State-of-the-Art Review: Thrombophilia and Pregnancy: Review of the Literature and Some Original Data

Arkel, Yale S.; Ku, De-Hui W.

doi:10.1177/107602960100700402

Cited by 21 publications

(10 citation statements)

References 56 publications

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“…VTE is the leading cause of morbidity and mortality during pregnancy and puerperium, with the high incidence of late complication – postthrombotic syndrome, which significantly impairs the quality of life [4,5,6,7]. …”

Section: Introductionmentioning

confidence: 99%

Clinical Characteristics and Type of Thrombophilia in Women with Pregnancy-Related Venous Thromboembolic Disease

Mitić

Kovač

Jurisic

et al. 2011

Gynecol Obstet Invest

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Background: Normal pregnancy is characterized by numerous changes in the hemostatic system, creating the hypercoagulable state which increases the risk of venous thromboembolic event (VTE) occurrence. The risk is further increased by the presence of inherited or acquired thrombophilia. Objective: In this study, we aimed to determine the prevalence of different types of thrombophilia in women with pregnancy-related VTE, and to investigate the possible connection between the type of thrombophilia and localization of VTE as well as the gestational age of VTE occurrence. Participants and Methods: Two hundred and two women with the first episode of pregnancy-related VTE and 130 controls were investigated. The antithrombin, protein C and protein S activity, APC resistance, FVG1691A, and FIIG20210A were determined. None of the investigated women was pregnant at the time of thrombophilia testing, and none was using oral contraceptives. Results: Thrombophilia was diagnosed in 95 patients (47%) and 7 controls (5.4%). The prevalence of FV Leiden, FIIG20210A mutations, antithrombin, PC and PS deficiencies taken together and combined thrombophilia was 22.3, 10.4, 6.9 and 6.9%, respectively. Significantly more frequent antepartum occurrence of VTE (11 vs. 3, p < 0.05) was found in women with natural coagulation inhibitor deficiency. Pulmonary embolism occurred more frequently in nonthrombophilic women (25 vs. 3, p < 0.001). Conclusion: Inherited thrombophilia was found to be considerably more frequently present in women with pregnancy- and puerperium-related VTE compared to healthy controls. Women with thrombophilia are at higher risk of developing thromboses localized in the iliacofemoral region, and women without thrombophilia are at higher risk of developing pulmonary embolism. Deficiency in natural coagulation inhibitors is associated with antepartum VTE occurrence.

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Section: Introductionmentioning

confidence: 99%

Clinical Characteristics and Type of Thrombophilia in Women with Pregnancy-Related Venous Thromboembolic Disease

Mitić

Kovač

Jurisic

et al. 2011

Gynecol Obstet Invest

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“…A significant added risk to thrombosis is the presence of coexistent inherited thrombophilia during pregnancy [19]. The presence of genetic thrombophilia markers such as FVL, PGM 20210A mutation, AT III deficiency, and antiphospholipid antibodies significantly increases a patient's risk of thrombotic event [20, 21]. Thromboembolic events are reported in approximately one-third of antiphospholipid-positive patients [22].…”

Section: Discussionmentioning

confidence: 99%

Review of Management and Outcomes in Women with Thrombophilia Risk during Pregnancy at a Single Institution

Khalafallah

Ibraheem

Teo

et al. 2014

ISRN Obstetrics and Gynecology

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Pregnancy is a hypercoagulable state associated with an increased risk of venous thromboembolic disease (VTE). We retrospectively studied 38 Caucasian pregnant women with thrombophilia risk and compared their obstetric outcomes with a matched cohort without known thrombophilia risk during the period between January 2007 and December 2010. There were (2) cases with factor V Leiden, (6) prothrombin gene mutation, (1) antithrombin III deficiency, (2) protein C deficiency, (3) protein S deficiency, (10) MTHFR mutation, (7) anti-cardiolipin antibodies, and (1) lupus anticoagulant. Patients without thrombophilia who presented with recurrent unprovoked VTE were considered as high risk (6 cases). Most patients received anticoagulation (34/38) with aspirin only (6), enoxaparin (27), and warfarin (1). Twenty-six out of thirty-eight pregnant women (68.4%) with an increased risk of thrombophilia experienced one or more obstetric complications defined as hypertension, preeclampsia, placenta abruptio, VTE, and oligohydramnios, compared with 15 out of 40 (37.5%) pregnant women in the control group (OR 3.6; 95% CI 1.42, 9.21, P < 0.001). The incidence of obstetric complications was significantly higher in the thrombophilia group compared to the controls. However, these complications were the lowest among patients who received full-dose anticoagulation. Our study suggests that strict application of anticoagulation therapy for thrombophilia of pregnancy is associated with an improved pregnancy outcome. The study was registered in the Australian and New Zealand Clinical Trials Registry under ACTRN12612001094864.

