Abstract
Antiphospholipid antibodies (aPL) are a cluster of autoantibodies directed against plasma proteins with affinity for membrane phospholipids. The most frequently tested aPL are lupus anticoagulant (LA), anti-cardiolipin antibodies (aCL), and anti-β2-glycoprotein I antibodies (anti-β2GPI). aPL play a key pathogenic role in the development of the antiphospholipid syndrome (APS), a systemic autoimmune disease characterized by recurrent thrombotic and/or pregnancy complications in patients with persistent aPL. However, aPL positivity is occasionally documented in patients with no previous history of thrombotic or pregnancy morbidity. LA activity, multiple aPL positivity, high-titer aPL, and a concomitant systemic autoimmune disease are recognized risk factors for future thrombotic events in asymptomatic carriers. Moreover, an accelerated atherosclerosis with increased cardiovascular (CV) risk has also been associated with aPL positivity, thus exposing aPL carriers to fatal complications and chronic disability requiring cardiac rehabilitation. Overall, an accurate risk stratification is recommended for aPL-positive subjects in order to prevent both venous and arterial thrombotic complications. In this review, we provide an overview of the main antithrombotic and risk assessment strategies in aPL carriers.
Highlights
Antiphospholipid antibodies are a cluster of autoantibodies directed against plasma proteins with affinity for membrane phospholipids [1]
Congress on AntiPhosphoLipid Antibodies (APLA 2010) recommendations, the high-risk group is represented by subjects with multiple aPL positivity, or lupus anticoagulant (LA) positivity, or persistent aCL positivity at medium-high titer [50]
Data from clinical studies strongly support the hypothesis that aPL may have a direct physiopathological role in systemic atherosclerosis, with aPL positivity being related to an increased risk of CV events regardless of the thrombotic risk [7,12,51]
Summary
Antiphospholipid antibodies (aPL) are a cluster of autoantibodies directed against plasma proteins with affinity for membrane phospholipids [1]. APS, known as Hughes syndrome, is a systemic autoimmune disease characterized by recurrent thrombotic and/or pregnancy complications in patients with persistent aPL positivity [1]. Persistent aPL positivity can be occasionally found in subjects without a history of thrombotic or pregnancy morbidity, calling into question the need for adequate prevention strategies [5]. In this regard, multiple aPL positivity, high-titer aPL, and concomitant systemic lupus erythematosus. A timely risk assessment may help define individualized antithrombotic strategies for aPL-positive subjects. An accurate risk stratification is recommended for aPL-positive subjects in order to prevent both venous and arterial thrombotic complications. We provide an overview of the main antithrombotic and risk assessment strategies in aPL carriers
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