ABSTRACT
The term “lupus” anticoagulant was first used by Feinstein and Rapaport in 1972,1 to describe the in vitro anticoagulant phenomenon observed mainly in patients with systemic lupus erythematosus. It has since been shown that this anticoagulant effect was due to the presence of antibodies directed against phospholipids and could not be corrected by the addition of normal plasma.2-3 This “anticoagulant” was paradoxically associated with thrombotic events. In 1984 a strong correlation was found between the lupus anticoagulant, antibodies to cardiolipin and the occurrence of these thrombotic events, which affected both the venous and arterial circulations, and the term anti-phospholipid syndrome was proposed by Harris et al. Spinal syndromes including Transverse Myelitis and the Guillain-Barre have been infrequently documented in association with anti-phospholipid antibodies. A familial clotting disorder or the presence of anti-phospholipid antibodies in family members may also be demonstrable.
