[Neurological aspects in antiphospholipid syndrome].
Antiphospholipid syndrome is considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack. Antiphospholipid antibodies (aPL) comprise a heterogeneous group of autoantibodies. Among them, lupus anticoagulant (LA) and beta 2-glycoprotein I dependent anticardiolipin antibody (beta 2-GPI aCL) are important and commonly measured. Recently, LA has been considered to be closely related to phosphatidylserine anti-prothrombin antibody. APL is an independent risk factor for first-ever ischemic stroke and a prognostic marker of recurrent stroke. The precipitating factors for the occurrence of stroke are the presence of beta 2-GPI-dependent aCL, a GPL aCL level of more than 40, and the simultaneous presence of lupus anticoagulant. Several mechanisms are believed to be involved in the thrombotic process in patients with antiphospholipid antibodies. Human activated protein C functions as a potent anticoagulant in human plasma by inhibiting the activity of coagulation cofactors Va and VIIIa. Activation of protein C is impaired in patients with aPL. Recently, the presence of aPL has been considered to be contributory factor for the development of atherosclerotic lesions. Transgenic mouse lacking the LDL receptor develop accelerated arteriosclerosis upon immunization with beta 2-GPL Several therapeutic options are available for the prevention of ischemic stroke in patients with aPL, such as antiplatelet, anticoagulant, and immunosuppressive therapy. The rate of recurrence in patients undergoing antiplatelet and anticoagulation combination therapy was found to be lower than that in patients receiving other forms of therapy. The WARSS-APASS collaborative study showed that there was no difference in the recurrence rate between aPL patients receiving antiplatelet or anticoagulation therapy alone. APL has been investigated in other neurological disorders such as multiple sclerosis, chorea, migraine and convulsion. The association of aPL with multiple sclerosis remains debatable. APL could be a contributory factor for the development of convulsion, but not for migraine.
Kitagawa
Yasuhisa
Y
Department of Neurology, Tokai University, Oiso Hospital.
D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000097:blood; D000925:Anticoagulants / Q000627:therapeutic use; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000188:drug therapy; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000517:prevention & control; D051379:Mice; D008875:Middle Aged; D009103:Multiple Sclerosis / Q000209:etiology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011486:Protein C / Q000502:physiology; D012307:Risk Factors; D055502:Secondary Prevention; D012640:Seizures / Q000209:etiology; D020521:Stroke / Q000209:etiology / Q000517:prevention & control; D019851:Thrombophilia / Q000209:etiology / Q000517:prevention & control
D017152:Antibodies, Antiphospholipid; D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D011486:Protein C