Antiphospholipid Syndrome—Pathophysiology

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Abstract

The antiphospholipid syndrome (APS) was first defined as a syndrome in 1983,1 consisting of recurrent thrombotic events and/or pregnancy loss, associated with the persistent presence of antiphospholipid antibodies (aPL). Several aPL subtypes are known, with the three formal diagnostic assays anticardiolipin (ACL), anti β-2 glycoprotein 1 (β2GP1), and lupus anticoagulant (LAC).2 Over the past few decades since initially defined, this syndrome has become known to be systemic, potentially affecting almost every organ system in the body. There is no single specific cause for APS but rather, as in other autoimmune diseases, a combination of environmental, hormonal, and genetic factors has been proposed.3-5 Specifically within this definition, obstetric APS refers to pregnancy morbidity occurring in patients with persisting antiphospholipid antibodies.6 Criteria used to define obstetric APS are one fetal loss after 10 weeks gestation; three or more early miscarriages with no other apparent explanation; preeclampsia or placental insufficiency, associated with a premature birth before 34 weeks of gestation.7-9 It is recognized today that the presence of aPL represents the most frequent acquired risk factor for a treatable cause of recurrent pregnancy loss and associated obstetric complications.2 The aPL are not only a diagnostic tool of APS, but rather participate in its pathophysiology with an active pivotal role, mediating several different manifestations of the syndrome.

Original languageEnglish
Title of host publicationRecurrent Pregnancy Loss
Subtitle of host publicationCauses, Controversies, and Treatment, Second Edition
PublisherCRC Press
Pages155-166
Number of pages12
ISBN (Electronic)9781482216158
ISBN (Print)9781482216141
DOIs
StatePublished - 1 Jan 2014

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