The thrombophilic fetus.

Thrombophilia is the increased tendency to thrombosis. Inherited and acquired factors may determine thrombophilia. Some physiologic conditions, such as pregnancy are themselves "thrombophilic". In pregnancy, in fact, there is a decrease of all natural anticoagulant systems, such as antithrombin, protein C and protein S that are partially compensated by an increased fibrinolysis. It has been well established that women with thrombophilic disorders are at greater risk of venous thromboembolism in pregnancy and puerperium. It has also been observed that those women have higher prevalence of those obstetric complications in which microplacental thrombosis may play a pathogenetic role, such as placental abruption, preeclampsia, intrauterine growth restriction, intrauterine fetal death, repeated spontaneous miscarriage. Given that those complications are not always associated with maternal thrombophilia, controversy still exists on the exact impact of the disorders with the adverse pregnancy outcomes. While we are convinced that thrombophilias are extensively implicated in pregnancy complications, we feel that there has not been completely elucidated the role of the different factors, the gestational age at which those factors may intervene, nor has been given enough relevance to the weight of fetal thrombophilias in the origin of some specific form of those obstetric complications. We should bear in mind that some thrombophilias may be inherited from the mother, the father or both. Our hypothesis is that maternal thrombophilias may be responsible for venous thromboembolism, preeclampsia HELLP and eclampsia, whereas fetal thrombophilia, may account for IUGR or stillbirth. This last would also explain some stillbirth or repeated late (>10 gestational weeks) miscarriage observed in non-thrombophilic mothers. The two sides of thrombophilia may, of course, concur, resulting in the more severe clinical presentations.