Obstetric Complications in Patients With Hereditary Thrombophilia Identified Using the LCx Microparticle Enzyme Immunoassay: A Controlled Study of 5,000 Patients

Kocher, Olivier; Cirovic, Christine; Malynn, Elizabeth; Rowland, Charles M.; Bare, Lance A.; Young, Bradford A.; Henslee, Jerry G.; Laffler, Thomas G.; Huff, Jeffrey B.; Kruskall, Margot S.; Wong, Geoffrey Yuet Mun; Bauer, Kenneth A.

doi:10.1309/j64r-8020-2j71-2k80

Cited by 18 publications

(19 citation statements)

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“…Thus, as regards the FVL mutation among women with recurrent early pregnancy loss, thanks to appropriate controls and the large population enrolled, our study can be considered capable of detecting a clinically relevant difference between cases and controls. Our negative results are in accordance with an earlier study with a large recruitment of cases [20], some more recent studies [30,31] and the most advanced opinions, concerning first trimester recurrent loss, which do not consistently suggest an association with FVL mutation [27,29]. Our study should avoid the heterogeneity of cases and controls studied in meta‐analyses which have until now supported this growing point of view.…”

Section: Discussionsupporting

confidence: 88%

Inherited thrombophilias and unexplained pregnancy loss: an incident case‐control study

Pasquier

Bohec

Mottier

et al. 2009

Journal of Thrombosis and Haemostasis

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Summary. Background: Despite an initial impressive impact, a critical appraisal of the link between pregnancy loss and inherited thrombophilias is currently growing. Furthermore, little is known about the paternal thrombophilic phenotype and pregnancy loss. Objective: We sought an association between unexplained pregnancy loss and parental factor V Leiden (FVL) and Prothrombin G20210A (PTG) mutations. Methods: Design -Incident case-control study. Setting -University Hospital of Brest (France). Patients -Women and their partners from the West Brittany area, consecutively referred for unexplained pregnancy losses (two or more consecutive losses at or before 21 weeks of gestation, or at least one later loss). Controls -Women and their partners with no history of pregnancy loss and at least one normal pregnancy, from the same geographic area, recruited using electoral lists. Statistical analysis -Comparison of FVL and PTG allele frequency between cases and controls using the chi-square test. Separate analyses were performed according to the type of pregnancy loss (early recurrent or later loss). Results: 311 women (mean age: 32.8) and 284 of their partners were enrolled as cases while 599 women (mean age: 34.3) and 297 of their partners were recruited as controls. The prevalence of female, male or couple thrombophilic mutations was not statistically different between cases and controls whatever the definition of pregnancy loss retained. Conclusions: Presently, there is no clinical indication to routinely test for FVL and likely PTG mutations in women with early recurrent pregnancy loss. Moreover, our results did not reveal that paternal thrombophilic polymorphism should be further explored.

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Section: Discussionsupporting

confidence: 88%

Inherited thrombophilias and unexplained pregnancy loss: an incident case‐control study

Pasquier

Bohec

Mottier

et al. 2009

Journal of Thrombosis and Haemostasis

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“…The overall cohort included 118 women who were heterozygous and four who were homozygous for the prothrombin gene G20210A mutation 26. Recently, Kocher and colleagues assessed a large cohort of unselected pregnant women for the factor V Leiden and prothrombin G20210A mutations 27. The factor V Leiden mutation was associated with an increased risk of stillbirth (OR 11.6, 95% CI 1.93–69.43).…”

Section: Discussionmentioning

confidence: 99%

Prothrombin Gene G20210A Mutation and Obstetric Complications

Silver

Zhao

Spong

et al. 2010

Obstetrics &Amp; Gynecology

154

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OBJECTIVE To estimate whether maternal carriage of the prothrombin gene G20210A mutation is associated with pregnancy loss, preeclampsia, placental abruption, or small for gestational age (SGA) neonates in a low-risk, prospective cohort. METHODS This was a secondary analysis of the Eunice Kennedy Shriver National Institute of Child Health and Human Development factor V Leiden study, a multicenter, prospective, observational cohort of 5,188 unselected singleton gestations. A total of 4,167 first-trimester samples were available for analysis and were tested for the prothrombin G20210A mutation. Obstetric complications were compared between women with and without the prothrombin G20210A mutation by univariable and multivariable analysis. RESULTS A total of 157 (3.8%) women had the prothrombin gene mutation (156 heterozygous and one homozygous). Carriers of the prothrombin G20210A mutation had similar rates of pregnancy loss, preeclampsia, SGA neonates, and abruption compared with noncarriers. Results were similar in a multivariable analysis controlling for age, race, prior pregnancy loss, prior SGA neonates, and family history of thromboembolism. Three thromboembolic events occurred in women testing negative for the mutation. CONCLUSION There was no association between the prothrombin G20210A mutation and pregnancy loss, preeclampsia, abruption, or SGA neonates in a low-risk, prospective cohort. These data raise questions about the practice of screening women without a history of thrombosis or adverse pregnancy outcomes for this mutation. LEVEL OF EVIDENCE II

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“…Studies examining the role of Factor V Leiden and the prothrombin 20210 gene mutations are not conclusive, with some studies suggesting an important role in incidence of fetal loss and others being less clear [22, 23]. Another study which included over 5000 women found that there was indeed a strong association between Factor V Leiden and risk of stillbirth with an odds ratio of 10.9 [24]. In this study, there was not a similar association established for early fetal loss, and the prothrombin gene mutation was not associated with any increased risk.…”

Section: Outcomes Related To Thrombophilias In Pregnancymentioning

confidence: 99%

The Role of Thrombophilia in Pregnancy

2013

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Thrombotic disease is a major cause of peripartum morbidity and mortality worldwide. Development of thrombosis in pregnancy is multifactorial due to the physiologic changes of pregnancy—which induce a relative hypercoagulable state—as well as physical changes leading to increased stasis and also the effects of both the inherited and the acquired thrombophilias. In this review, we discuss the impact of each of these factors on the development of thrombosis as well as the evidence for the impact of pregnancy-associated thrombosis on pregnancy outcome. We then discuss the use of both prophylactic and therapeutic anticoagulation during pregnancy and the puerperium. We review the indications and dosing recommendations for administration of anticoagulation in a context of discussing the evidence including the lack of evidence and formal guidelines in this area. We briefly address the role of the new oral anticoagulants in pregnancy and conclude that significant further research in women with thrombophilias and pregnancy-associated thrombosis may help clarify the management of this condition in the future.

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Obstetric Complications in Patients With Hereditary Thrombophilia Identified Using the LCx Microparticle Enzyme Immunoassay: A Controlled Study of 5,000 Patients

Cited by 18 publications

References 0 publications

Inherited thrombophilias and unexplained pregnancy loss: an incident case‐control study

Inherited thrombophilias and unexplained pregnancy loss: an incident case‐control study

Prothrombin Gene G20210A Mutation and Obstetric Complications

The Role of Thrombophilia in Pregnancy

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