Abstract:
Antiphospholipid syndrome is an autoimmune disorder characterized by vascular thrombosis and/or pregnancy morbidity associated with persistent antiphospholipid antibody positivity. Cases fulfilling the Sydney criteria for obstetric morbidity with no previous thrombosis are known as obstetric antiphospholipid syndrome (OAPS). OAPS is the most identified cause of recurrent pregnancy loss and late-pregnancy morbidity related to placental injury. Cases with incomplete clinical or laboratory data are classified as obstetric morbidity APS (OMAPS) and non-criteria OAPS (NC-OAPS), respectively. Inflammatory and thrombotic mechanisms are involved in the pathophysiology of OAPS. Trophoblasts, endothelium, platelets and innate immune cells are key cellular players. Complement activation plays a crucial pathogenic role. Secondary placental thrombosis appears by clot formation in response to tissue factor activation. New risk assessment tools could improve the prediction of obstetric complication recurrences or thromboses. The standard-of-care treatment consists of low-dose aspirin and prophylactic low molecular weight heparin. In refractory cases, the addition of hydroxychloroquine, low-dose prednisone or IVIG improve pregnancy outcomes. Statins and eculizumab are currently being tested for treating selected OAPS women. Finally, we revisited recent insights and concerns about the pathophysiology, diagnosis and management of OAPS.
摘要:
抗磷脂综合征是一种自身免疫性疾病,其特征是与持续的抗磷脂抗体阳性相关的血管血栓形成和/或妊娠发病率。符合悉尼产科发病率标准且以前没有血栓形成的病例被称为产科抗磷脂综合征(OAPS)。OAPS是与胎盘损伤相关的复发性妊娠丢失和妊娠晚期发病率的最确定的原因。临床或实验室数据不完整的病例分为产科发病率APS(OMAPS)和非标准OAPS(NC-OAPS),分别。炎症和血栓形成机制涉及OAPS的病理生理学。滋养层,内皮,血小板和先天免疫细胞是关键的细胞参与者。补体激活起着至关重要的致病作用。继发性胎盘血栓形成通过响应于组织因子激活的凝块形成而出现。新的风险评估工具可以改善产科并发症复发或血栓形成的预测。标准治疗包括低剂量阿司匹林和预防性低分子量肝素。在难治性病例中,添加羟氯喹,低剂量泼尼松或IVIG可改善妊娠结局。他汀类药物和依库珠单抗目前正在测试用于治疗选定的OAPS女性。最后,我们重新审视了最近对病理生理学的见解和关注,OAPS的诊断和管理。