The persistent presence in plasma of medium to high levels of IgG and/or IgM class anticardiolipin antibodies (aCL) and/or the lupus anticoagulant (LAC) is associated with both “recurrent pregnancy loss” and venous and arterial thrombosis.1 This clinicoserological entity, first described in the early eighties in patients with systemic lupus erythematosus was termed the antiphospholipid syndrome (APS).1 ,2 The recognition that APS also occurs in otherwise healthy people led to the term primary antiphospholipid syndrome.3 The classic laboratory markers of APS, aCL, and LAC belong to the family of so-called antiphospholipid antibodies (aPL). Clinical studies indicate that aPL are related to both early pregnancy losses and fetal demise in advanced pregnancy and that placental thrombosis and infarction are common findings in aPL related intrauterine fetal deaths.4 Studies in animal models for APS support a causative role for aPL in pregnancy loss.5 Prospective clinical studies have confirmed that aPL are risk factors for pregnancy loss, both in patients with systemic lupus erythematosus (60% versus 13% pregnancy loss)6 and in healthy nulliparous women (16% versus 7% pregnancy loss).7 In women with a history of three or more consecutive pregnancy losses persistently positive tests for aPL are found in up to 15%,8 and in these, subsequent fetal loss rates up to 60–90% are noted without specific treatment.8 ,9 Apart from being risk factors for fetal demise, aPL associate with high frequencies of pre-eclampsia, intrauterine growth restriction, fetal distress, and premature delivery.9 ,10