Abstract

Antiphospholipid syndrome (APS) is characterized by a combination of clinical features consisted of thrombotic or pregnancy-related events and autoimmune antiphospholipid antibodies. In the 1998 International Consensus Preliminary Criteria, APS is defined by the concomitant presence of these clinical features and laboratory tests, including solid immunoassay and lupus anticoagulant (LAC). Current concept of antiphospholipid antibodies directed against plasma proteins with affinity for negatively charged phospholipids, mainly beta2-glyoprotein 1 (beta2GP1) and prothrombin, that is, anti-beta2GP1 and anti-prothrombin antibodies have been shown as a key antibody in the APS, while the pathophysiological mechanisms remain still uncertain. In the recent investigations potential mechanisms, such as endothelial activation induced by bivalent-formed antiphospholipid antibodies and complement activation, have emerged. Recurrent pregnancy losses or fetal death, and increased rates of preeclampsia and placental insufficiency are the clinical features in the APS. It is now accepted that unfractionated or low-molecular-weight heparin in combination with low-dose aspirin represents the current standard treatment for pregnant women with anti-phospholipid antibodies, and high-dose immunoglobulin is considered as a salvage therapy for refractory APS. This review highlights the characteristics of APS and the recent consensus for obstetrical managements in APS.

Keywords: antiphospholipid syndrome, beta glycoprotein, lupus anticoagulant, prothrombin, recurrent pregnancy loss, preeclampsia, endothelial activation, anticoagulant