ABSTRACT
The presence of antibodies to phospholipid (aPL) is associated with several distinct features, including venous and arterial thrombosis. aPL are identified clinically in two different ways, either as immunoglobulins reacting with anionic phospholipids, usually cardiolipin, or as lupus anticoagulants. The former antibodies are detected in solid-phase enzyme-linked immunosorbent assays, the latter by their ability to prolong phospholipid-dependent coagulation tests. Studies have either looked at fibrinolysis in patients or used patient sera or purified immunoglobulins in in vitro experiments. In addition to tissue plasminogen activator and urokinase-type plasminogen activator, a third route to plasminogen activation is via the contact system. It is apparently mediated by kallikrein, generated from prekallikrein by factor Xlla in the presence of high-molecular-weight kininogen. Laboratory studies gave evidence of inhibitory activity directed against prekallikrein, though using assays of prekallikrein based on the activated partial thromboplastin time with difficulties of interpretation in the presence of lupus anticoagulant.
