Systemic Autoimmune Disease Unit, Department of Internal Medicine I, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
Obstet Gynecol Surv. 2010 Jan;65(1):39-45. doi: 10.1097/OGX.0b013e3181c97809.
Pregnancy loss is the main obstetrical complication of the obstetric antiphospholipid syndrome. Classically, such losses have been attributed to placental thrombosis and infarcts, although in many cases there is no evidence of decidual thrombosis or placental vasculopathy, and instead inflammatory signs are present. In addition, the prevalence of systemic thrombosis is low in obstetric antiphospholipid syndrome, suggesting an alternative pathogenesis. There is evidence that antiphospholipid antibodies, mainly beta2-glycoprotein-I/anti-beta2-glycoproteina-I complexes, activate both classical and alternative complement pathways. Complement proteins may injure trophoblast cells, recruiting and activating monocytes and neutrophils. Free radicals and proteolytic enzymes could also attack trophoblastic cells, and amplification of the causal loop between tissue factor, inflammatory cells, and complement proteins could also be a factor. Overall, these diverse mechanisms may explain both inflammatory and thrombotic placental alterations. The role played by certain pro-inflammatory cytokines, mainly tumor necrosis factor-alpha, and the altered balance between angiogenic and anti-angiogenic factors remains to be clarified. In the end, obstetric antiphospholipid syndrome seems to be a clinical subset of classical APS. In these women, systemic thrombotic risk seems to be low. Current knowledge about inflammatory pathway involvement in obstetric antiphospholipid syndrome will permit us to modify the time to start heparin treatment, currently recommended to begin it as soon as possible after pregnancy confirmation.
Obstetricians & Gynecologists, Family Physicians.
After completion of this article, the reader will be able to recall manifestations of obstetric antiphospholipid syndrome, describe nonthrombotic mechanisms that may affect obstetric outcomes in women with antiphospholipid syndrome, and predict changes in the evaluation and treatment of obstetric patients with antiphospholipid syndrome should inflammatory factors prove to be an important feature of antiphospholipid syndrome.
妊娠丢失是产科抗磷脂综合征的主要产科并发症。传统上，此类丢失归因于胎盘血栓形成和梗死，尽管在许多情况下，没有蜕膜血栓形成或胎盘血管病变的证据，而存在炎症迹象。此外，产科抗磷脂综合征中系统性血栓形成的患病率较低，提示存在替代发病机制。有证据表明，抗磷脂抗体，主要是β2-糖蛋白 I/抗β2-糖蛋白 I 复合物，激活经典和替代补体途径。补体蛋白可能会损伤滋养层细胞，招募和激活单核细胞和中性粒细胞。自由基和蛋白水解酶也可能攻击滋养层细胞，组织因子、炎症细胞和补体蛋白之间的因果关系的放大也可能是一个因素。总的来说，这些不同的机制可能解释了炎症和血栓形成的胎盘改变。某些促炎细胞因子（主要是肿瘤坏死因子-α）和血管生成和抗血管生成因子之间平衡的改变的作用仍有待阐明。最终，产科抗磷脂综合征似乎是经典 APS 的一个临床亚型。在这些女性中，全身性血栓形成风险似乎较低。目前对抗磷脂抗体相关产科疾病中炎症途径参与的认识将使我们能够改变开始肝素治疗的时间，目前建议在怀孕确认后尽快开始。
妇产科医生、家庭医生。
完成本文后，读者将能够回忆起产科抗磷脂综合征的表现，描述可能影响抗磷脂综合征妇女产科结局的非血栓形成机制，并预测抗磷脂综合征产科患者评估和治疗的变化，如果炎症因子被证明是抗磷脂综合征的一个重要特征。
