AI Article Synopsis

  • Lupus anticoagulant is a key risk factor for pregnancy complications and impacts placental function by increasing cell death (apoptosis) and reducing cell growth and invasion of trophoblasts.
  • Heparin administration can counteract these negative effects, promoting trophoblast viability and invasion.
  • This study suggests that modulating trophoblast development with heparin could be a potential therapeutic approach in pregnancies affected by lupus anticoagulant.

Article Abstract

Objective: Lupus anticoagulant poses a significant risk factor for obstetric complications, whereas heparin improves live birth rates in those pregnancies. Pathophysiology of antiphospholipid antibodies on placental function involves coagulopathies and thrombosis but also dysregulated trophoblast turnover.

Study Design: With the use of placental explant cultures, we assessed the effect of lupus anticoagulant positive sera (LA + sera) on apoptosis, mitosis, and invasion of trophoblast and determined the role of unfractionated heparin in regulating these functions.

Results: LA + sera were associated with increased placental apoptosis (TUNEL, M30 formation, DNA laddering). LA + sera decreased villous trophoblast proliferation and reduced extravillous trophoblast invasion through matrigel. Heparin attenuated LA + sera-induced apoptosis and facilitated trophoblast invasion.

Conclusion: Lupus anticoagulant may impair placentation by increasing apoptosis, attenuating mitosis and reducing invasion of the trophoblast. The direct effects on trophoblast viability by heparin demonstrate an alternative biologic function for this anticoagulant and raise the possibility that anomalous trophoblast development may be therapeutically regulated.

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Source
http://dx.doi.org/10.1016/j.ajog.2004.05.014DOI Listing

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