Contents


Preface

Antiphospholipid syndrome (APS) is a systemic autoimmune disorder characterized by vascular thrombosis and/or pregnancy-related morbidity in the presence of persistently positive antiphospholipid antibodies (aPL). APS is considered the most common acquired form of thrombophilia worldwide. Obstetric APS is a complex entity that can affect both the mother and the fetus throughout pregnancy with high morbidity. At least one clinical criterion (vascular thrombosis or pregnancy morbidity) and one laboratory-based criterion (positive test result for lupus

anticoagulant, anticardiolipin antibodies, and/or anti-β2-glycoprotein-1 antibodies) must be met for a patient to be classified as having APS. In the general population, the incidence of clinical manifestations significant for APS is high and could often be triggered by other underlying factors. Therefore, the diagnosis of APS relies primarily on laboratory measurements of aPL. However, current laboratory-based tests for aPL are hampered by technical limitations. Despite numerous attempts to increase their specificity, a high number of patients are still misdiagnosed. There is a need for novel, robust, and reliable biomarkers to firstly detect APS and secondly

This book consists of three sections. The first section contains the introductory chapter. The second section discusses important clinical aspects of APS and the cellular and/or molecular mechanisms potentially involved. Topics covered in this section include stroke and APS, obstetric manifestations of APS, and bleeding complications in APS. The third section discusses novelties in the diagnosis and pathogenesis of APS. The two chapters in this section examine the diagnostic utility of a novel autoantibody against β2-glycoprotein I/HLA class II complexes and recent findings in the field of extracellular vesicles, which offer promising aspects

**Polona Žigon**

Ljubljana, Slovenia

Department of Rheumatology, University Medical Centre Ljubljana,

to monitor the risk for recurrent events over time.

that may explain their role in the pathogenesis of APS.
