ABSTRACT
The etiology of pregnancy loss often remains an enigma, even after exclusion of uterine abnormalities and of genetic, immunological, infectious, or endocrine disorders. Recently, thrombophilias, whether hereditary or acquired, have been found in a significant number of women with recurrent abortions without apparent cause. The evidence for pregnancy loss having a thrombotic basis is due to the widely reported association between antiphospholipid antibodies (aPL) and recurrent pregnancy loss (RPL). aPL are thought to cause pregnancy loss by thrombosis in decidual vessels, impairing the blood supply to the fetus and leading to fetal death. Due to the assumption that aPL induce thrombosis causing pregnancy loss, it has been assumed that any prothrombotic state may also increase the chance of pregnancy loss due to a thrombotic mechanism, and that if this process recurs three or more times, there is recurrent miscarriage. Hereditary thrombophilias that have been reported to be associated with recurrent pregnancy loss include antithrombin, protein C, and protein S deficiencies, factor V Leiden (FVL), the G20210A mutation in the factor II (FII) gene, and homozygosity for the thermolabile variant of methylenetetrahydrofolate reductase (MTHFR C677T), which leads to hyperhomocysteinemia specifically in the presence of low folate levels. In addition, deficiencies of factor XIII (FXIII) and fibrinogen are associated with pregnancy loss. Both of these are bleeding diatheses that become apparent in childhood, and are associated with impaired wound repair in addition to pregnancy loss and excessive bleeding. This chapter deals with the association between decreased or increased levels of coagulation factors
and pregnancy loss. The various factors and their association with the trophoblast are shown in Figure 10.1.
