Peripartum thromboprophylaxis for homozygous and heterozygous FVL mutation carriers yields similar pregnancy outcome.

KeY words: P regnancy is characterized by a physiological state of hypercoagulability. Moreover, a significant portion of pregnant patients suffering from severe obstetric complications – such as stillbirth [1,2], preeclampsia [3], placental abruption and intrauterine growth restriction [4] – were found to have some form of inherited or acquired thrombophilia [5,6]. Up to 50% of gestational venous thromboembolic events are associated with heritable thrombophilias [7,8]. Congenital thrombophilias were found to be present in up to 15% in several ethnic groups [7]. The wide diversity of thrombophilias makes research in this field challenging. Although women with adverse pregnancy outcome are more likely to test positive for thrombophilia, it is unclear which specific thrombophilia is implicated in each outcome [5]. Moreover, the exact mechanisms underlying placental dysfunction in women with thrombophilia are not fully understood [9]. Since published series are rather small or combine different forms of thrombophilias [5,7], differentiating and defining a precise clinical management strategy for each type is difficult. The most commonly recognized inherited thrombophilia is factor V Leiden mutation [10,11], an autosomal dominant trait occurring mostly in the Caucasian population (5%) with variations by regions [12]. The clinical manifestation of the FVL1 mutation is variable [10]. It is recognized that homozygosity carries a greater risk of venous thromboembolism than heterozygosity, with both an earlier age of onset and recurrence as well as shorter time between episodes [10]. The association between pregnancy and recurrent VTE2 in homozygous carriers has been emphasized [13]. Bates et al. [14] demonstrated that the risk of VTE during pregnancy in homozygous FVL carriers is high as compared with other inherited thrombophilias. Homozygous carriers of factor V Leiden have an up to 80-fold increased risk of venous thrombosis [15,16], but the risk of obstetric complications in FVL homozygosity has yet to be determined. Biron-Andreani and colleagues [17] observed that without anticoagulation, late fetal loss was more frequent in homozygotes than heterozyFVL = factor V Leiden VTE = venous thromboembolism