Factor V Leiden in pregnancies complicated by placental abruption Martin Procha ´zka a , Catharina Happach b , Karel Mars ˇa ´l c , Bjo ¨rn Dahlba ¨ck d , Pelle G. Lindqvist b, * Objective Recent studies suggest an increased prevalence of obstetric complications in female carriers of hereditary or acquired thrombophilias. The aim of the study was to determine if carriership of the factor V (FV) Leiden mutation (activated protein C [APC] resistance) is higher in women who have had of placental abruption during pregnancy. Design A retrospective case –control study. Setting University Hospital MAS, Malmo ¨, Sweden. Methods A comparison of 102 women with placental abruption with 2371 prospectively collected controls. Carriership of FV Leiden was determined and the women were interviewed. Main outcome measures Proportion of FV Leiden carriership, first degree heritage of thrombosis and previous placental abruption in cases and controls. Results Carriage of FV Leiden was found in 15.7% of women who have had placental abruption as compared with 10.8% of controls ( P ¼ 0.12, odds ratio [OR] ¼ 1.5, 95% confidence interval [CI] ¼ 0.9 – 2.7). Around 20% of women with placental abruption reported first degree heritage for venous thrombosis, as compared with 6.7% of controls ( P  0.001). Conclusions FV Leiden carriership was not significantly different in women with placental abruption. However, there was an increased prevalence of first degree heritage for venous thrombosis in women with placental abruption, indicating a higher prevalence of thrombophilia among women with placental abruption. INTRODUCTION Placental abruption is a major cause of fetal and mater- nal morbidity and mortality, occurring in 0.4–1.3% of all pregnancies. It usually presents as a combination of vaginal bleeding, uterine contractions and pain. The aetiology of placental abruption is unknown, but it occurs more fre- quently among smokers, in hypertensive pregnancies, in pregnancies with IUGR, in chorioamnionitis, in instances of trauma, with advancing maternal age, with male fetal gender and in women with previous placental abruption 1 . Placental abruption is defined as the separation of the normally implanted placenta, usually by haemorrhage into the decidua basalis. Placental abruption accounts for 20–25% of antepartum haemorrhages 2 . The perinatal mor- tality rate varies between 2% and 67%, depending on gestational age, fetal weight and the degree of abruption. Over 50% of perinatal deaths due to placental abruption occur before delivery 2 . Activated protein C (APC) resistance caused by the factor V (FV) Leiden mutation is the most common known inherited risk factor for venous thrombosis in white Euro- pean populations 3 . The gene for FV Leiden mutation results in replacement of arginine (R) at position 506 by glutamine (Q) 4 . This affects one of the cleavage sites for APC in FV and causes impaired anticoagulation. The resulting hyper- coagulable state is a lifelong risk factor for venous throm- bosis. FV Leiden is not only common among thrombosis cases (30–50%), but also highly prevalent (3–15%) in the general populations of white European ancestry. Recent studies suggest an increased prevalence of obstet- ric complications in female carriers of hereditary or ac- quired thrombophilias 5,6 . The placental circulation, which resembles a venous circulation with low pressure and flow velocity, may be particularly susceptible to thrombotic complications at the maternal – placental interface, causing premature separation of the placenta. Weiner-Megnagi et al. 7 recently found that 8 out of 27 women (30%) who had had placental abruption were carriers of FV Leiden, as compared with 1 of 29 among controls. In addition, Kupferminc et al. 5 found FV Leiden to be present in 5 out of 20 women with placental abruption (25%), as compared BJOG: an International Journal of Obstetrics and Gynaecology May 2003, Vol. 110, pp. 462–466 D RCOG 2003 BJOG: an International Journal of Obstetrics and Gynaecology doi:10.1016/S1470-0328(03)02969-0 www.bjog-elsevier.com a Department of Obstetrics and Gynaecology, Palacky ´ University, Olomouc, Czech Republic b University Hospital, Malmo ¨ Allma ¨nna Sjukhus, Sweden c Lund University, Sweden d Department of Coagulation Research, Malmo ¨ University Hospital, Malmo ¨ Allma ¨nna Sjukhus, Sweden * Correspondence: Dr P. Lindqvist, Department of Obstetrics and Gynaecology, University Hospital, Malmo ¨ Allma ¨nna Sjukhus (MAS), Ingang 74, 20502 Malmo ¨, Sweden.