Espinosa Gerard, Cervera Ricard, Font Josep, Shoenfeld Yehuda
Department of Autoimmune Diseases, Institut Clínic d'Infeccions i Immunologia, Hospital Clínic, Villarroel 170, 08036 Barcelona, Catalonia, Spain.
Autoimmun Rev. 2003 Mar;2(2):86-93. doi: 10.1016/s1568-9972(02)00144-1.
Despite the strong association between antiphospholipid antibodies (aPL) and thrombosis, the pathogenic role of aPL in the development of thrombosis has not been fully elucidated. Proposed pathophysiological mechanisms may be categorized into two types. First, aPL may act in vivo by disrupting the kinetics of the normal procoagulant and anticoagulant reactions occurring on cell membranes. Second, aPL may stimulate certain cells thereby altering the expression and secretion of various molecules. In this article, we review the mechanisms by which aPL may develop thrombotic events.
尽管抗磷脂抗体（aPL）与血栓形成之间存在密切关联，但aPL在血栓形成过程中的致病作用尚未完全阐明。提出的病理生理机制可分为两类。第一，aPL可能通过破坏细胞膜上正常促凝和抗凝反应的动力学在体内发挥作用。第二，aPL可能刺激某些细胞，从而改变各种分子的表达和分泌。在本文中，我们综述了aPL可能引发血栓事件的机制。
