Postpartum thyroiditis (PPT.) is a type of autoimmune thyroiditis (AIT). The prevalence of PPT is 1.1% to 21.1%, with an average prevalence of 7% in iodine-sufficient areas. Etiology and pathology PPT is a clinical form of underlying AIT under the influence of immunosuppressive mechanisms that are lifted after childbirth. The association of thyroid autoantibodies with PPT is well established. Thyroid peroxidase antibody (TPOAb) positive women will develop the disease in 40% to 60% of women, and the risk of PPT in TPOAb positive women is 20 times higher than in TPOAb negative women, so TPOAb is an important predictor of PPT in pregnant women. Excessive iodine intake is a predisposing factor for the development of PPT. According to the type of thyroid function abnormalities occurring in PPT, there are three subtypes, namely hyperthyroidism hypothyroidism biphasic, hyperthyroidism monophasic and hypothyroidism monophasic. 42.9% of PPTs are hyperthyroidism hypothyroidism biphasic, 11.4% are hypothyroidism monophasic and 45.7% are hyperthyroidism monophasic. Hyper- and hypothyroidism biphasic is the typical clinical course of PPT. The hyperthyroid phase occurs 1-6 months after delivery (usually at 3 months) and is maintained for l to 2 months. It manifests as palpitations, fatigue, fear of heat, and emotional agitation. The cause is the destruction of the thyroid tissue by inflammation. Thyroid hormones leak out, leading to thyrotoxicosis. The characteristic laboratory test is a “bidirectional separation” between serum thyroid hormone levels and thyroid iodine uptake, i.e., elevated serum T4 and T3 levels and a significant decrease in thyroid iodine uptake. Hypothyroidism occurs 3-8 months after delivery (usually around 6 months) and lasts for 4-6 months. It is characterized by muscle and joint pain and stiffness, fatigue, lack of concentration, constipation, and other symptoms. The cause is a decrease in thyroid hormone synthesis after inflammatory damage to the thyroid follicular epithelium. Laboratory tests show a gradual increase in TSH levels and a decrease in serum thyroid hormone levels. The recovery period occurs 6-12 months after delivery. Thyroid hormone levels and thyroid iodine uptake rates gradually return to normal. However, about 20% of cases can remain as persistent hypothyroidism. In a small number of cases, hypothyroidism may occur 3-10 years after recovery from PPT, and the thyroid gland may be mildly to moderately enlarged with a moderate texture but no tenderness. Ultrasonography shows hypoechoic or hypoechoic nodules. Diagnosis: Thyroid function abnormalities occur within 1 year after delivery and can take 3 forms: hyperthyroidism-hypoparathyroidism biphasic, hyperthyroidism-monophasic and hypoparathyroidism-monophasic; no history of thyroid abnormalities before delivery; exclude postpartum Graves’ disease. PPT can be diagnosed if the above conditions are met. PPT should be differentiated from the following diseases: ① Postpartum hyperthyroxinemia: This disease is caused by increased thyroid binding globulin (TBC) during pregnancy, which is manifested by increased triiodothyronine (T3) and thyroxine (T4). 4 weeks after delivery, as TBG returns to normal, T3 and T4 are normal, while FT4, FT3 and TSH are always normal. ② Differentiate from postpartum Graves’ disease recurrence. Postpartum Graves’ disease often has a history of prenatal Graves’ disease or is accompanied by characteristic manifestations of Graves’ disease, such as infiltrative proptosis, and more severe hyperthyroidism; thyroid iodine uptake rate: PPT is reduced during hyperthyroidism; postpartum Graves’ disease is increased, but patients restricted by breastfeeding cannot have their thyroid iodine uptake rate checked; TSH receptor antibody (TRAb): postpartum Graves’ disease TBAb positive, while PPT is negative. Hashimoto’s disease: The clinical manifestations of this disease are similar to those of PPT and are difficult to differentiate, relying mainly on fine needle aspiration biopsy of the thyroid gland and follow-up. hashimoto’s thyroiditis shows characteristic germinal center cells and eosinophilia. thyroid pathology in patients with PPT shows mild lymphocytic infiltration but no germinal center and no Hürthle cells. Subacute thyroiditis: Mostly caused by viral infection, with fever, neck pain, thyroid tenderness, negative anti-thyroid antibodies, and increased sedimentation. V. Treatment and prognosis Most cases of PPT show a self-limiting course. Anti-thyroid drugs are not required in the hyperthyroid phase. Symptomatic treatment such as β-adrenergic receptor blocking drugs can be given to those with severe hyperthyroidism. In hypothyroidism, serum TSH <10 mIU/L does not require thyroid hormone replacement therapy, and TSH can recover on its own. For the group with >10uIU/L, thyroid hormone replacement therapy is recommended. Women who have had PPT have a significantly increased risk of permanent hypothyroidism 5-10 years after delivery, and annual TSH monitoring is recommended, and hypothyroidism should be treated promptly if it occurs. Prevention: Iodine-containing drugs should be avoided in women with a history of this disease to avoid inducing hypothyroidism. The measurement of TPO-Ab in pregnant women before delivery is important in predicting the development of the disease, and in women with known positive TPOAb, serum thyroid hormone and TSH should be monitored 3-6 months postpartum. there is not enough evidence on the relationship between postpartum depression and PPT and thyroid antibodies; however, because hypothyroidism as a cause of postpartum depression is curable, it is advocated that it be treated in postpartum depression. Therefore, it is advocated to screen for hypothyroidism in postpartum depression in order to treat it.