[Ischemic stroke with antiphospholipid antibody].
Antiphospholipid syndrome is considered to be associated with a hypercoagulable state that leads to stroke and other ischemic events, and is currently diagnosed based on the modified Sapporo criteria that was proposed in 2006. Antiphospholipid antibodies (aPL) comprise a heterogeneous group of autoantibodies. Among them, the level of beta2-glycoprotein I-dependent anticardiolipin antibody, lupus anticoagulant (LA), and IgG anticardiolipin antibody are commonly measured. Recently, phosphatidylserine dependent anti-prothrombin antibody has been suggested to be closely related to LA. aPL is an independent risk factor for a first-ever ischemic stroke, especially in young female patients. It is still debatable whether aPL is a marker for recurrent stroke risk. The precipitating factors for the occurrence of stroke are beta2-GPI-dependent aCL, aGPL, and aCL levels of greater than 40, and the simultaneous presence of LA. Several mechanisms are considered to be involved in the thrombotic process in patients with antiphospholipid antibodies. Activation of protein C is impaired in patients with aPL. Beta2-GPI has simultaneous procoagulant and anticoagulant effects. Cardiac valvular involvement, which could be the cause of cardiogenic embolism, is prevalent in patients with aCL. In addition, the presence of aPL is associated with the development of atherosclerosis. Recently, it has been proposed that endothelial cells, monocytes, and platelets were reported to be activated by beta2-GPI: further, p38 mitogen-activated protein kinase has been reported to be phosphorylated. Several therapeutic options are available for the prevention of ischemic stroke in patients with aPL. For cases of cryptogenic ischemic stroke and positive aPL antibodies, antiplatelet therapy is reasonable. Oral anticoagulation with a target international normalized ratio (INR) of 2 to 3 is reasonable for patients with ischemic stroke who meet the criteria for antiphospholipid syndrome with venous and arterial occlusive disease in multiple organs.
Kitagawa
Yasuhisa
Y
Department of Neurology, Hachioji Hospital, Tokai University School of Medicine, 1838 Ishikawa cho, Hachioji-shi, Tokyo 192-0032, Japan.
Ohkuma
Hirohisa
H
Tokuoka
Kentaro
K
D017668:Age of Onset; D017152:Antibodies, Antiphospholipid / Q000097:blood; D000925:Anticoagulants / Q000008:administration & dosage; D016736:Antiphospholipid Syndrome / Q000150:complications* / Q000175:diagnosis; D001241:Aspirin / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D002986:Clinical Trials as Topic; D005260:Female; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D011379:Prognosis; D012307:Risk Factors; D020521:Stroke / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology* / Q000517:prevention & control; D014859:Warfarin / Q000008:administration & dosage
D017152:Antibodies, Antiphospholipid; D000925:Anticoagulants; D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D014859:Warfarin; D006493:Heparin; D001241:Aspirin