The association between adverse pregnancy outcomes and maternal factor V Leiden genotype: a meta-analysis

2004 ◽  
Vol 91 (04) ◽  
pp. 700-711 ◽  
Author(s):  
John Attia ◽  
Tracy Dudding
Keyword(s):  
Pregnancy Outcomes ◽  
Odds Ratio ◽  
Fetal Loss ◽  
Factor V Leiden ◽  
Adverse Pregnancy Outcomes ◽  
Factor V ◽  
Third Trimester ◽  
Factor V Leiden Mutation ◽  
Increased Risk ◽  
Adverse Pregnancy

SummaryThe conclusions of studies to date which evaluate a possible association between factor V Leiden and adverse pregnancy outcome have been conflicting. This study was undertaken to further investigate this association. Our objective was to evaluate the association between adverse pregnancy outcomes and maternal factor V Leiden genotype by meta-analysis. Inclusion criteria were: (a) cohort or case control design; (b) outcomes clearly defined as one of the following: first or second/ third trimester miscarriage or intrauterine death, preeclampsia, fetal growth retardation, or placental abruption; (c) both the case and control mothers tested for the factor V Leiden mutation; (d) sufficient data for calculation of an odds ratio. Both fixed and random effect models were used to pool results and heterogeneity and publication bias were checked. For first trimester fetal loss, the pooled odds ratio was heterogeneous (p=0.06) and no dose-response curve could be found. For second/third trimester fetal loss, there was a consistent and graded increase in risk: the odds ratio was 2.4 (95% CI 1.1-5.2) for isolated (non-recurrent) third trimester fetal loss, rising to 10.7 (95% CI 4.0-28.5) for those with 2 or more second/third trimester fetal losses. FactorV Leiden is associated with a 2.9 fold (95% CI 2.0-4.3) increased risk of severe preeclampsia, and a 4.8 fold (95% CI 2.4-9.4) increased risk of fetal growth retardation. These results support factor V Leiden testing for women with recurrent fetal loss in the second/third trimester. Women with only 1 event may also warrant testing if the fetal loss occurred in the third trimester. Conversely, in those women known to have the factor V Leiden mutation, monitoring for adverse pregnancy outcomes is warranted; whether this means increased vigilance or anti-coagulant prophylaxis is still contentious.

Homozygous factor V Leiden mutation in a woman with multiple adverse pregnancy outcomes

2000 ◽  
Vol 264 (3) ◽  
pp. 164-165 ◽  
Author(s):  
H.-U. Pauer ◽  
J. Neesen ◽  
M. Schloesser ◽  
B. Hinney ◽  
R. Rauskolb
Keyword(s):  
Pregnancy Outcomes ◽  
Factor V Leiden ◽  
Adverse Pregnancy Outcomes ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Adverse Pregnancy

scholarly journals Factor V Leiden Mutation and its Impact on Pregnancy Complications

2011 ◽  
Vol 54 (3) ◽  
pp. 117-121 ◽  
Author(s):  
Ľubica Hammerová ◽  
Ján Chabada ◽  
Juraj Drobný ◽  
Angelika Bátorová
Keyword(s):  
Venous Thromboembolism ◽  
Pregnancy Outcomes ◽  
Factor V Leiden ◽  
Adverse Pregnancy Outcomes ◽  
Intrauterine Fetal Death ◽  
Control Group ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Significant Difference ◽  
Adverse Pregnancy

Objective: The aim of this prospective study was to find the association between the factor V Leiden mutation and adverse pregnancy outcomes. Methods: This study is an analysis of a prospective observational study of the frequency of placenta-mediated complications of factor V Leiden mutation carriers. We compared pregnancy outcomes of 11 women with a heterozygous form of the factor V Leiden mutation with 41 women of a control group. Results: All pregnancies ended with delivery of a living infant. None of the 52 pregnancies were complicated by venous thromboembolism. There were a few significant differences regarding placenta-mediated complications. The gestational age at delivery showed small significant differences. There was a significant difference in the birth weight deviation in percentage between FVL carriers and controls. The incidence of blood loss exceeding 1000 ml was higher in the control group. Conclusions: Carriership of the factor V Leiden mutation did not affect the incidence of preeclampsia. Adverse pregnancy outcomes such as placental abruption were rare. Eclampsia, intrauterine fetal death and venous thromboembolism did not occur. Our results provide evidence that the maternal heterozygous FVL mutation did not increase the risk of an adverse pregnancy outcome.

scholarly journals Potential role of Factor V Leiden mutation in adverse pregnancy outcomes: An updated systematic review

2017 ◽  
Vol 4 (12) ◽  
pp. 1832 ◽  
Author(s):  
Nasibeh Roozbeh ◽  
Farzaneh Banihashemi ◽  
Mitra Mehraban ◽  
Fatemeh Abdi
Keyword(s):  
Systematic Review ◽  
Pregnancy Outcomes ◽  
Placental Abruption ◽  
Factor V Leiden ◽  
Adverse Pregnancy Outcomes ◽  
Factor V ◽  
Spontaneous Abortions ◽  
Factor V Leiden Mutation ◽  
Adverse Pregnancy ◽  
Fvl Mutation

