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Antiphospholipid syndrome

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Karen Schreiber1,2, Savino Sciascia3, Philip G. de Groot4, Katrien Devreese5,

Soren Jacobsen2, Guillermo Ruiz-Irastorza6, Jane E. Salmon7, Yehuda Shoenfeld8,9,

Ora Shovman8,10 and Beverley J. Hunt1

Abstract |

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by thepresence of antiphospholipid antibodies, such as lupus anticoagulant, anticardiolipin antibodiesand anti‑β2‑glycoprotein 1 antibodies. APS can present with a variety of clinical phenotypes, including thrombosis in the veins, arteries and microvasculature as well as obstetrical complications.

The pathophysiological hallmark is thrombosis, but other factors such as complement activation might be important. Prevention of thrombotic manifestations associated with APS includes lifestyle changes and, in individuals at high risk, low-dose aspirin. Prevention and treatment of thrombotic events are dependent mainly on the use of vitamin K antagonists. Immunosuppression and anticomplement therapy have been used anecdotally but have not been adequately tested. Pregnancy morbidity includes unexplained recurrent early miscarriage, fetal death and late obstetrical manifestation such as pre-eclampsia, premature birth or fetal growth restriction associated with p lacental insufficiency.

Current treatment to prevent obstetrical morbidity is based on low-dose aspirin and/or lowmolecular-weight heparin and has improved pregnancy outcomes to achieve successful live birth in >70% of pregnancies. Although hydroxychloroquine and pravastatin might further improve pregnancy outcomes, prospective clinical trials are required to confirm these findings.

Source: nature.com/articles/nrdp201...

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