ABSTRACT
The hemostatic balance in the placenta may be determined by both maternal and fetal factors cooperatively regulating coagulation at the feto-maternal interface. The maternal spiral arteries become remodeled by pregnancy hormones and trophoblast into uteroplacental arteries toward the end of the first trimester. The evidence for pregnancy loss having a thrombotic basis is due to the association between antiphospholipid antibodies and recurrent pregnancy loss. Case-control studies can only show associations between thrombophilias and pregnancy losses. The presumed benefit of antithrombotic therapy and the absence of side effects has led many clinicians to prescribe low molecular weight heparin, aspirin, or both to women with recurrent pregnancy loss and hereditary thrombophilia. Cytokine imbalances have been described in recurrent pregnancy loss, antiphospholipid syndrome, preeclampsia, preterm births, and intrauterine growth restriction. Afibrinogenemia—a defect in hepatic fibrinogen secretion or release—is inherited as an autosomal recessive trait and is associated with bleeding diathesis, impaired wound repair, and recurrent pregnancy loss.
