The prethrombotic state (PTS) is a pathological process in which multiple factors cause dysfunction or impairment of the hemostatic, coagulation, anticoagulation, and fibrinolytic systems. Numerous studies have shown that thrombosis occurs as a result of a combination of alterations in vascular endothelial cells, platelets, coagulation, anticoagulation, fibrinolytic systems, and blood rheology, which have been altered to varying degrees prior to thrombosis. PTS includes both congenital and acquired, the former being due to mutations in genes related to coagulation and fibrinolysis, and the latter mainly due to antiphospholipid antibody syndrome (APS), acquired homocysteinemia, and the presence of various diseases in the body that cause a hypercoagulable state of the blood. Antiphospholipid antibody syndrome (APS) is a general term for a group of clinical signs caused by antiphospholipid antibodies (APL antibodies), a group of antibodies that can react immunologically with a variety of antigenic substances containing phospholipid structures, mainly lupus anticoagulant (LA), anti-cardiolipin antibody (ACA), anti-phosphatidic acid antibody and anti-phosphatidylserine antibody. The clinical manifestations associated with APL antibodies are mainly thrombosis, habitual abortion, thrombocytopenia and neuropsychiatric symptoms. APL is a group of specific autoantibodies against phospholipid negatively charged protein complexes in the body. Some plasma proteins in the body such as β2-glycoprotein (β2-GPI) have the antigenic determinant cluster of ACA on their molecules, and ACA can recognize negatively charged phospholipid complexes after binding to β2-GPI, and cause changes in the surface structure of β2-GPI and the appearance of epitopes recognized by ACA. GPI has the ability to inhibit platelet aggregation caused by thrombinogen, adenosine diphosphate (ADP), and thrombin generation on its surface, and block phospholipid-dependent coagulation reactions, which predispose to thrombus formation when ACA reacts with it. Pre-thrombotic state tests for recurrent miscarriage: thyroid function, blood rheology, anti-nuclear antibody, anti-double-stranded DNA, sedimentation, anti-cardiolipin antibody, anti-β2 glycoprotein 1 antibody, D-dimer, platelet agglutination rate, platelet aggregation test (PAGT), partial thromboplastin time, plasma α-granule membrane protein. What is the relationship between prethrombotic state and miscarriage? The prethrombotic state is closely associated with recurrent miscarriage. It is widely believed that the hypercoagulable state of blood may lead to altered blood flow in the placental area of the uterus, which may predispose the local tissues to microthrombosis, formation of placental fibrous deposits and placental infarct foci, thus causing placental ischemia and hypoxia, and eventually leading to embryonic dysplasia or miscarriage. How can anti-cardiolipin antibodies cause miscarriage? (1) Acting on endothelial phospholipids to inhibit the release of arachidonic acid and prostaglandin production, promoting platelet aggregation in vasoconstrictors; (2) Binding to platelet phospholipids to induce platelet activation, aggregation, destruction and release of thrombocyclin, leading to intravascular thrombosis; (3) Interfering with the activation of thrombomodulin tissue protein C and also inhibiting the activation of fibrinogen and protein activation; (4) inhibits the anticoagulant activity of β2-GPI by binding to β2-GPI. The main pathological changes are endothelial damage, platelet aggregation, hypercoagulable state and finally lead to intravascular thrombosis.