Abstract
Antiphospholipid syndrome (APS) is an autoimmune condition characterized by the presence of antiphospholipid antibodies (aPL) in subjects presenting with thrombosis and/or pregnancy loss. The currently used classification criteria were updated in the international consensus held in Sidney in 2005. Vascular events seem to result of local procoagulative alterations upon triggers influence (the so called “second-hit theory”), while placental thrombosis and complement activation seem to lead to pregnancy morbidity. The laboratory tests suggested by the current classification criteria include lupus anticoagulant, a functional coagulation assay, and anticardiolipin and anti-β2-glycoprotein-I antibodies, generally detected by solid phase enzyme-linked immunosorbent assay. The real challenge for treating physicians is understanding what is the actual weight of aPL in provoking clinical manifestations in each case. As thrombosis has a multi-factorial cause, each patient needs a risk-stratified approach. In this review we discuss the role of thrombotic risk assessment in primary and secondary prevention of venous and arterial thromboembolic disease in patients with APS, focusing on new antibody specificities, available risk scoring models and new coagulation assays.
Highlights
The strive for personalised medicine can be traced in its origin to Hippocrates’ times: the assessment of the four humours—blood, phlegm, yellow bile and black bile—were essential to determine the correct treatment for each individual patient
APL comprehends a heterogeneous group of circulating immunoglobulins including lupus anticoagulant (LA), anticardiolipin antibodies and anti-β2glycoprotein-I
The prevalence of antiphospholipid antibodies (aPL) is higher in patients with other autoimmune conditions such as rheumatoid arthritis or systemic lupus erythematosus (SLE), where up to 40 % are persistently positive for aPL [10, 11]
Summary
Thrombotic risk assessment in antiphospholipid syndrome: the role of new antibody specificities and thrombin generation assay. Savino Sciascia1*†, Simone Baldovino1†, Karen Schreiber, Laura Solfietti, Massimo Radin, Maria J.
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