Postpartum thyroiditis is a type of autoimmune thyroiditis (AIT). PPT has a prevalence of 1.1%-21.1%, with an average prevalence of about 7% in iodine-sufficient areas. Etiology and pathology: PPT is the transformation of underlying AIT into its clinical form under the influence of the lifting of immunosuppressive mechanisms after delivery. The association of thyroid autoantibodies with PPT is well established. Thyroid peroxidase antibody (TPOAb) positive women will develop the disease in 40-60% of cases. 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, it can be divided into 3 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. The hyper- and hypo-hyperthyroid biphasic type is the typical clinical course of PPT. The hyperthyroid phase occurs 1-6 months (usually at 3 months) after delivery and is maintained for l-2 months. It manifests as palpitations, fatigue, fear of heat, and emotional agitation. It arises when thyroid tissue is destroyed by inflammation and 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., increased 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: Abnormal thyroid function occurs within 1 year after delivery and can manifest in 3 forms: hyperthyroidism-hypoparathyroidism biphasic, hyperthyroidism-monophasic and hypoparathyroidism-monophasic; no prenatal history of abnormal thyroid function; exclusion of postpartum Graves’ disease. PPT can be diagnosed if the above conditions are met. PPT should be differentiated from the following diseases: 1. Posthyperthyroidism: This disease is caused by an increase in thyroid binding globulin (TBC) during pregnancy, manifested by an increase in 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, postpartum Graves’ disease recurrence identification. Postpartum Graves’ disease often has a history of prenatal Graves’ disease or is accompanied by characteristic manifestations of Graves’ disease, such as infiltrative proptosis, with heavy hyperthyroidism; thyroid iodine uptake rate: PPT is reduced during hyperthyroidism; postpartum Graves’ disease is increased, but patients restricted by breastfeeding cannot do thyroid iodine uptake rate examination; TSH receptor antibody (TRAb): postpartum Graves’ disease TBAb positive, while PPT is negative. 3. Ben’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. 4. Acute thyroiditis: Mostly caused by viral infection, with fever, neck pain, thyroid tenderness, negative anti-thyroid antibodies, and increased blood sedimentation. 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 monitoring of TSH is recommended; once hypothyroidism occurs, it should be treated promptly. Iodine-containing medications should be avoided in women with a history of this disease to avoid inducing hypothyroidism. Prenatal measurement of TPO-Ab in pregnant women is important in predicting the development of the disease, and serum thyroid hormone and TSH should be monitored 3-6 months after delivery in women known to be positive for TPOAb. There is insufficient evidence on the association of postpartum depression with PPT and thyroid antibodies; however, because hypothyroidism is curable as a cause of postpartum depression, it is advocated to screening for hypothyroidism for treatment.