Abstract
Antiphospholipid syndrome is an autoimmune disorder characterized by vascular thrombosis and/or pregnancy morbidity associated with persistent antiphospholipid antibody positivity. Cases fulfilling the Sydney criteria for obstetric morbidity with no previous thrombosis are known as obstetric antiphospholipid syndrome (OAPS). OAPS is the most identified cause of recurrent pregnancy loss and late-pregnancy morbidity related to placental injury. Cases with incomplete clinical or laboratory data are classified as obstetric morbidity APS (OMAPS) and non-criteria OAPS (NC-OAPS), respectively. Inflammatory and thrombotic mechanisms are involved in the pathophysiology of OAPS. Trophoblasts, endothelium, platelets and innate immune cells are key cellular players. Complement activation plays a crucial pathogenic role. Secondary placental thrombosis appears by clot formation in response to tissue factor activation. New risk assessment tools could improve the prediction of obstetric complication recurrences or thromboses. The standard-of-care treatment consists of low-dose aspirin and prophylactic low molecular weight heparin. In refractory cases, the addition of hydroxychloroquine, low-dose prednisone or IVIG improve pregnancy outcomes. Statins and eculizumab are currently being tested for treating selected OAPS women. Finally, we revisited recent insights and concerns about the pathophysiology, diagnosis and management of OAPS.
Highlights
Introduction iationsAntiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by the occurrence of vascular thrombosis—arterial or venous—and/or pregnancy morbidity [1]
From early studies in 1929, we have identified several mechanisms for this effect, including the inhibition of C1q binding to immune complexes, interference with the interactions of C4 with C1s and C2, blockade of the formation of the C3 amplification convertase by the alternative pathway and inhibition of the formation of the membrane attack complex (MAC)
When a patient meets all four criteria but it involves only two organs, systems and/or tissues; the absence of laboratory confirmation owing to the early death of a patient never tested for aPL; no confirmation by histopathology analyses or when the development of a third event occurs between one week and one month after presentation, despite anticoagulation, the patient is classified as probable catastrophic APS (CAPS) [134,136]
Summary
Antiphospholipid antibodies are a heterogeneous group of immunoglobulins directed against negatively charged phospholipids, cofactors or phospholipid–cofactor complexes that are usually present in monocyte, trophoblast, endothelial and platelet cell membranes [13,14,15]. Cases with low titers of aPL or only one positive test, and not in agreement with the Sydney recommendations, are classified as noncriteria OAPS (NC-OAPS; see Table 1). These women could present autoantibodies against other phospholipids, such as phosphatidic acid, phosphatidylserine, phosphatidylinositol, phosphatidylglycerol, phosphatidylethanolamine or phosphatidylcholine; cofactors such. The significant psychological sequelae that may affect the couple, as well as the feeling of blame related to recurrent pregnancy losses and the fear to have more losses, should be considered These recurrent poor obstetric outcomes suppose an important economic burden for both patients and health systems. The aim of this article is to thoroughly review the concepts related to the pathogenesis, diagnostic, clinical concerns and management of OAPS, as well as to update new data on them
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