1049) now find that maternal genes are only partly responsible. The rest of the blame falls on genetic defects that the fetus inherits from the father.
Recurrent miscarriages are associated with mutations known as Leiden polymorphisms, which prevent the factor V coagulant from being destroyed by the anticoagulation machinery. The assumption has been that clots formed in the placenta of Leiden mothers might cripple fetal growth by blocking nutrient supply.
Examination of placental tissue from Leiden mothers, however, shows no correlation between placental clotting and fetal loss. And female mice with Leiden mutations give birth successfully despite their propensity to form blood clots.
Sood et al. predicted that risk factors from the father might increase the risk of fetal loss. They found that crossing Leiden female mice with males that had mutations in anticoagulation factors now caused the loss of only those fetuses that were less able to break down maternal factor V. The synergy between maternal and fetal defects suggests that screening both parents for anticoagulant mutations may be a better indicator of high-risk pregnancies than screening only the mother.
The mouse fetal losses were not due to placental clotting, but fetal loss was prevented by blocking the activation of the mother's platelets. The authors hypothesize that fetal loss must involve an as yet unknown action of maternal platelet factors on the fetal cells at the interface of maternal and fetal tissue.