Defects of genes encoding inhibitors of coagulation and their application in early miscarriage aetiology.

Properly functioning coagulation in gravidity is not necessary only to provide the continuity of circulation in placenta. Today we recognize that proteins and cells of haemostasis in the maternal blood cooperate with the components of a coagulation cascade produced by embryonic trophoblast cells. Such coordination on the embryomaternal interface is necessary for an intact embryogenesis. Other findings discuss the ability of coagulation components to act also outside the hemocoagulation process, especially as signal molecules, regulators of immune reactions, cell proliferation and others. Haemostasis is thus a complex system and we still do not know all of its pathways. This is perhaps also the reason that in the case of known procoagulant mutations (FV Leiden, gene mutation for prothrombine G20210A) we cannot explain why some carriers suffer recurrent miscarriages and others have uncomplicated pregnancies. The expert community believes that the phenotype manifestation of these mutations in terms of pregnancy losses could be connected to the simultaneous presence (synergistic effect) of other polymorphisms of gene-encoding proteins of haemostasis or the lack thereof (antagonistic effect) (Ref. 59).