ABSTRACT
Antiphospholipid syndrome (APS) was first defined as a syndrome in 1983,1 consisting of a triad of manifestations involving arterial and/or venous thrombosis, recurrent fetal loss, accompanied by mild to moderate thrombocytopenia and elevated titers of antiphospholipid (aPL) antibodies: lupus anticoagulant (LA) and/or anticardiolipin antibodies (aCL). Today, this syndrome is known to be systemic and may affect almost every organ and tissue in the body. The cause of APS is still considered a mystery – yet, as in many other autoimmune diseases, a combination of environmental and genetic factors has been proposed. Recent data indicate that infectious agents may play a major role in the etiology of APS. The pathophysiology of APS includes all arms of the coagulation system, as well as other mechanisms not related to hypercoagulability. In fact, aPL have been shown to be directly toxic to the developing fetus, as these antibodies can be passively transferred from humans to naive mice and will induce pregnancy loss in those mice2 (Figure 7.1). Active immunization with human pathogenic monoclonal anticardiolipin antibody induces clinical manifestations of APS in BALB/c mice.3 Additionally, the serum from women with APS is highly teratogenic to rat embryos in culture and also affects embryonic growth.4
Moreover, purification of the immunoglobulin G (IgG) fraction of the sera of women with APS directly affects the embryo and yolk sac, reducing their growth.5 This chapter discusses the etiology and pathophysiology of APS, with special emphasis on the reproductive system.
