In recent years, clinical syndromes involving lupus anticoagulants and anti
phospholipid antibodies have come into increasing clinical prominence. Sinc
e the discovery that most antiphospholipid antibodies require the presence
of anionic phospholipid-binding proteins such as B2-glycoprotein I and prot
hrombin, a large number of studies have attempted to delineate the specific
ity of these antibodies. Several mechanisms have been proposed to explain t
he hypercoagulable state associated with these antibodies. This review atte
mpts to summarize these data and the challenges that confront efforts to de
lineate the pathogenesis of the prothrombotic state associated with the pre
sence of these antibodies.