[Diagnosis and potential treatment of antiphospholipid syndrome-related mainly on ischemic stroke]

Antiphospholipid syndrome (APS) was defined in 2006 by an international consensus as an autoimmune disease that manifests clinically as recurrent thrombotic complications or fetal loss and serologically as elevated plasma levels of antiphospholipid antibodies (aPLs). aPLs are a heterogeneous group of antibodies directed against anionic phospholipids, phospholipid-binding plasma proteins, and phospholipid-protein complexes. Standard ELISA for anticardiolipin (aCL) and anti-β2-glycoprotein I antibodies and clotting assays for lupus anticoagulant (LA) are recommended for detecting aPLs. Phosphatidylserine-dependent anti-prothrombin antibody (aPS/PT) assay may also be useful as a confirmatory test for APS. aPLs are an independent risk factor for initial occurence of ischemic stroke, especially in young adults. APS patients with thrombotic stroke frequently have other, often conventional, vascular risk factors. Guidelines issued in 2011 by the American Heart Association and American Stroke Association recommended antiplatelet therapy for patients with cryptogenic ischemic stroke or TIA and who test positive for aPL. In contrast, oral anticoagulants with a target international normalized ratio (INR) of 2.0-3.0 are recommended for patients with ischemic stroke who meet all the criteria for APS. Recently, 3 new anticoagulants for stroke prevention, dabigatran, rivaroxaban, and apixaban, have been studied in phase 3 clinical trials in patients with atrial fibrillation. However, optimal treatment for catastrophic APS is unknown. Current treatment guidelines emphasize the importance of early diagnosis and recommend aggressive therapies to avoid a fatal outcome. Combinations of high doses of intravenous heparin, steroids, and immunoglobulins and/or repeated plasma exchanges can be considered as treatments of choice for this severe condition.