1. Do all prenatal tests need to be performed? If there is no hyperthyroidism before pregnancy, but high T3 and T4 are found after pregnancy, does it mean that the pregnant woman has hyperthyroidism? Does this need to be treated? According to domestic and international data, the prevalence of combined hyperthyroidism in pregnancy is 0.02-0.2%, combined with clinical hypothyroidism is 0.6%, combined with subclinical hypothyroidism is 5.27%, combined with low T4 blood is 2.15%. Therefore, the number of patients with thyroid abnormalities in pregnancy is still very high, but it is still controversial whether all patients need to have their thyroid function checked before pregnancy. It is generally accepted that pregnant women with risk factors should be tested for thyroid function: personal history of thyroid disease; family history of thyroid disease; goiter; positive thyroid antibodies with signs and symptoms suggestive of hyper- or hypothyroidism; type 1 diabetes mellitus; other autoimmune diseases; infertility; history of miscarriage and preterm delivery; and history of head and neck radiation therapy, among ten other conditions. This is because certain physiological changes in the metabolism of thyroid hormones occur during pregnancy, such as increased levels of estrogen and progesterone stimulating the liver to synthesize thyroid binding globulin (TBG), and increased glycosylation of TBG slowing down its metabolic clearance, resulting in serum TBG levels up to 2-3 times higher than during non-pregnancy. The increase in TBG leads to an increase in serum total thyroid hormone (T3, T4) levels, but free thyroid hormone (FT3, FT4) levels are normal. This condition cannot be diagnosed as hyperthyroidism and certainly does not require treatment. 2. Is there a case that hyperthyroidism does not exist before pregnancy but occurs during pregnancy and continues? If hyperthyroidism does not exist before pregnancy but occurs during pregnancy, there are two cases: The first case is that the placenta produces a large amount of chorionic gonadotropin (hCG) in early pregnancy, which has the activity of thyroid stimulating hormone (TSH) and stimulates the thyroid gland, causing the serum thyroid hormone to rise and TSH to be suppressed, resulting in hyperthyroidism in pregnant women. This is called transient hyperemesis gravidarum (THHG), which is mild, often accompanied by severe pregnancy vomiting, and resolves spontaneously in mid- to late pregnancy. The second type of hyperthyroidism occurs during pregnancy and is characterized by the same features as general hyperthyroidism, which is more severe and does not resolve easily. However, the latter condition is relatively rare, and the autoimmune disease usually reduces or remits due to the presence of immune tolerance during pregnancy. 3. What is the difference between transient hyperthyroidism in pregnancy and true hyperthyroidism? Transient hyperthyroidism in pregnancy occurs in the early stages of pregnancy and naturally resolves in the middle and late stages of pregnancy. The thyroid autoantibodies are often elevated, long-lasting and not easily relieved, and often require treatment. 4. What are the effects of hyperthyroidism on the mother and fetus? The incidence of preeclampsia, eclampsia, congestive heart failure and hyperthyroidism crisis increases significantly in late pregnancy. The incidence of stillbirth, preterm delivery, placental abruption and infection is much higher than in early to mid pregnancy when hyperthyroidism is well controlled. The main effects on the fetus are intrauterine growth retardation, prematurity, small full-term babies, congenital malformations, stillbirth and premature closure of cranial suture. The incidence of fetal malformation in untreated patients with hyperthyroidism is 6%, while the incidence of fetal malformation in treated patients is 1.7%, and the incidence of fetal malformation in normal pregnancies is only 0.2%. 5. Some patients start to show hyperthyroidism during pregnancy, but later the hyperthyroidism is relieved and then recurs after delivery. Hyperthyroidism in pregnancy is characterized by an increase in hyperthyroidism in early pregnancy, a remission in the middle and late pregnancy, and a recurrence of hyperthyroidism after delivery. The beginning of hyperthyroidism in pregnancy may be related to the increase of serum hCG concentration in early pregnancy, because hCG has TSH-like effect. In the middle and late pregnancy, with the emergence of immune tolerance, decrease of TSAb titer, increase of serum TBG and decrease of iodine available in maternal thyroid, hyperthyroidism will be reduced or improved, or even become hypothyroidism. In the postpartum period, most of the remitted hyperthyroidism will recur as the immune tolerance is lifted.