Institute of Human Genetics, UKM and University of Muenster, Germany.
Lupus. 2012 Jun;21(7):796-8. doi: 10.1177/0961203312438235.
This concise review summarizes the role of reduced ANXA5 expression through carriage of the M2/ANXA5 haplotype as a predisposing factor for various thrombophilia related obstetric complications. A revised ANXA5 'protective shield' model is emphasized, where decreased coverage resulting of M2 carriage at placental villi could lead directly to the observed pathology and on the other hand through exposing of antiphospholipid antigenic determinants, to the development of antiphospholipid antibodies (aPL). The aPL then can further disrupt the ANXA5 protective shield. Available and prospective evidence for this revised model is discussed. Conclusions are made about the diagnostic implications of M2 carriage and possible therapeutic strategies with anticoagulants, proven successful in obstetric antiphospholipid syndrome (APS) treatment.
这篇简明综述总结了携带 M2/ANXA5 单倍型导致 ANXA5 表达减少，从而成为各种与血栓形成相关的产科并发症易患因素的作用。强调了改良的 ANXA5“保护盾”模型，携带 M2 的情况下，胎盘绒毛中覆盖的 ANXA5 减少，可能直接导致观察到的病理变化；另一方面，通过暴露抗磷脂抗原决定簇，导致抗磷脂抗体(aPL)的产生。aPL 进一步破坏 ANXA5 保护盾。讨论了这个改良模型的现有和预期证据。还对 M2 携带的诊断意义以及可能的抗凝治疗策略进行了总结，该策略在产科抗磷脂综合征（APS）治疗中已被证明是有效的。
