An insight into the pathophysiology of thrombosis in antiphospholipid syndrome.
The antiphospholipid syndrome (APS) is a disorder which is characterized by the presence of autoimmune antiphospholipid antibodies (APL) and increased risk of thrombosis and fetal loss. APL are associated with recurrent abortions in APS patients and participate in the pathogenesis of venous or arterial thrombosis, although the underlying mechanisms are poorly understood. Antigens that are targeted by APL include beta 2 glycoprotein I and prothrombin. Pathological mechanisms of APL encompass inhibition of natural anticoagulants (protein C system, tissue factor pathway inhibitor, and annexin A5), inhibition of the fibrinolytic system, activation of endothelial cells, monocytes and platelets, and complement activation. In this review, we discuss the main targets of APL and prothrombogenic mechanisms of APL.
Palomo
Ivan G
IG
Department of Clinical Biochemistry and Immunohematology, Cardiovascular Risk Factor Disease Research Program, Faculty of Health Sciences, Universidad de Talca, Chile. ipalomo@utalca.cl
Segovia
Fabian M
FM
Alarcon
Marcelo L
ML
Fuentes
Barbara Y
BY
Pereira
Jaime G
JG
Rojas
Armando
A
Forastiero
Ricardo
R
D000925:Anticoagulants / Q000627:therapeutic use; D000937:Antigen-Antibody Reactions; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000276:immunology / Q000503:physiopathology*; D001324:Autoantigens / Q000276:immunology; D006801:Humans; D013927:Thrombosis / Q000150:complications / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*
D000925:Anticoagulants; D001324:Autoantigens