Recognized for its associated thrombosis in the 1950s, antiphospholipid syndrome (APS) and lupus anticoagulant (LAC) are associated with pregnancy complications that include fetal loss, fetal growth restriction,preeclampsia, thrombosis, and autoimmune thrombocytopenia. It is characterized by an autoimmune process that is separate in many women from systemic lupus erythematosus (SLE) and other connective tissue diseases. Diagnosis requires clinical and laboratory findings with the clinical criteria being the primary method of diagnosis. Women with the clinical features should be tested for LAC and anticardiolipin (aCL) antibodies; most patients with APS have both LAC and aCL immunoglobulin G (IgG) antibodies.
APS is classified as primary or secondary depending on its association with other autoimmune disorders. Primary antiphospholipid syndrome is diagnosed in patients demonstrating the clinical and laboratory criteria without other recognized autoimmune disease. Secondaryantiphospholipid syndrome is diagnosed in patients with other autoimmune disorders such as SLE.
Antiphospholipid (aPL) antibodies belong to the large family of antibodies that react with negatively charged phospholipids (PLs) including cardiolipin, phosphatidylglycerol, phosphatidylinositol, phosphatidylserine, phosphatidylcholine, and phosphatidic acid.
LAC and aCL predispose to clotting in vivo, predominantly by interfering with the antithrombotic role of PLs; thus, it is associated with clinical thrombosis, not bleeding. The aPL autoantibodies bind moieties on negatively charged PLs or moieties formed by the interaction of negatively charged PLs with other lipids, PLs, or proteins.