Hyperthyroidism (hereafter referred to as hyperthyroidism) occurs in women of childbearing age. The increase of thyroid hormone in pregnancy combined with hyperthyroidism increases the excitability of nerves and muscles and increases the oxygen consumption of the body, while norepinephrine and angiotensin also increase, causing vascular spasms in the body and strengthening contractions, making pregnancy hypertension, miscarriage and preterm delivery easy to occur. On the other hand, excessive secretion of thyroid hormones will inhibit the secretion of gonadotropins by the pituitary gland. This may lead to low birth weight, fetal growth restriction and stillbirth. When hyperthyroidism is severe and involves the heart, coupled with increased blood volume and hyperemesis during pregnancy, heart failure and hyperthyroid crisis may occur, directly threatening the life of the pregnant woman and the fetus. The causes of hyperthyroidism during pregnancy are basically the same as those of hyperthyroidism during non-pregnancy, including Graves’ disease, toxic nodular goiter, and autonomic hyperfunctional adenoma of the thyroid, among which Graves’ disease is the most common, accounting for 85%. In addition to the above-mentioned causes of hyperthyroidism, hyperthyroidism during pregnancy also includes hyperemesis gravidarum, hyperemesis gravidarum, malignant hyperemesis gravidarum and transient hyperthyroidism due to chorioepithelial carcinoma. All of these patients have significantly increased serum hCG levels, resulting in increased serum thyroid hormone levels and decreased serum TSH levels, resulting in clinical manifestations of hyperthyroidism, collectively referred to as hyperthyroidism in pregnancy (SGH). The treatment of SGH is based on supportive therapy and ATD is not recommended. SGH hyperthyroidism tends to follow the changes in blood hCG and usually returns to normal by 14-18 weeks of gestation. During pregnancy, since normal pregnant women can also show symptoms similar to thyrotoxicosis such as excessive sweating, fear of heat, rapid heartbeat and short temper, it is difficult to make a diagnosis of hyperthyroidism during pregnancy relying solely on clinical manifestations. During pregnancy, hyperthyroidism should be suspected if a pregnant woman has weight loss that does not increase with the number of months of pregnancy, or muscle wasting in the proximal extremities, or a heart rate of 100 beats/min or more at rest; if blood FT3 and FT4 are elevated and TSH is less than 0.1 mlU/L (the lower limit of normal value is 0.5 mlU/L), hyperthyroidism can be diagnosed. Graves’ disease may be diagnosed if there is also infiltrative proptosis, diffuse goiter, tremor or vascular murmur in the thyroid area, and positive serum TRAb or TsAb. Once the diagnosis of hyperthyroidism is confirmed during pregnancy, prompt and adequate treatment should be given. If hyperthyroidism is not well controlled during pregnancy, pregnant women are at a significantly increased risk of developing pregnancy complications. Conversely, when hyperthyroidism is adequately controlled during pregnancy, the prognosis for the mother and her offspring is significantly better than in those with uncontrolled hyperthyroidism. Patients with hyperthyroidism who become pregnant after normal thyroxine levels can pass through all stages of pregnancy to full term delivery just as well as normal pregnancies. The ability of a woman with preconception hyperthyroidism to become pregnant depends on the severity of the hyperthyroidism. It has been reported in the literature that mild hyperthyroidism has no significant effect on pregnancy, and pregnancy can lead to varying degrees of remission of hyperthyroidism, which may be related to changes in body immune function during pregnancy. If patients with moderate or severe hyperthyroidism and uncontrolled symptoms become pregnant, the rates of miscarriage, gestational toxicity, preterm birth, small full-term infants and perinatal mortality are increased. Therefore, patients are advised not to become pregnant. If the patient is on antithyroid drug (ATD) therapy and the thyroid function is in the normal range on laboratory tests, stopping or applying the minimum dose of ATD, pregnancy is possible. After the minimal dose maintains normal thyroid function for several weeks, the drug can be discontinued. However, pregnant women with high levels of TRAb need to maintain treatment until 32 to 36 weeks of gestation to avoid recurrence of hyperthyroidism. In case of recurrence of hyperthyroidism, treatment can be repeated. If pregnancy is combined with subclinical hyperthyroidism, it can be closely observed and temporarily left untreated. Treatment should be started only when symptoms worsen or hyperthyroidism worsens on thyroid function tests. Strictly speaking, it is better to get pregnant one year after the diagnosis of hyperthyroidism is confirmed, and contraception should be used during the treatment period (ATD or radioactive iodine). If a patient develops hyperthyroidism during pregnancy, after informing her of the possible risks to pregnancy and the fetus, she