Hyperthyroidism in pregnancy includes hyperthyroidism diagnosed before pregnancy, hyperthyroidism diagnosed at the beginning of pregnancy, and hCG-associated hyperthyroidism (transient emetic hyperthyroidism). The prevalence is about 0.2%~2%. 95% of hyperthyroidism in pregnancy is caused by Graves’ disease. The pattern of clinical manifestation is that the symptoms of hyperthyroidism increase in early pregnancy and decrease in late pregnancy. First, the impact of hyperthyroidism on pregnancy and the fetus 1, the impact of hyperthyroidism in pregnancy on the mother: hyperthyroidism condition reproduction or aggravation, menstrual disorders, amenorrhea, menstrual cycle anovulatory, the chances of conception is reduced. The adverse effects of uncontrolled hyperthyroidism on pregnant women include miscarriage, preterm delivery, hypertensive syndrome of pregnancy, congestive heart failure, thyroid crisis, placental abruption and infection. 2.The effects of hyperthyroidism in pregnancy on the fetus include neonatal hyperthyroidism, intrauterine growth retardation, preterm birth, small full-term babies, low birth weight neonatal risk, stillbirths, fetal malformations, and so on. Effective control of hyperthyroidism can significantly improve the outcome of pregnancy. The relationship between hyperthyroidism in pregnancy and the incidence of congenital malformations is inconclusive. Studies have reported a high incidence of fetal malformations in untreated hyperthyroidism and a low incidence in the ATD-treated group. However, there are also reports in the literature that hyperthyroidism is not associated with fetal malformations. Second, the clinical manifestations and diagnosis of hyperthyroidism in pregnancy are very similar to hyperthyroidism in terms of hypermetabolic syndrome and physiologic goiter. Due to the increase of TBG, blood TT3 and TT4 are also increased accordingly. Hyperthyroidism should be suspected if weight does not increase with the number of months of gestation, proximal wasting of the extremities, and HR above 100 beats/minute at rest. Hyperthyroidism can be diagnosed if serum TSH decreases and FT3 or FT4 increases. If accompanied by infiltrative proptosis, diffuse goiter, tremor or vascular murmur in the thyroid region, and positive serum thyroid stimulating antibodies (TSAb), Graves’ disease can be diagnosed. Third, transient hyperthyroidism of pregnancy and severe vomiting about 40% of patients with severe vomiting of pregnancy have abnormal thyroid function tests, may appear FT4 elevation or TSH suppression, or both at the same time. Most often seen in severe severe vomiting of pregnancy, after the disappearance of severe vomiting (hCG back to normal) recovery. This is due to an increase in the thyrotropically active component of hCG leading to TSH receptors. It occurs early in pregnancy and is characterized by prolonged severe nausea and vomiting, weight loss of more than 5%, and in severe cases dehydration and ketosis. There are no positive thyroid signs. Serum TSH levels are decreased and FT4 or FT3 are increased; serum hCG levels are increased and correlate with the extent of the condition, helping to differentiate it from Graves’ disease in pregnancy. The key to treatment is correction of the metabolic disturbances caused by persistent vomiting, as well as mitigation of further vomiting. There is no indication for the use of antithyroid drugs (ATDs). Treatment and monitoring of hyperthyroidism in pregnancy: Whether to terminate the pregnancy and remove the fetus should be decided on a case-by-case basis. If the fetus is retained, the principle of treatment: ATD is preferred, a few patients need to choose surgical treatment, and radioactive iodine treatment is prohibited. (I) ATD treatment At present, there are two kinds of ATDs commonly used: propylthiouracil (PTU) and methimazole (MMI). 1, the effect of ATD on the fetus: some studies have shown that the placental passage rate of PTU is lower than that of MMI, and the amount of PTU passing through the placenta is 1/4 of that of MMI. this difference is related to the fact that MMI is more likely to be bound to plasma proteins and to be more easily ionized under the condition of physiological pH value. Studies have shown that neither PTU nor MMI application during pregnancy increases the incidence of congenital malformations in the fetus. Currently, PTU is preferred for the treatment of early hyperthyroidism in pregnancy (0-12 weeks), and MMI is used as a second-line choice; methimazole (MMI) treatment is preferred in the middle and late stages of pregnancy (13 weeks to delivery). 2, the use of ATD hyperthyroidism in pregnancy treatment goal is to use the smallest amount of ATD, in the shortest possible time to normalize thyroid function, to ensure maternal and fetal health. ATD dose should be as small as possible, the indicator is to maintain the serum FT4 in the upper limit of the normal value. The minimum dose of ATD to maintain normal thyroid function for several weeks can be discontinued. Maintenance therapy until late in pregnancy is currently advocated to avoid recurrence of hyperthyroidism. If hyperthyroidism recurs, treatment with ATD can be repeated. Those who have previously suffered from hyperthyroidism can become pregnant after discontinuing ATD if the serum TSH reaches the normal range during ATD treatment; or they can become pregnant if the dose of ATD is reduced so that the serum FT4 is at the upper limit of the normal value. Some scholars advocate that MMI should be discontinued before pregnancy and PTU should be used instead to avoid possible malformations caused by MMI. Since the dose of ATD to control hyperthyroidism needs to be increased after the combined use of levothyroxine (L-T4), the combined use of L-T4 is not recommended during pregnancy. 3, the monitoring of thyroid function during the treatment period of ATD to check the thyroid function every 2 weeks at the beginning of the treatment, and then extended to 4~6 weeks. FT4 is used as an indicator for monitoring thyroid function. Months after the serum FT4 reaches normal, the serum TSH level may still be in a suppressed state, so the TSH level cannot be used as a monitoring index at the beginning of the treatment, and the normalization of the TSH level is an indicator of the effective control of hyperthyroidism. （Surgery is rarely used. Surgery should be performed in the fourth to sixth month of pregnancy. Surgery in the third trimester of pregnancy is likely to cause miscarriage. Indications for surgical treatment: ① Significantly enlarged thyroid gland, requiring a large dose of ATD to control, PTU dose of more than 400mg / d, and some people believe that PTU dose of more than 300mg / d should be surgical treatment. ② Allergic to ATD. (iii) heavy psychological burden, excessive worry about the side effects of drugs on the fetus or can not follow the doctor’s instructions to take medication regularly. （Radioactive iodine therapy is prohibited. After 1O weeks of pregnancy, the fetal thyroid gland can concentrate 131I and cause fetal goiter and hypothyroidism. Confirmation of pregnancy is necessary before administering 131I therapy to a female patient with hyperthyroidism. If 131I treatment is chosen, pregnancy should be avoided for 6 months after treatment. (d) Other treatments 1. Beta-blockers: Use with caution. beta-blockers such as pranolol have been associated with spontaneous abortion. Pranolol may also cause intrauterine growth retardation, prolonged labor, neonatal bradycardia, hypotension, hypoglycemia and hyperbilirubinemia and other complications. 2, iodide:Iodide can cause neonatal goiter and hypothyroidism, try not to use in pregnancy, but before thyroid surgery and thyroid crisis rescue can be applied for a short period of time.