No abstract

The antiphospholipid antibody syndrome (APS) is characterized by thrombocytopenia, recurrent thromboembolic phenomena and recurrent fetal loss, in association with anticardiolipin antibodies (aCL) and/or lupus anticoagulant (LA). Owing to the ethical and practical restrictions of experimentation on humans, we have to look to animal experimentation to broaden our knowledge of the pathogenesis and management of APS. Work has been carried out predominantly on strains of naive mice in which APS has been induced, passively and actively, using autoantibodies, autoantigens and other antigens. Studies of autoimmune-prone mice and naive rabbits are present in the literature, to a lesser degree. We review the various animal models of the pathogenesis of APS, whether spontaneous or induced, which have been developed over the years. Although several of the models have provided insights into the relationship between antiphospholipid antibodies and fetal loss, very few give guidance to explain the link with thrombosis. Novel or experimental therapeutic regimens have to be tested on appropriate animal models before any kind of human clinical trials may proceed. The regimens devised thus far are also reviewed.

Genetic factors, shared by patients and their relatives, seem to have some effect on the prevalence of aPL in the subjects studied, while environmental factors shared by spouses appear to have no influence.