Ten years ago we described a group of patients with a combination of c
linical features associated with the presence of antiphospholipid anti
bodies. These features included a tendency to both arterial and venous
thrombosis, livedo reticularis, recurrent abortions and occasional th
rombocytopenia. This striking clinical constellation was originally na
med the anticardiolipin syndrome and is now more appropriately called
the antiphospholipid syndrome (APS). Although our early studies were c
entred on systemic lupus erythematosus in which up to a third of patie
nts demonstrated features of the syndrome, it was clear even a decade
ago that the APS would increasingly become the domain of neurologists
and cardiovascular physicians. The consensus is that antiphospholipid
antibodies have a pathogenetic role in the vasculopathy of the APS, bu
t the mechanisms are still unknown. The establishment of good animal m
odels for the APS is the best opportunity to develop rational and more
targeted therapies. In our experience, treatments directed against th
e secondary thrombotic event have proved more successful than those di
rected against the underlying immunological abnormality.