At present, many patients with recurrent fetal arrest come to the Department of Rheumatology and Immunology to check the relevant items in the hope of finding the cause of fetal arrest, so what items should be checked? 1, antiphospholipid syndrome and thrombosis items: antiphospholipid antibodies (including IgM, IgA and IgG anti-cardiolipin antibodies and anti-β2 glycoprotein I antibodies and lupus anticoagulant), easy embolism combination (containing lupus anticoagulant and protein S and protein C, etc.), antithrombin III, coagulation III (containing D-dimer and fibrinogen, etc.), platelet aggregation rate. Antiphospholipid antibodies are a group of specific autoantibodies produced against phospholipid components of self-glycerol. In the physiological state, negatively charged phospholipids are not exposed to the exterior of the cell membrane, while in the pathological state, negatively charged phospholipids are distributed to the exterior surface of the cell, and binding to the phospholipids of the endothelial cell membrane can change the stability of the cell membrane; binding to platelets can increase the adhesion and aggregation ability of platelets, thus promoting thrombosis, and with the aggravation of placental vascular thrombosis, causing placental infarction and leading to miscarriage. 2, thyroid function project: many women have hypothyroidism or hyperthyroidism, which can also lead to recurrent miscarriage due to abnormal thyroid function. 3.Blood group and blood group antibodies check: the couple’s blood group does not match, especially O blood group mothers are prone to recurrent spontaneous abortion (because O mothers can produce IgG antibodies to AB antigens and can pass the placental barrier). The abnormally high blood group antibodies act on the trophoblast cells or enter the fetus through the placenta, resulting in damage to the fetal-placental unit and miscarriage. 4, HLA genetic examination: large HLA similarity between husband and wife (large common antigen similarity) may be one of the causes of recurrent spontaneous abortion. Under normal circumstances, the HLA antigen of the father can stimulate the mother to produce the corresponding HLA antibodies to protect the fetus from the maternal immune system. If the HLA compatibility between the couple is too high and the maternal immune recognition of the paternal antigen of the embryo is incomplete, the mother cannot be effectively stimulated to produce protective antibodies and the fetus is exposed to the surveillance of the maternal immune system, causing the mother to have a rejection reaction, leading to miscarriage and The fetus is exposed to the surveillance of the maternal immune system, resulting in rejection by the mother, leading to miscarriage and stillbirth. The frequency of HLA CDR, HLA-A and HLA-B in couples with recurrent spontaneous abortions is significantly higher than that in couples with normal births. 5, closed antibody: the lack of closed antibody is also one of the important causes of recurrent spontaneous abortion. The fetal placental unit is not rejected by the mother and relies on maternal production of confinement antibodies and other immunosuppressive substances, thus preventing harmful maternal reactions. Containment antibodies are produced mainly against embryonic HLA-II antigens and lymphocyte cross-reacting antigens, and help to maintain pregnancy by binding to fetal placental trophoblast antigens or maternal lymphocytes to prevent embryonic paternal antigens from being recognized and killed by the maternal immune system and to prevent immune attack on the embryonic trophoblast. Currently, there are a number of antibody types detected, including: (1) anti-warm B-cell antibodies (anti-HLA-DR antibodies); (2) anti-lymphocyte cross-reactive antigen antibodies; (3) anti-FC (i.e. antibody FC segment) receptor antibodies; (4) microlymphotoxic antibodies; (5) anti-cold B-cell antibodies (non-HLA cold B-cell antibodies); and (6) anti-father complement-dependent antibodies. Anti-HLA- DR antibodies and anti-lymphocyte cross-reacting antigen antibodies can bind to local trophoblast-related antigens at the maternal-fetal interface, blocking fetal antigens and preventing the attack of maternal immune cells; anti-FC receptor antibodies can prevent certain IgG antibodies that are harmful to the fetus from passing through the placental barrier, thus protecting the fetus. In addition, the mother also produces anti-closing antibody unique type of antibody, which can not only localize in the mother-fetal immune interface, but also in the circulation with harmful immune active cells (such as killer T cells, natural killer cells, etc.) and related factors such as IL-2, blocking the harmful immune response, and forming an important immune protection network with the closing antibody. 6. Anti-reproductive immune antibodies include anti-sperm antibodies, anti-endometrial antibodies, anti-ovarian antibodies, anti-chorionic gonadotropin antibodies, anti-nuclear antibody profile (including ANA, ENA and ds-DNA, etc.) and anti-hyaluronic antibodies. Anti-sperm antibodies not only interfere with sperm metabolism and energy acquisition, but also affect fertilization, fertilized egg implantation and embryonic development, eventually leading to miscarriage. The serum and cervical mucus of normal fertile women do not contain anti-sperm antibodies, while the seropositivity rate of women with recurrent spontaneous abortions is 36.4%. The endometrium of women of childbearing age is regulated by ovarian hormones and exfoliates periodically, and the exfoliated endometrium flows out of the body with menstrual blood, which generally does not induce autoimmune reactions. Due to endometrial injury and inflammation, the endometrial tissues stimulate the body to produce anti-endometrial antibodies as self-antigens, which can bind with the target antigens in the endometrium and activate the complement reaction, destroying the structure of the endometrium, causing endometrial dysplasia and reducing the acceptability of the pregnant egg, which is not conducive to the implantation of the pregnant egg, leading to infertility and miscarriage. 7. T and B lymphocyte subsets and natural killer (NK) cells, immunoglobulins and complement, interleukin 2, interferon γ and tumor necrosis factor: imbalance of Th1 /Th2 type cytokines is associated with recurrent spontaneous abortion. CD4+ helper T cells can be divided into subsets with two different functions according to the cytokines they secrete, namely Th1 (T helper 1) and Th1 cells mainly secrete interleukin 2, interferon gamma and tumor necrosis factor; Th2 cells mainly produce interleukins 4, 5, 6 and 10. Th2 cytokines mainly promote B-cell proliferation and antibody production, mediate humoral immunity, and are involved in mediating immune tolerance formation. Pregnancy is a physiological phenomenon dominated by Th2 cytokines, and in women with recurrent spontaneous abortions, the meconium immune cells produce excessive amounts of embryotoxic cytokines and the Th1/Th2 balance is biased toward Th1, while Th2 is suppressed. 8. Hysteroscopy to assess the morphology and environment of the uterine cavity for adhesions, polyps, mediastinum, and inflammatory lesions. 9.Karyotype examination of both spouses. If available, fetal chorionic villi are retained for chromosomal examination at the time of abortion.