The use of antithyroid drugs (ATDs) during pregnancy and lactation has always been the subject of controversy. Many prospective clinical studies have now clarified that ATDs can be used appropriately during pregnancy and lactation without adverse effects on the fetus and infant. I. Risks of untreated hyperthyroidism in pregnancy Discussing the pros and cons of treatment with ATD in pregnancy, the risks of untreated hyperthyroidism in pregnancy to the mother and fetus should also be taken into account. The adverse effects of uncontrolled hyperthyroidism on pregnant women include miscarriage, preterm delivery, pre-eclampsia, congestive heart failure, thyroid crisis, placental abruption, and infection. The effects on the fetus include neonatal hyperthyroidism, intrauterine growth retardation, preterm infants, full-term small sample babies, and stillbirths. Effective control of hyperthyroidism can significantly improve the outcome of pregnancy. In a retrospective study of 181 women with hyperthyroidism in pregnancy done in 1989, the study population was divided into three groups: women who started with normal thyroid function and remained normal (group 1), women who started with hyperthyroidism and had it controlled during pregnancy (group 2), and women who had uncontrolled hyperthyroidism (group 3). Risk factors for low birth weight babies associated with hyperthyroidism included: hyperthyroidism lasting more than 30 weeks at the time of gestation; onset of Graves’ disease before age 20 with a history of more than 10 years The risk factors include: hyperthyroidism lasting more than 30 weeks at the time of gestation; onset of Graves’ disease before the age of 20 and a history of more than 10 years; and TSH binding inhibitory immunoglobulin (TBII) values greater than 30%. They also found that the risk of preterm delivery was 2.8 and 16.5 in the second and third groups, respectively, and the risk of gestational hypertension was 4.7 in the third group. In 1989, Davis et al. reported that they collected data on 342 pregnant women with hyperthyroidism between 1972 and 1988, and the analysis showed that the risk of stillbirth, preterm delivery, thyroid crisis and fetal developmental abnormalities in both the ATD-treated and thyroid surgery groups. The incidence of stillbirth, preterm delivery, thyroid crisis, and fetal growth abnormalities was significantly lower in both the ATD-treated and thyroid surgery-treated groups than in the untreated group. The relationship between untreated hyperthyroidism and the incidence of congenital malformations is uncertain; Momotani et al. reported a 6% incidence of fetal malformations in untreated hyperthyroid patients, 1.7% in the ATD-treated group, and 0.2% in the normal thyroid group. However, it has also been reported that hyperthyroidism is not associated with fetal malformations. Reports suggest that the incidence of congenital malformations in women with untreated or poorly treated hyperthyroidism in pregnancy may be mildly increased, but there is a lack of additional information to support this. Second, which drug is chosen to treat hyperthyroidism in pregnancy: PTU or MMI? There are two types of ATDs commonly used to treat hyperthyroidism: propylthiouracil (PTU) and methimazole (tabazol, MMI). 1, placenta through the only human in vivo study reported that seven women at 8 to 20 weeks gestation, 2h before termination of pregnancy, took 35S-labeled compounds. The ratio of cord blood and fetal serum to maternal serum drug concentrations ranged from 0.27 to 0.35 for those taking PTU and 0.72 to 1.0 for those taking MMI, indicating that the placental transmission rate of PTU was lower than that of MMI. A recent study using isolated perfused human placentas found no difference in placental transmission rates between PTU and MMI. There was no difference in placental transmission between PTU and MMI, although PTU protein binding was higher and placental transmission was not dependent on the concentration of perfusate protein, suggesting a high degree of placental selectivity for unbound drugs. This is consistent with the clinical observation of similar fetal outcomes (thyroid function and congenital malformations) regardless of the drug used. 2. congenital malformations that may be associated with ATD Many studies have confirmed that neither PTU nor MMI applied during pregnancy leads to an increased incidence of congenital malformations in the fetus. It has been reported that MMI may lead to dermal dysplasia (congenital localized skin defects) and embryonic dysplasia, including congenital head skin defects, posterior nostril atresia, trachea. Esophageal leakage, nipple hypoplasia, facial dysmorphism, and psychomotor retardation have been reported. Previous studies have suggested that propylthiouracil is the preferred treatment for hyperthyroidism during pregnancy and lactation. The American Thyroid Association (ATA) and the Chinese Medical Association’s Guidelines for the Management of Thyroid Disorders in Pregnancy and the Postpartum Period recommend that propylthiouracil is preferred for the treatment of hyperthyroidism only in early pregnancy (0-12 weeks) and that methimazole is preferred for the treatment of hyperthyroidism in mid- and late pregnancy and during lactation. The use of ATD for hyperthyroidism in pregnancy is described in the diagnosis and treatment of hyperthyroidism in pregnancy. IV. ATD and breastfeeding The traditional view is that women taking AIDs should not breastfeed and are often advised to stop breastfeeding because of the belief that the concentration of these drugs in breast milk can affect the function of the fetal thyroid gland. In 1980 Kampmann et al. published a report with a very striking title? “Propylthiouracil in human breast milk: a dogmatic reworking”, proposing that PTU is not significantly concentrated in breast milk. 9 lactating women were given 200 mg of PTU and the drug concentrations in serum and breast milk were measured for 4 hours and the amount of PTU in breast milk was found to be 0.025% of the administered dose (range 0.007% to It was found that the amount of PTU in milk was 0.025% of the dose (range 0.007% to 0.077%), and the drug concentration in milk was 10% of the serum drug concentration during the same period. Based on this amount, if a mother takes 600 mg of PTU per day, which is equivalent to giving 149 μg to her infant, the drug concentration for a 4-kg infant is equivalent to a 70-kg adult taking 3 mg of PTU per day. Regarding the ratio of the drug concentration of MMI in breast milk to that in serum of 1.0, the amount of drug in breast milk after the mother has taken the drug for 8 h is 0.1% to 0.17% of the dose taken In 2000, Azizi found that if a hyperthyroid patient took 2O-3Omg of MMI per day, the drug concentration in the infant’s serum was 0.03mg/L after the mother took the drug for 2h, which was much lower than the dose of the drug in play. The higher milk excretion rate of MMI compared to PTU is due to little binding to serum proteins, so PTU should be preferred for the treatment of hyperthyroidism during lactation. The administration of PTU 300 mg or MMI 20 mg daily during lactation has no significant effect on fetal thyroid function, but the infant’s thyroid function should be monitored; no complications such as intellectual and physical developmental effects, granulocytopenia, or liver function impairment have been observed in the offspring of mothers taking ATD during lactation. It is recommended that mothers should take ATD after finishing breastfeeding, with an interval of 3 to 4 h before the next breastfeeding session. In conclusion, it is safe for mothers to use ATD therapy during breastfeeding, whether it is continued after pregnancy or started after delivery.