The development of this syndrome is associated with the formation of antibodies directed against negatively charged phospholipids and phospholipid-binding proteins, called antiphospholipid antibodies. The actual incidence of the syndrome is not known, but variations between 1 and 6% have been suggested. Females are more commonly affected (male/female ratio is 5:1), with peak incidence between 30 and 40 years of age. In some immune diseases, the syndrome is detected with a higher frequency. such are rheumatoid arthritis, lupus, Sjogren’s syndrome. In addition, the recurrence of certain infections such as hepatitis B, HIV, syphilis, Lyme disease and others is also important. It should always be kept in mind that positive antiphospholipid antibodies are found in about 2% of healthy individuals. In addition, they can become positive during various infections, as well as during treatment with some of the following medications – Procainamid, Quinidin, Propranolol, Chlorpromazin, Interferon-alfa and others. But in these cases, clinical signs of the syndrome are less often found. With increasing age, the frequency of detection of antibodies increases, and in persons over 70 years of age it reaches 12%. The presence of positive antibodies, but without characteristic clinical manifestations, does not indicate disease. This warrants further research. In the pathogenesis of antiphospholipid syndrome, special attention is paid to the mechanisms leading to platelet activation, coagulation disorders and damage to the endothelium – the inner lining of blood vessels. This mechanism is related to providing favorable conditions for the development of atherosclerosis. Vascular thromboses include both deep venous thrombosis and/or pulmonary embolism and arterial thromboses, which may present with limb ischemia, cerebrovascular accidents, transient ischemic attacks, myocardial infarction, ischemic colitis with necrosis, skin ulcers, and others . The clinical picture of the disease may include spontaneous abortions, premature birth, sudden unexplained embryonic death. Patients with antiphospholipid syndrome are at increased risk for early manifestation of severe preeclampsia, elevated liver enzymes and HELLP syndrome, which can develop as early as 15-20 weeks of gestation and progress rapidly, necessitating termination of pregnancy for medical reasons. Fetal thrombosis is rare, but fetal damage is most often due to placental insufficiency, corresponding to growth retardation, which is most often diagnosed after 20 weeks of gestation. Tests may show thrombocytopenia – a low level of platelets, as well as proteinuria (presence of protein in the urine), due to the development of microangiopathic renal thrombosis. The term “catastrophic” antiphospholipid syndrome was introduced to define a form of the syndrome characterized by multiorgan involvement and rapid evolution. It is also known as Asherson’s syndrome. It is a life-threatening condition.In a few days, patients develop multiorgan failure with pulmonary distress, renal failure with severe hypertension, cerebral, cardiac, gastrointestinal thrombosis. Diagnostic criteria are the simultaneous appearance of thrombosis in three or more organs, as well as thrombosis of small vessels. In patients with thrombosis, it is necessary to perform imaging studies in order to confirm the diagnosis. Doppler ultrasonography can help to demonstrate deep venous thrombosis, especially in the extremities. An MRI can also detect deep vein thrombosis. Chest computed tomography angiography is essential to demonstrate pulmonary embolism, ischemic stroke, or cerebral venous sinus thrombosis. Echocardiography can detect the presence of valvular vegetations and valvular dysfunctions.