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Thrombolysis in antiphospholipid syndrome: current hematologic perspectives

René Y McNall-Knapp1

  • 1University of Oklahoma Health Sciences Center, Jimmy Everest Section of Pediatric Hematology/Oncology, University of Oklahoma Children's Physicians Building, Oklahoma City, OK 73104, USA. rene-mcnall@ouhsc.edu

Current Rheumatology Reports
|May 7, 2008
PubMed

Antiphospholipid antibodies (aPL) can cause thromboembolic events, but the reason for the thrombogenesis has not been fully elucidated. Studies show that the true pathogenic targets of aPL are plasma proteins involved in hemostasis (eg, beta(2)-glycoprotein I and prothrombin). These plasma proteins in turn bind to phospholipids, leading to the misclassification as "antiphospholipid" antibodies. The hemostatic system has abundant checks and balances to avoid excess hemorrhage and thrombosis. Thus, thrombosis requires more than interrupting one protein in the complex system. This review examines host genetic factors important in predisposition to thrombosis associated with aPL and concentrates on how antibodies in antiphospholipid syndrome interact with our natural anticoagulants and lead to thrombosis.

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