should opt for anti-thyroid medication if she continues to choose pregnancy or opt for surgery during the 6th month of pregnancy. The pattern of clinical manifestations of hyperthyroidism during pregnancy is that hyperthyroidism worsens in the first 5 months of pregnancy, decreases in the second 5 months, and worsens again in the first 3 months after delivery. Thus, pregnant women have a tendency to have a recurrence of hyperthyroidism after delivery. The main antithyroid drugs (ATD) are propylthiouracil (PTU) and methimazole (MMI). Previous studies have concluded that methimazole passes through the placenta in significantly greater amounts than propylthiouracil, leading to an increased risk of hypothyroidism in the fetus and newborn, while other studies have found that methimazole taken early in pregnancy leads to a significantly increased risk of congenital malformations in the newborn, while propylthiouracil has not been reported to lead to an increased risk of congenital malformations in the newborn. Therefore, it is proposed that propylthiouracil is the best choice during pregnancy. However, on June 4, 2009, the U.S. Food and Drug Administration (FDA) issued an alert to healthcare professionals advising adults and pediatric patients of the risk of serious liver injury, including liver failure and death, associated with the use of propylthiouracil. Therefore, propylthiouracil may be more appropriate for the treatment of patients with Graves’ hyperthyroidism in the first trimester of pregnancy, with methimazole preferred for the treatment of hyperthyroidism in mid- and late pregnancy. The equivalent dose ratio of PTU to MMI is 10:1 to 15:1 (i.e., PTU 100 mg = MMI 7.5 to 10 mg). β-blockers such as propranolol may cause intrauterine growth retardation, prolonged labor, fetal bradycardia and neonatal hypoglycemia as complications of long-term treatment, and should therefore be used with caution. When using antithyroid drugs to treat hyperthyroidism in pregnancy, care must be taken to use the minimum effective dose to prevent overtreatment leading to maternal and fetal hypothyroidism. The dose of propylthiouracil is 300 mg/d, and the dose of methimazole is 15-20 mg/d, starting with small doses; secondly, we should pay attention to monitoring thyroid function, testing pregnant women’s serum TSH and free thyroxine every 4 weeks or so, so that thyroid function is maintained at the high limit of normal. Currently, the dosage of ATD that maintains FT4 at the upper limit of normal or mild hyperthyroidism is considered to be the appropriate dosage; it generally takes 4 weeks for FT4 to improve and 6-8 weeks for TSH to normalize. Since the time to normalize TSH lags behind that of thyroid hormones, it is not used as an observational indicator to adjust medication during pregnancy, but normal TSH levels suggest that ATD should be reduced or discontinued. In addition, because TSH receptor antibodies (TRAb) can cause fetal hyperthyroidism through the placenta and can persist in the newborn for more than a month after delivery. Serum TRAb should be measured at 20-24 weeks of gestation in the presence of Graves’ hyperthyroidism or a previous history of iodine-131 therapy and surgical treatment of Graves’ hyperthyroidism, and fetal and neonatal thyroid function should be monitored if high levels of TRAb are present in the pregnant woman. Combined use of LT4 during pregnancy is not recommended. Surgery may be considered if ATD therapy is not effective, if there is an allergy to ATD, or if the thyroid gland is so enlarged that a high dose of ATD is required to control the hyperthyroidism. The timing of surgery is usually chosen in the sixth month of pregnancy. Surgery in early and late pregnancy is likely to cause miscarriage and preterm delivery. Anti-thyroid medication is only suitable for patients with mild hyperthyroidism. For patients with moderate or severe hyperthyroidism or those with recurrent hyperthyroidism, Iodine-131 therapy is recommended before pregnancy. This is because iodine-131 therapy has the advantages of being safe, non-invasive, convenient, with few side effects and a high cure rate, and has no effect on fertility or offspring. Although, some patients may develop hypothyroidism, with early detection and thyroxine supplementation, pregnancy can be normalized six months after treatment. I-131 treatment for hyperthyroidism is contraindicated in women during pregnancy and lactation. Women of childbearing age must be certain that they are not pregnant prior to I-131 treatment. Pregnancy should be avoided for 6 months after treatment. The use of PTU 300 mg/d or MMI 20 mg/d during lactation has no significant effect on fetal thyroid function; it is safe for mothers to take moderate amounts of ATD during lactation, but the infant’s thyroid function should be monitored. It is recommended that mothers should take ATD after breastfeeding is completed, with an interval of 3 to 4 h before the next breastfeeding session. Because of the risk of serious liver injury with propylthiouracil, methimazole (MMI) should be preferred for ATD in divided doses during lactation.