Theodore E. Woodward Award: antiphospholipid syndrome revisited: a disorder initiated by inflammation. Article uri icon

Overview

MeSH Major

  • Antiphospholipid Syndrome
  • Inflammation

abstract

  • The antiphospholipid syndrome (APS), characterized by thrombosis and pregnancy loss that occur in the presence of antiphospholipid (aPL) antibodies, is a leading cause of miscarriage and maternal and fetal morbidity. Using a mouse model of APS induced by passive transfer of human aPL antibodies, we have shown that complement activation plays an essential and causative role in pregnancy loss and fetal growth restriction, and that blocking activation of the complement cascade rescues pregnancies. Given that the primary treatment for APS patients is anticoagulation throughout pregnancy, usually with sub-anticoagulant doses of heparin, we considered the possibility that heparin prevents pregnancy loss by inhibiting complement. We found that heparin inhibits activation of complement on trophoblasts in vivo and in vitro and that anticoagulation, in and of itself, is not sufficient to prevent pregnancy complications in our experimental model of APS. Our studies underscore the importance of inflammation in fetal injury associated with aPL antibodies and emphasize the importance of developing and testing targeted complement inhibitory therapy for patients with APS.

publication date

  • December 2007

Research

keywords

  • Article

Identity

Language

  • eng

PubMed Central ID

  • PMC1863598

PubMed ID

  • 18528494

Additional Document Info

start page

  • 99

end page

  • 114

volume

  • 118