Anti-phosphate syndrome (antiphospholipid syndrome, APS) is a systematic autoimmune disease, which is explained in detail below:
The main clinical characteristics of anti-phosphate syndrome are the formation of an artery, angiogenesis, and/or pathological pregnancy (e.g. early pregnancy and mid-term foetal death), reduction of slabs, and the persistence of moderately or highly positive antiphosphate antibodies. The disease is usually divided into primary APS and secondary APS, which are repeated in the form of systematic erythalamus, dry syndrome, etc.
1. Blood clot formation: APS patients may have repeated artery or intravenous blood clots, which may occur in any part of the body, including deep veins, pulmonary vessels, lower cavity veins, kidneys and liver veins. Blood embolism incidents can spread and are not related to antibody levels. Pathological pregnancy: APS patients may also have pathological pregnancies, such as early pregnancy, mid-term and late-mortality. These complications in pregnancy may be related to the formation of a clot or to the direct effects of anti-phosphate antibodies on placenta function. 3. Declining slabs: Reductions in slabs can occur in some patients, which may be related to the damage to slabs by antiphosphate antibodies. 4. Other manifestations: APS patients may also have non-specific clinical manifestations, such as mesh blue spots, lower limb ulcer, autoimmune soluble blood, heart valve disease, etc.
The causes of APS are not yet fully explained, but research has shown that anti-phosphate antibodies (aPLs) play a key role in APS morbidity. These antibodies are a group of self-activated antibodies that target phosphorus and/or phosphate in combination with proteins, and can cause clinical manifestations such as sembling formation and pathological pregnancy through various mechanisms.
Diagnosis and diagnostics The diagnosis of APS is based on clinical performance, laboratory examinations and visual examinations. Patients suspected of APS should be tested for anti-phosphate antibodies, including anti-cardophosphate antibodies, anti-beta 2-sugar protein-I antibodies, etc. At the same time, a combination of patient history, clinical performance and video screening is required. The diagnosis needs to be identified with other autoimmune diseases, diseases of the blood system and infectious diseases.
The treatment of APS includes, among others, anticondensation treatment, anti-sphygmoplat therapy and immunization treatment. Anticondensation treatment is an important measure for APS patients to prevent haematosis, and commonly used anticondensants include low molecular heparin, Wafalin, etc. Anti-sculpture treatment is used mainly to prevent slab accumulation and leopard formation, and commonly used drugs include aspirin. Immunization treatment is used primarily to regulate the immune function of patients, reduce the generation of anti-phosphate antibodies and reduce their pathological effects. In terms of prognosis, the prognosis of APS patients varies according to individual differences, but in general, early diagnosis, active treatment and regular monitoring help to improve the prognosis of patients.
In summary, anti-phosphate syndrome is a complex self-immunological disease with diverse clinical performance and prone to recurrence. Patients suspected of APS should be diagnosed and treated as early as possible in order to reduce the occurrence of complications and improve the quality of life of patients.
