Alijotas-Reig Jaume
Unidad de Enfermedades Sistémicas Autoinmunes, Servicio de Medicina Interna I, Hospital Universitario Vall d'Hebrón, U.A.B., Barcelona, España.
Med Clin (Barc). 2010 Jan 23;134(1):30-4. doi: 10.1016/j.medcli.2009.05.027. Epub 2009 Aug 5.
Pregnancy losses are the main obstetrical complications of the obstetric antiphospholipid syndrome (obstetric-APS). Classically, they have been strongly attributed to thrombosis and further placental infarcts. But in some cases is not possible to show evidence of decidual thrombosis or placental vasculopathy, and sometimes inflammatory signs are present. Besides, the prevalence of systemic thrombosis is low in obstetric APS patients. Some cases have low plasma C4/C3 levels. Animal models show a local inflammatory mechanism. The beta2-glycoprotein-I/anti-beta2-glycoprotein-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. In addition, an amplifier loop between the tissue factor, inflammatory cells and complement proteins could exist. Overall, these diverse mechanisms may explain both, inflammatory and thrombophilic placental alterations. In the end, the role played in this binomial by certain pro-inflammatory cytokines, mainly TNF-alpha, remains to clarify.
妊娠丢失是产科抗磷脂综合征（obstetric-APS）的主要产科并发症。传统上，它们被强烈归因于血栓形成及进一步的胎盘梗死。但在某些情况下，无法显示蜕膜血栓形成或胎盘血管病变的证据，且有时会出现炎症迹象。此外，产科APS患者中系统性血栓形成的患病率较低。一些病例血浆C4/C3水平较低。动物模型显示存在局部炎症机制。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。补体蛋白可能损伤滋养层细胞，募集并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。此外，组织因子、炎症细胞和补体蛋白之间可能存在一个放大环路。总体而言，这些不同的机制可能解释炎症性和血栓形成性胎盘改变。最后，某些促炎细胞因子，主要是肿瘤坏死因子-α，在这一双重过程中所起的作用仍有待阐明。
