ABSTRACT
In recent years, defects in coagulation factors both hereditary and acquired have been widely investigated as causes of pregnancy loss, both sporadic and recurrent. 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 leading to fetal death. Due to the assumption that aPL induces 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. Hereditary thrombophilias have been classified into groups.1 (1) Defects in endogenous inhibitors of the coagulation pathway (antithrombin, protein C, protein S, tissue factor pathway inhibitor, and thrombomodulin deficiency). (2) Increased levels or function of procoagulation factors (factor V Leiden [FVL], prothrombin gene mutation G20210A, dysfibrinogenemia and hyperfibrinogenemia, and increased levels of factors VII, VIII, IX, and XI). (3) Hyperhomocysteinemia, mainly due to C677T homozygosis of the methylenetetrahydrofolate reductase (MTHFR) gene. (4) Defects of the fibrinolytic system, involving plasminogen, tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), thrombinactivatable fibrinolysis inhibitor (TAFI), factor XIII, and lipoprotein A. (5) Altered platelet function (platelet glycoproteins GPIb-IX, GPIa-IIa, and GPIIb-IIIa). However, the prevalence of each hereditary thrombophilia varies in different ethnic groups.