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“…In addition, there is a decrease in vasculo-syncytial membranes,an increase in fibrosis and an increase in hypovascular villi all which can lead to fetal growth restriction or demise [20][21][22]. Pregnancy itself is a hypercoagulable state with fetal demise, thrombosis and pre-eclampsia being related to Factor V Leiden mutation, prothrombin gene mutation 20210A, and deficiencies of anti-thrombin III, protein C and protein S [23]. Thus, SLE specific thrombophilic factors are additive to the background of pregnancy related hypercoagulability (multiple hits), and this increases the occurrence of adverse fetal outcomes in lupus.…”

Section: Pregnancy Lossmentioning

confidence: 99%

Thrombophilia in Systemic Lupus Erythematosus: A Review of Multiple Mechanisms and Resultant Clinical Outcomes

Dhar¹,

Sokol²

2013

Pregnancy Thrombophilia - The Unsuspected Risk

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cardiovascular disease and clotting, the multiple mechanisms for hypercoagulability in SLE, and discuss the complexity of this problem in this population.Pregnancy Thrombophilia -The Unsuspected Risk Premature cardiovascular diseaseLupus-specific thrombophilic factors contribute to premature cardiac disease and atherosclerosis in this population. These lupus specific factors can affect the endothelium resulting in premature arterial vascular disease contributing to the accelerated/premature atherosclerosis observed in SLE [24]. Atheroma formation is initiated when oxidized low density lipoprotein (LDL) is taken up by foam cells in vascular endothelium [24][25]. High density lipoprotein (HDL) and Apo-A1 are protective factors against atherosclerosis. β-2 glycoprotein-1 binding to oxidized LDL facilitates uptake by foam cells [26]. Patients with SLE have antibodies to LDL/ β-2 glycoprotein-1 complexes, HDL, and Apo -A1 [26][27]. Antibodies to HDL and Apo A-1 cross react with cardiolipin and prevent HDL and Apo-1 protection against atherosclerosis. Antibodies to oxidized LDL may cross react with β-2 glycoprotein-1 and may enhance uptake, thus promoting plaque formation [25][26][27][28]. Anticardiolipin antibody binding exposes immunogenic and normally hidden (or cryptic) epitopes on β-2 glycoprotein-1, which can bind to anti-β-2 glycoprotein-1 antibodies. These antibodies bind to adhered β-2 glycoprotein-1 on endothelial cells which causes endothelial activation and subsequent up regulation of inflammatory and procoagulant factors [24][25][26]. In addition, adhered β-2 glycoprotein-1 on oxidized LDL promotes LDL uptake by macrophages, thus facilitating plaque formation [24][25][26]28]. During the acute phase response, HDL can be converted to pro-inflammatory molecules which promote LDL oxidation. Chronic inflammation can cause HDL dysfunction in SLE. HDL has been found to be pro-inflammatory in women with SLE and is termed pro-inflammatory HDL or piHDL [25][26]28]. More than 85% patients with SLE and carotid plaques had piHDL vs. 40% in those without plaques [27]. Pro-inflammatory HDL is an independent risk factor for atherosclerosis in rheumatoid arthritis and antiphospholipid antibody syndrome [26,28]. The prevalence of moderate to severe atherosclerosis in SLE at autopsy is 52% [29]. There is a higher prevalence of coronary artery disease in SLE than general population which is not predicted by traditional risk factors or increase in lupus activity alone [30][31][32][33][34][35][36][37][38][39]. Mortality studies show coronary artery disease (CAD) /myocardial infarction (MI) is a frequent cause of death in SLE and occurs in 11-48% of SLE patients [3,[30][31][32][33][34][35]. Death from CAD in SLE is disproportionately larger in late disease, with CAD/MI being the leading cause of death in SLE survivors. This accounts for the late peak in mortality in SLE [36][37][38]. Although there are a greater number of CAD risk factors (hypertension, diabetes mellitus, dyslipidemia, sedentary life style) in SLE patients than ...

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State-of-the-Art Review: Thrombophilia and Pregnancy: Review of the Literature and Some Original Data

Cited by 21 publications

References 56 publications

Clinical Characteristics and Type of Thrombophilia in Women with Pregnancy-Related Venous Thromboembolic Disease

Clinical Characteristics and Type of Thrombophilia in Women with Pregnancy-Related Venous Thromboembolic Disease

Review of Management and Outcomes in Women with Thrombophilia Risk during Pregnancy at a Single Institution

Thrombophilia in Systemic Lupus Erythematosus: A Review of Multiple Mechanisms and Resultant Clinical Outcomes

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