Gestational transient thyrotoxicosis (GTT): The incidence of GTT in pregnant women is 2-3%. It is associated with increased concentrations of human chorionic gonadotropin (hCG). hCG has the same alpha subunit, similar beta subunit and receptor subunit as thyrotropin (TSH), so hCG has a mild stimulatory effect on TSH receptors in thyroid cells. The syndrome is characterized by reduced serum TSH levels and increased FT4 or FT3. The clinical picture is one of hyperthyroidism, the degree of the disease correlates with the degree of increased serum hCG levels, but there is no proptosis and the thyroid gland is negative for autoantibodies. In severe cases, severe nausea, vomiting, weight loss of 5% or more, dehydration and ketosis may occur in severe cases. This is why it is also called transient hyperthyroidism of hyperemesis gravidarum (THHG). Most cases require only symptomatic treatment, while severe cases require short term antithyroid medication. Diagnosis of Graves’ disease in pregnancy: Hypermetabolic syndrome and physiologic goiter during pregnancy are very similar to Graves’ disease, and due to elevated TBG and correspondingly elevated TT3 and TT4, these make the diagnosis of hyperthyroidism difficult. Hyperthyroidism should be considered if the weight does not increase with the number of months of pregnancy, if the proximal muscles of the limbs are wasted, and if the heart rate at rest is above 100 beats/min. Hyperthyroidism can be diagnosed if serum TSH is decreased and FT3 or FT4 is increased. Graves’ disease may be diagnosed if accompanied by infiltrative proptosis, diffuse goiter, tremor or vascular murmur in the thyroid area, and positive serum TRAb or TSAb. Hyperthyroidism and pregnancy: Uncontrolled hyperthyroidism increases the incidence of miscarriage, preterm delivery, pre-eclampsia, and placental abruption in pregnant women, and increases the risk of preterm infants, intrauterine growth retardation, and full-term microsomnias. Maternal thyroid-stimulating antibodies (TSAb) can cause fetal or neonatal hyperthyroidism by stimulating the fetal thyroid gland through the placenta. Therefore, if the patient has uncontrolled hyperthyroidism, it is recommended not to get pregnant; if the patient is on antithyroid drug (ATD) therapy and the serum TT3 or FT3, TT4 or FT4 reaches the normal range, stop ATD or apply the minimum dose of ATD and you can get pregnant; if the patient is hyperthyroidism found during pregnancy, after informing the possible risks of pregnancy and fetus, if the patient chooses to continue the pregnancy ATD treatment is preferred, or surgical treatment during the 4th-6th months of pregnancy. Fetal development should be monitored during pregnancy. Effective control of hyperthyroidism can significantly improve the poor outcome of pregnancy. ATD treatment in pregnancy: Because PTU has a high plasma protein binding ratio and a lower placental passage rate than MMI, PTU passes the placenta in only 1/4 of the amount of MMI, and because skin dysplasia (aplasia cutis) due to MMI is more common than PTU, PTU is preferred for treatment of hyperthyroidism in pregnancy, with MMI as a second-line agent. The goal of ATD therapy is to achieve and maintain the upper limit of normal serum FT4 in the shortest possible time using the smallest effective dose of ATD and to avoid ATD from affecting fetal brain development through the placenta. The starting dose of methimazole (MMI) 10-20 mg once daily or propylthiouracil (PTU) 50-100 mg three times daily orally, with monitoring of thyroid function and timely reduction of drug dose. Thyroid function was checked every 2-4 weeks at the beginning of treatment and extended to 4-6 weeks later. TSH levels can remain suppressed for several weeks after serum FT4 has reached normal, so TSH levels cannot be used as a monitoring indicator during treatment. Combined use of L-T4 is not recommended during pregnancy because the dose of ATD for controlling hyperthyroidism needs to be increased with the combination of levothyroxine (L-T4). Surgery may be considered if ATD therapy is not effective, if there is an allergy to ATD, or if the thyroid gland is significantly enlarged and a high dose of ATD is required to control hyperthyroidism. The timing of surgery is usually chosen between the 4th and 6th month of pregnancy. Surgery in early and late pregnancy is likely to cause abortion. β-blockers such as propranolol are associated with spontaneous abortion and may also cause complications such as intrauterine growth retardation, prolonged labor, and neonatal bradycardia, so they should be used with caution. ATD therapy during lactation: Studies over the past 20 years have shown that the application of ATD during lactation is safe for the offspring. The use of PTU 150 mg/day or MMI 10 mg/day during lactation has no significant effect on the infant’s brain development, but the infant’s thyroid function should be monitored; no complications such as granulocytopenia or liver function damage have been found in the offspring of mothers who were treated with ATD during lactation. The mother should take ATD after breastfeeding is completed, followed by an interval of 3-4 hours before the next breastfeeding. the amount of milk excreted by MMI is 7 times higher than that of PTU, so PTU should be the first choice for treatment of hyperthyroidism during breastfeeding. Pregnancy and 131I therapy: 131I therapy for hyperthyroidism is contraindicated in women during pregnancy and lactation. Women of childbearing age must be certain that they are not pregnant before 131I therapy is administered. If 131I therapy is chosen, pregnancy should be avoided for 6 months after treatment.