Case ReportsSevere Preeclampsia Associated with Coinheritance of Factor V Leiden Mutation and Protein S Deficiency
Section snippets
Case
A 29-year-old white primigravida presented at 31 weeks’ gestation with generalized edema, weight gain of 2 lb per week, elevated blood pressure and 4+ dipstick proteinuria. At regular prenatal visits her blood pressure was 100/60 mmHg, urine dipstick was normal, and a glucose screen at 28 weeks’ gestation was negative. At age 17, she had a spontaneous superficial thrombophlebitis of the left saphenous vein while taking oral contraceptives but was otherwise healthy. There was no history of
Comment
Our patient had severe early onset preeclampsia and postpartum deep vein thrombosis during her first pregnancy associated with coinheritance of the factor V Leiden mutation and protein S deficiency. Heparin prophylaxis was administered during two subsequent pregnancies, without recurrence of hypertension, preeclampsia, or venous thromboembolism.
Information on the prevalence of the factor V Leiden mutation or protein S deficiency in other family members is not available. However, the high
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Cited by (20)
Factor V Leiden mutation in pregnancy
2004, JOGNN - Journal of Obstetric, Gynecologic, and Neonatal NursingCitation Excerpt :A systematic review by Alfirevic and colleagues (2002) revealed that women with placental abruption were more often heterozygous or homozygous for factor V Leiden mutation (odds ratio of 16.9) and that women with unexplained stillbirth were more likely to have the factor V Leiden mutation (odds ratio of 6.1). In multiple reports, activated protein C resistance has been associated with severe, early-onset preeclampsia (Dizon-Townson et al., 1996; Kahn, 1998). Women with hemolysis, elevated liver enzymes, and low platelet count (HELLP syndrome) have been noted to have a higher incidence of factor V Leiden mutation and activated protein C resistance due to unknown causes (Krauss et al., 1998).
Thalassemia intermedia and cavernous transformation of portal vein thrombosis in pregnancy
2003, European Journal of Obstetrics and Gynecology and Reproductive BiologyThrombophilia, preeclampsia, and fetal demise: A case report
2002, Journal of Clinical AnesthesiaMaternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia
2001, American Journal of Obstetrics and GynecologyPathogenesis and genetics of pre-eclampsia
2001, LancetCitation Excerpt :Genes that affect blood pressure have come under investigation and work on angiotensin has produced both positive and negative results.34–37 Associations with other genetic markers have been studied; examples are lipoprotein lipase;38 methylenetetrahydrofolate reductase;39 factor V Leiden;40 and apolipoprotein E.41 There have been many studies on the population association/candidate gene approach but there are no clear conclusions. In principle, a whole-genome linkage study is the most powerful way of identifying disease-susceptibility genes wherever there is a strong genetic component.
Outcome of pregnancy in women with hereditary thrombophilia
2001, International Journal of Gynecology and Obstetrics