1. The most prominent manifestation of thrombosis in antiphospholipid syndrome is thrombosis, which can occur in the arteries or in the veins. The most common of these is recurrent deep vein thrombosis, including renal, retinal and inferior vena cava thrombosis, but the greater threat to patients is arterial thrombosis. Non-inflammatory obstructive vascular lesions are found to be segmental in the histopathology of ACA-positive SLE patients, and the lesions are rare but severe. There was fibrous thrombosis in the intracardiac arteries and caused myocardial infarction, and capillaries and small arteries were obstructed by fibrous material; these pathological changes were probably the result of the action of APL antibodies. ACA-positive women are prone to recurrent miscarriage in early pregnancy and intrauterine fetal death in mid- and late pregnancy, especially in those with moderate to highly elevated ACA-IgG levels. In a retrospective study of women with more than 2 miscarriages tested for ACA, Oshiro found that intrauterine fetal death in ACA-positive women was a more characteristic type of miscarriage than early pregnancy. The study by Lockshin et al. revealed that ACA predicted spontaneous miscarriage earlier and more sensitively. (1) ACA may cause a decrease in the level of PG12 in the myometrium, making the placenta prone to infarction and leading to miscarriage. (2) ACA causes placental vasculitis, resulting in fetal death due to insufficient oxygen supply and nutrition. (3) ACA acts on placental thrombosis and vasoconstriction, reducing placental blood flow, resulting in fetal distress and death. ACA can cause thrombocytopenia by binding to platelet membrane phospholipids, which can activate platelets and accelerate their aggregation, leading to thrombocytopenia. ACA binds to platelet membrane phospholipids and increases platelet phagocytosis and destruction by the mononuclear macrophage system, leading to thrombocytopenia; ACA promotes platelet activation, thus making it easy to form thrombi, while platelet consumption decreases. Other clinical manifestations: reticulocutaneous cyanosis is the most common cutaneous manifestation of APS, seen in about 80% of patients. Non-stroke neurological manifestations are often caused by small-vessel embolic disease, which can be mental disturbance or transient ischemic attack. Recent literature reports that ACA is associated with neuropsychiatric disorders, and those with positive ACA in CNS lesions may present with epilepsy, migraine, transient cerebral ischemia and transient blackouts, psychiatric abnormalities, hemiparesis, cerebral infarction, stroke, etc. Some non-embolic neurological diseases such as chorea and Guillain-Barré syndrome are also associated with ACA.