Thyroid function status during pregnancy is directly related to pregnancy outcome. Poorly controlled thyrotoxicosis is associated with miscarriage, gestational hypertension, preterm delivery, low birth weight, intrauterine growth restriction, stillbirth (death of the fetus during delivery), thyroid crisis, and maternal congestive heart failure. It is best to consider pregnancy in women with existing hyperthyroidism after thyroid function has been controlled to normal, and at least 6 months in patients with hyperthyroidism treated with 131 iodine. (1) Methimazole (MMI) and propylthioxypyrimethamine (PTU) have risks for both mother and fetus; (2) MMI has a risk of fetal malformation, so it is recommended to discontinue MMI and switch to PTU before planning pregnancy; (3) PTU is preferred in the T1 stage of pregnancy, with MMI as a second-line option; ( (3) After the T1 period, then switch to MMI to avoid the occurrence of hepatotoxicity of PTU. MMI has been reported to cause fetal developmental malformations, mainly skin dysplasia and “methimazole-related embryopathy”, including atresia of the posterior nasal aperture and esophagus, and facial malformations. The use of PTU may cause liver damage and even acute liver failure, so it is recommended to use PTU only during T1 of pregnancy, except during T1, when MMI is preferred. monitor thyroid function for adverse drug reactions (especially blood and liver function). ATD is safe in moderation during lactation. MMI should be preferred because of the hepatotoxicity of PTU. 20 – 30 mg/d of MMI is safe for both mother and baby. 300 mg/d of PTU can be used as a second-line drug and is also safe. Dosing is done in divided doses after breastfeeding and the infant’s thyroid function is monitored.