Lithology of the Kennebec Valley esker

作者：Jared Trefethen, H. B. Trefethen · 发表于：American Journal of Science · 年份：1944 · DOI：10.2475/ajs.242.10.521 · 被引用次数：5 · 研究领域：Systemic Lupus Erythematosus Research、Blood disorders and treatments、Renal Diseases and Glomerulopathies

Antiphospholipid syndrome (APS) is prothrombotic systemic autoimmune disorder characterized with multisystem manifestation, most commonly venous and arterial thromboembolism and/or recurrent pregnancy loss. The varying clinical phenotype is associated with heterogeneity in the pathogenic antiphospholipid antibodies (aPL) that are central to the diagnosis of APS. According to the international consensus statement on classification criteria, APS is classified when persistently elevated levels of specific aPL, such as lupus anticoagulant (LA), anti-cardiolipin (aCL) and anti-β2 glycoprotein I (anti-β2GPI) antibodies, are confirmed in addition to clinical manifestations (1, 2). The exact pathogenesis of APS is unknown, but aPL have been described to activate monocytes, neutrophils, dendritic cells and placental tissue (3). Despite the fact that many different proteins have been identified as being involved in the pathogenesis of APS, accumulating evidence from in vitro experiments as well as animal studies has revealed that β2GPI is the main target for aPL. It was also shown that triple aPL positivity, defined by detection LA, high titres of aCL and anti-β2GPI antibodies, correlates better with both thrombosis and pregnancy morbidity than any other aPL profile (4). Several autoantibodies outside those included in APS classification criteria could be also relevant to APS pathogenesis (5) and therefore, antibodies against other antigen targets have been investigated. Current eviden...