**1. Introduction**

The antiphospholipid syndrome (APS) is an acquired autoimmune disorder, defined by the combination of generally accepted laboratory and clinical criteria [1]. The latest laboratory criteria include repeated (at least 12 weeks apart) positive testing for at least 1 of 3 selected antiphospholipid antibodies (aPL): lupus anticoagulant (LA), anticardiolipin (aCL), anti-beta2-glycoprotein I (anti-B2GPI) antibodies. Clinical criteria emphasize the arterial and venous thromboembolic and pregnancy-related (recurrent miscarriages in the first trimester, fetal death in the second or third trimesters, severe pre-eclampsia requiring delivery of a premature infant before 34 weeks of gestation) events. However, other laboratory

and clinical complications with clear association to aPL, referred to as non-criteria manifestations, have been described. Based on the affected organ system, the clinical non-criteria manifestations divide into several subgroups: cardiovascular, neurologic, skin, renal, hematologic, and other [2, 3]. Hematologic complications include thrombocytopenia, hemolytic anemia, and functional changes or deficiencies of coagulation factors with both thrombotic (acquired resistance to activated protein C, protein S deficiency) or bleeding tendencies. As mentioned above, the association of aPL with thromboembolic events is extensively and well documented. However, the acquired coagulopathy caused by the aPL is complex and
