I. Overview of postpartum thyroiditis Some studies have shown that the prevalence of PPT ranges from 1.1 to 16.7%, with a mean of 8.1%. In addition, women with other immune disorders are at increased risk of PPT; women who are being treated with L-T4 for Hashimoto’s thyroiditis have an increased risk of PPT once they become pregnant if their thyroid gland has not completely atrophied. PPT develops within 1 year of delivery and lasts for 6-12 months. Typical cases go through three clinical phases, namely the thyrotoxic phase, the hypothyroid phase and the recovery phase. Atypical cases may present with only the thyrotoxic phase or the hypothyroid phase. PPT occurs in 30-50% of TPOAb-positive women in early pregnancy. Etiology: Immunologically, PPT is the result of an underlying autoimmune thyroiditis (AIT) that transforms into a clinically dominant form under the influence of an “immune rebound” mechanism after delivery. The thyroid autoantibody TPOAb is an important predictor of PPT in pregnant women for two reasons: first, 30-50% of women with positive TPOAb in early pregnancy develop PPT; second, the risk of developing PPT in TPOAb-positive women is 20 times higher than in TPOAb-negative women. In addition, excessive iodine intake is also a predisposing factor for the development of PPT. Diagnostic criteria for postpartum thyroiditis (a) The diagnosis of postpartum thyroiditis is based on the following four aspects: 1. Abnormal thyroid function (thyrotoxicosis, hypothyroidism or both) occurs within one year after delivery 2. The course of the disease shows biphasic changes of hyperthyroidism and hypothyroidism or is self-limiting 3. The thyroid gland will be mildly or moderately enlarged with moderate texture but no tenderness 4. In addition to the above diagnostic basis, there are auxiliary diagnostic indicators for postpartum thyroiditis, and the following two points should be noted: 1. The differential diagnosis of postpartum Graves’ disease is required. The differential diagnosis can be made from the following three points: 1. PPT has positive laboratory tests for TPOAb or/and TgAb, TT4 and FT4 are elevated and then decreased, and 131 iodine uptake is first decreased and then increased. 2. 2. Thyrotoxicosis in PPT is due to destruction of thyroid tissue and leakage of thyroid hormones, whereas thyrotoxicosis in Graves’ disease is due to hyperthyroidism. 3. Graves’ disease hyperthyroidism is more severe, accompanied by eye signs and TRAb positive. III. Treatment of postpartum thyroiditis The treatment of postpartum thyroiditis is divided into the treatment of the thyroid virus phase and the treatment of the hypothyroidism phase. (a) Treatment of the thyroid virus phase of postpartum thyroiditis: The symptoms of the thyroid virus phase of postpartum thyroiditis are often mild and do not require intervention, and treatment with antithyroid drugs (ATD) is not effective at this time, so ATD is not given during the thyrotoxic phase. If symptoms are more severe during the thyrotoxic phase, beta-blockers (e.g., propranolol) can reduce symptoms and can be used, but the smallest dose possible should be used, and treatment needs to be continued for several months. (ii) Treatment of postpartum thyroiditis hypothyroidism: After the thyrotoxic phase, serum TSH needs to be rechecked every 2 months for the purpose of timely detection of the hypothyroid phase. The levothyroxine (L-T4) replacement therapy can be given during the hypothyroidism phase of postpartum thyroiditis. During the treatment period, regular follow-up is required and serum TSH should be rechecked every 4-8 weeks. After 6-12 months of continuous treatment of the hypothyroidism phase, a gradual reduction of the L-T4 dose can be attempted. If the patient is breastfeeding at this time, do not reduce the L-T4 dose for now. Regular follow-up of thyroid function should be maintained for 3-5 years, and L-T4 replacement therapy should be given to patients who develop permanent hypothyroidism. The therapeutic dose of L-T4 should not be reduced for women who intend to have another pregnancy, are already pregnant or are breastfeeding. IV. Prognosis of postpartum thyroiditis More than 20% of patients with PPT develop permanent hypothyroidism. Serum TSH needs to be checked annually for 8 years after the onset of the disease for early detection and treatment of permanent hypothyroidism. The use of L-T4 to prevent the development of PPT in TPOAb-positive pregnant women is ineffective. Data from studies have shown that 10-20% of women whose nail function has returned to normal within one year after delivery develop permanent hypothyroidism, while about 50% of women develop permanent hypothyroidism between 5 and 8 years. Therefore, it can be concluded that postpartum thyroiditis can easily develop into permanent hypothyroidism and requires regular monitoring and follow-up. So, what are the risk factors for developing permanent hypothyroidism? The main ones are the degree of hypothyroidism, TPOAb titer and maternal age and history of miscarriage. For regular follow-up and screening of patients with postpartum thyroiditis, the following two things should be done: First, patients with PPT should have their TSH retested annually within 8 years after the onset of the disease to detect hypothyroidism as early as possible and treat it as early as possible Second, screening for TPOAb and TSH is currently advocated for women of childbearing age before pregnancy, and the incidence of PPT in TPOAb-positive pregnant women reaches more than 60% V. Summary Postpartum thyroiditis is the result of postpartum self Postpartum thyroiditis is one of the types of postpartum autoimmune thyroiditis; its diagnosis needs to be based on its medical history and clinical manifestations; the treatment of postpartum thyroiditis is different between the viral and hypothyroid phases; postpartum thyroiditis is prone to develop into permanent hypothyroidism, so we need to pay more attention to it and do regular follow-ups and screenings.