidism in women of childbearing age is about 5%. High-risk groups for hypothyroidism include those with a personal and family history of thyroid disease; those with a history of goiter and thyroid surgery and 131I treatment; and those with a personal and family history of autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes mellitus. It is important to enhance education for women of childbearing age who already have hypothyroidism about the adverse effects of hypothyroidism on pregnancy and fetal brain development.