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 vasospasm in the body and intensifying contractions, making pregnancy hypertension, miscarriage and preterm delivery easy to occur. On the other hand, excessive secretion of thyroid hormone will inhibit the secretion of gonadotropin 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 during pregnancy and complications of gestational hypertension, heart failure and hyperthyroid crisis may occur, directly threatening the life of the pregnant woman and the fetus. Once the diagnosis of hyperthyroidism is confirmed during pregnancy, timely and adequate treatment should be given. If hyperthyroidism is not well controlled during pregnancy, the risk of pregnancy complications increases significantly in pregnant women. 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. The etiology of hyperthyroidism during pregnancy is basically the same as that of hyperthyroidism during non-pregnancy, including Graves’ disease, toxic nodular goiter, and autonomic hyperfunctioning adenoma of the thyroid, of 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 chorionic gonadotropin (hCG) levels, resulting in increased serum thyroid hormone levels and decreased serum thyroid stimulating hormone (TSH) levels, with clinical manifestations of hyperthyroidism, collectively known as hyperthyroidism in pregnancy syndrome (SGH). Most patients with SGH will have gastrointestinal symptoms such as severe nausea and vomiting. The physical examination is usually free of goiter and serious signs of hyperthyroidism such as Graves’ ophthalmopathy. tsAb and other thyroid autoantibodies are negative, but blood hCG is significantly elevated. SGH hyperthyroidism tends to wax and wane with changes in blood hCG, and serum thyroid hormones generally return to normal by 14-18 weeks of gestation. treatment for SGH is primarily supportive and ATD therapy is not recommended. During pregnancy, since normal pregnant women may also show symptoms similar to thyrotoxicosis such as excessive sweating, fear of heat, rapid heartbeat and short temper, it is difficult to make the diagnosis of hyperthyroidism during pregnancy solely by relying 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. Due to the altered physiological status of women during pregnancy, the values of thyroid function tests in normal women during pregnancy differ from those in non-pregnant women. Throughout pregnancy, a woman’s TSH values will be lower than those of non-pregnant women. This may be due to an increase in thyroid hormone secretion caused by high levels of hCG through a feedback mechanism. Therefore, it is instructive to establish a lower limit of serum TSH every 3 months of pregnancy. The normal reference values range from 0.1 to 2.5 mU/L in the first trimester, 0.2 to 3.0 mU/L in the second trimester, and 0.3 to 3.0 mU/L in the second trimester. Whether a woman with pre-pregnancy hyperthyroidism can become pregnant depends on the severity of the hyperthyroidism, and ATA guidelines recommend that women with hyperthyroidism should have their thyroid function normalized before pregnancy. Pregnancy in women with hyperthyroidism depends largely on the severity of the condition. Mild hyperthyroidism has no significant effect on pregnancy, while moderate or severe hyperthyroidism or uncontrolled symptoms may affect the outcome of pregnancy. Therefore, it is recommended that women with hyperthyroidism be treated aggressively prior to pregnancy. When treating patients with pre-pregnancy hyperthyroidism, they may choose medication, surgery or radioactive iodine therapy depending on their condition, as the effect on the fetus does not have to be considered. If the patient is receiving antithyroid drug (ATD) therapy and the thyroid function is stable in the normal range by laboratory tests, pregnancy can be stopped or the minimum dose of ATD can be applied. 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 32-36 weeks of gestation to avoid recurrence of hyperthyroidism. 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, those diagnosed with hyperthyroidism should preferably get pregnant after 1 year of stabilization and should use contraception during treatment. Anti-thyroid medication is only suitable for patients with mild hyperthyroidism. For patients with moderate or severe hyperthyroidism or those with recurrent hyperthyroidism, it is recommended to choose iodine-131 treatment 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. If a patient develops hyperthyroidism during pregnancy, if the patient does not develop severe hyperthyroidism complications and pregnancy complications, but only simple hyperthyroidism, medication may be chosen to normalize the thyroid function as soon as possible and the pregnancy may be considered to continue. On the contrary, if a pregnant woman develops serious complications, the pregnancy should be terminated as soon as possible and the hyperthyroidism should be treated actively at the same time. The pattern of clinical manifestation of hyperthyroidism during pregnancy is that the symptoms of hyperthyroidism increase in the first 5 months of pregnancy, decrease in the second 5 months, and increase again in the first 3 months after delivery. As a result, pregnant women have a tendency to have a recurrence of hyperthyroidism after delivery. The main antithyroid drugs (ATDs) 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 during the first trimester of pregnancy, with methimazole preferred for the treatment of hyperthyroidism in mid- to 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 pranolol may cause intrauterine growth retardation, prolonged labor, and fetal cardiac arrest with long-term treatment. The use of β-blockers such as ponerol may cause intrauterine growth retardation, prolonged labor, fetal bradycardia and neonatal hypoglycemia, and other complications. When using antithyroid drugs to treat hyperthyroidism in pregnancy, care should be taken to use the minimum effective dose to prevent overtreatment leading to hypothyroidism in pregnant women and fetuses. In general, the dose of PTU is 50-150 mg, 2-3 times/d; the dose of MMI is 5-15 mg, 1 time/d, starting from a small dose; secondly, we should pay attention to monitoring thyroid function, and test the serum TSH and free thyroxine of pregnant women every 4 weeks or so, so that thyroid function can be maintained at the normal high limit. 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 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 history of prior iodine-131 therapy and surgical treatment of Graves’ hyperthyroidism; if high levels of TRAb are present, fetal and neonatal thyroid function should be monitored; disappearance of TRAb suggests that ATD therapy can be discontinued, and continued use may increase the risk of fetal hypothyroidism. Combined use of L-T4 during pregnancy is not recommended. Surgery may be considered if ATD therapy is not effective, if the patient is allergic to ATD, or if the thyroid gland is so enlarged that a high dose of ATD is required to control hyperthyroidism. The timing of surgery is usually chosen in the 4th to 6th month of pregnancy. Surgery in early and late pregnancy is likely to cause miscarriage and preterm delivery. Hyperthyroidism during pregnancy may be triggered by infection, mental stimulation and mood swings. Although hyperthyroid crisis is rare, the death rate is very high, ranging from 10% to 20%, and can rise to 75% if not rescued in time. Therefore, once hyperthyroidism crisis occurs, the pregnancy should be rescued immediately and terminated 2 to 4 hours after the condition is stabilized. If the condition of hyperthyroidism is well controlled, there is usually no great risk during delivery. During labor, patients should be given spiritual comfort, encouraged to rest and eat, and closely observe the progress of labor to shorten the second stage of labor as much as possible to avoid increasing the burden on the heart, and if necessary, surgically assisted labor. The use of PTU 300mg/d or MMI 20mg/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 and follow up with the next breastfeeding 3 to 4 h apart. Although the excretion of propylthiouracil (PTU) in breast milk is much lower than that of methimazole (MMI), because of the risk of serious liver injury with propylthiouracil, ATA guidelines recommend that methimazole (MMI) should be given in divided doses as the first choice for ATD during lactation.