[Some considerations about the possible pathological mechanisms at work in antiphospholipid syndrome and stroke]

Over the last two decades antiphospholipid syndrome (APS) has started to be recognized from the association of apparently anionic phospholipid-specific antibodies with thrombosis, thrombocytopenia and recurrent foetal losses. This syndrome affects patients with systemic lupus erythematosus and is considered to be an important cause of thromboembolic disease. Antiphospholipid antibodies are serum immunoglobulins that react with negatively charged phospholipids, albeit directly or by means of a cofactor, affect the coagulation system, and promote thrombosis. Recent research has been directed towards gaining an understanding of the mechanisms by which these antibodies are able to play a direct role in the pathophysiology of thrombosis, and the extent to which certain risk factors, such as smoking, high blood pressure, lipid disorders and so on, exert an influence over the expression of phospholipids in the cerebral endothelium.

These antibodies have no single mechanism of action; different authors have described different pathological mechanisms, which help us to understand the heterogeneous clinical manifestations of APS.