Several years prior to this evaluation, this 45-year-old woman, with history of pregnancy-induced hypertension and preeclampsia, had her first stroke, affecting her left hemibody. The patient was treated with warfarin. Two years later, while on warfarin, she lost consciousness and was diagnosed with acute obstructive hydrocephalus due to a pineal gland hemorrhage requiring placement of a ventriculoperitoneal shunt. This was followed a year later by two additional hemispheric strokes. The patient received aspirin. Seven years on, she had an episode of vomiting, diarrhea, right-hand weakness, and difficulty speaking and was treated with aspirin and dipyridamole.

Our patient was diagnosed with the APAS. APAS is an acquired prothrombotic syndrome characterized by recurrent arterial or venous thromboembolism, unexplained fetal loss usually within the first 10 weeks of gestation, and thrombocytopenia, with the presence of circulating antiphospholipid antibodies. Primary APAS is an immune-mediated coagulopathy associated with cerebral ischemia in young adults, the etiology of which remains unknown. Secondary APAS can occur within the context of several diseases, mainly autoimmune or rheumatologic disorders, infections, malignancy, and drugs. Antiphospholipid antibodies are a heterogeneous group of autoantibodies directed against phospholipid-binding proteins. Several antiphospholipid antibodies have been described; the most thoroughly studied subsets include lupus anticoagulant (LA) and anticardiolipins (aCL) IgG, IgA, and IgM isotypes. The mechanism of anticoagulation by
aCL includes the formation of a complex between aCL and beta-1 glycoprotein 1 antibody (β2GPI), leading to a dysfunctional protein C pathway.