β-2-glycoprotein, IgM utoantibodies
Why this test?
Diagnosis of antiphospholipid syndrome.
To assess thrombotic risk in patients with systemic lupus erythematosus.
In what cases is it prescribed?
In case of various miscarriage, especially at the 10th week or more, when the death of the fetus due to genetic reasons is unlikely.
In the presence of venous or arterial thrombosis, especially at a young age, in particular heart attacks, strokes, transient disorders of cerebral blood circulation, pulmonary embolism, thrombosis of retinal vessels.
With the clinical prerequisites of the presence of APS and a negative analysis for antibodies to cardiolipin and lupus anticoagulant.
Antibodies to beta-2-glycoprotein (IgM) are one of the markers in the diagnosis of antiphospholipid syndrome (APS). Antiphospholipid syndrome (APS), or antiphospholipid antibody syndrome (APS, or SAFA), is an autoimmune condition of hypercoagulation accompanied by the appearance of antibodies to phospholipids. APS provokes the formation of blood clots (thrombosis) in both arteries and veins, as well as pregnancy-related complications such as miscarriage, stillbirth, premature birth and severe preeclampsia.
Diagnostic criteria for the diagnosis of APS require the presence of a single clinical feature, such as thrombosis or pregnancy complications, and two blood tests for antibodies, separated by three months from each other, that confirm the presence of either anti-beta-2-glycoprotein or red blood cell anticoagulant lupus Antiphospholipid syndrome can be primary or secondary.
The exact causes of the formation of such autoantibodies have not yet been determined. Primary antiphospholipid syndrome occurs in the absence of any other related diseases, is characterized by the development of venous and arterial thrombosis (or both at the same time), some types of pathology in obstetric practice, thrombocytopenia, the development of various cardiovascular, hematological, skin and neurological disorders.
A characteristic feature of APS is recurrence of thrombosis. Secondary antiphospholipid syndrome occurs together with other autoimmune diseases, such as rheumatological diseases, scleroderma, systemic lupus erythematosus (SLE), rheumatoid arthritis, dermatomyositis, etc. In some cases, APS leads to rapid multiple organ failure due to generalized thrombosis, this phenomenon is called catastrophic antiphospholipid syndrome (or Asherson's syndrome) and is associated with a high risk of death. Antiphospholipid syndrome occurs in approximately 5% of pregnant women and in some cases is the main cause of miscarriage.
APS can develop in other autoimmune rheumatic and non-rheumatic diseases, malignant neoplasms, against the background of infections and taking a number of medicines. It is an autoimmune disease in which antiphospholipid antibodies (anticardiolipin antibodies and lupus coagulant) interact with proteins that bind to anionic phospholipids on plasma membranes. Like many other autoimmune diseases, this syndrome is more common in women than in men.
Beta-2-glycoprotein is a cofactor necessary for the interaction of antiphospholipid antibodies with phospholipids. It is synthesized in the liver. It is a blood plasma protein that binds to negatively charged phospholipids, in particular cardiolipin. It is also an inhibitor of the internal coagulation pathway. Beta-2-glycoprotein inhibits the formation of prothrombinase (factor Xa) in the presence of platelets, and also inhibits the activation of factor XII. Has anticoagulant activity.
Therefore, the detection of antibodies to cardiolipin in blood serum simultaneously with IgM antibodies to beta-2-glycoprotein increases the specificity of the diagnosis of APS, and in patients with SLE it correlates with the development of APS as a whole and its main clinical manifestations separately - venous and arterial thrombosis, obstetric pathology and thrombocytopenia . Antibodies to β-2-glycoproteins belong to the class of antiphospholipid antibodies and were included in the laboratory classification criteria for the diagnosis of antiphospholipid syndrome in 2006 (Miyakis et al., 2006).