Background: Thrombophilia is an inherited or acquired predisposition for development of thrombosis. One of the common thrombophilia polymorphisms is Factor V Leiden (FVL) mutation, which may contribute to negative pregnancy outcomes. This systematic review study seeks to describe the potential effects of factor V Leiden mutation on adverse pregnancy outcomes. Methods: Pubmed, Embase, ISI Web of Sciences, Scopus, ScienceDirect, Proquest and Google Scholar, for articles published during 1996-2017. Articles were evaluated by the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for standard reporting. As well, the quality of studies was assessed by the Newcastle-Ottawa Scale (NOS). Results: A total of 14 studies were eligible based on the inclusion criteria. The papers were scored by the STROBE checklist. The range of STROBE score was 15-20. Only 37.5% of the studies confirmed the relationship between fetal loss and FVL. The effect of FVL mutation on spontaneous abortions and In Vitro Fertilization (IVF) failures was demonstrated in all the studies. In the reviewed studies, there was no observed relationship between FVL mutation with intrauterine growth restriction (IUGR), preeclampsia, placental abruption or small for gestational age (SGA). Conclusion: The reviewed studies showed an unclear association between FVL mutation and stillbirth, IUGR, preeclampsia, or placental abruption. The exact effects of hereditary thrombophilia on pregnancy outcome is also still controversial. However, FVL mutation appeared to have an effect on spontaneous abortions and IVF failures. Therefore, screening patients for thrombophilic polymorphisms might be helpful.

scholarly journals High Hemoglobin Level is a Risk Factor for Maternal and Fetal Outcomes of Pregnancy in Chinese Women: A Retrospective Cohort Study

2021 ◽  
Author(s):  
Lanlan Wu ◽  
Ruifang Sun ◽  
Yao Liu ◽  
Zengyou Liu ◽  
Hengying Chen ◽  
...  
Keyword(s):  
Pregnancy Outcomes ◽  
Chinese Women ◽  
Adverse Pregnancy Outcomes ◽  
Multivariate Logistic Regression ◽  
Third Trimester ◽  
Low Birth Weight Infants ◽  
The Third ◽  
Increased Risk ◽  
Adverse Pregnancy ◽  
Multivariable Adjustment

Abstract Background To examine the association of hemoglobin (Hb) levels during gestation with the risk of selected adverse pregnancy outcomes in Chinese women. Methods A total of 1911 singleton mothers were included. Hb levels were measured during the second (16-18th weeks) and third (28-30th weeks) trimesters of pregnancy, and pregnancy outcomes were followed. Statistical analysis was performed using multivariate logistic regression. Results After multivariable adjustment, Hb levels > 130 g/L in the second trimester increased the risk of low-birth-weight infants (LBW) (odds ratio [OR], 2.54; 95% confidence interval [CI], 1.12–5.77). In the third trimester of gestation, compared with women whose Hb levels between 110–119 g/L, women with Hb levels > 130 g/L had an increased risk of LBW (OR, 2.17; 95% CI, 1.05–4.48) and small-for-gestational-age infants (SGA) (OR, 1.98; 95% CI, 1.04–3.78). In addition, maternal Hb levels of < 110 g/L or > 130 g/L at the second week that were restored vs not restored in the third trimester decreased the risk of preterm birth (PTB) by 80% (95% CI, 0.07–0.58) and 86% (95% CI, 0.03–0.84), respectively. Conclusion Maternal Hb > 130 g/L was associated with increased risk of adverse pregnancy outcomes. Reduction of PTB risk was observed with correction of Hb level during the third trimester.

Maternal thrombophilias are not associated with early pregnancy loss

2004 ◽  
Vol 91 (02) ◽  
pp. 290-295 ◽  
Author(s):  
Michael Paidas ◽  
Edmund Funai ◽  
Edward Kuczynski ◽  
Charles Lockwood ◽  
Henry Roqué
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Fetal Loss ◽  
Factor V Leiden ◽  
Anticardiolipin Antibodies ◽  
Prothrombin G20210a ◽  
Factor V ◽  
Increased Risk ◽  
Pregnancy Wastage ◽  
Adverse Pregnancy

SummaryWe investigated the association between inherited and acquired maternal thrombophilias and adverse pregnancy events. A cohort of 491 patients with a history of adverse pregnancy outcomes was evaluated for activated protein C resistance, factor V Leiden and prothrombin G20210A mutations, hyperhomocysteinemia, deficiencies of antithrombin, protein C and S and both anticardiolipin antibodies and lupus anticoagulants. The study had an 80% power to detect a 15% difference in the prevalence of thrombophilia for 1st trimester loss. In our high-risk cohort the presence of 1 maternal thrombophilia or more than one thrombophilia were found to be protective of recurrent losses at < 10 weeks (1 thrombophilia: OR: 0.55, 95% CI: 0.33–0.92; >1 thrombophilia: OR: 0.48, 95%CI:0.29–0.78). In contrast, the presence of maternal thrombophilia(s) was modestly associated with an increased risk of losses ≥ 10 weeks (1 thrombophilia: OR:1.76, 95%CI: 1.05–2.94, >1 thrombophilia: OR:1.66, 95%CI:1.03–2.68). Women who experienced only euploid losses were not more likely to have an identified thrombophilia than women who experienced only aneuploid losses (OR 1.03; 0.38–2.75). The presence of maternal thrombophilia was associated with an increased risk of fetal loss after 14 weeks, fetal growth restriction, abruption and preeclampsia. There was a significant “dose-dependent” increase in the risk of abruption (OR:3.60, 95%CI: 1.43–9.09) and preeclampsia (OR:3.21, 95%CI:1.20–8.58). In conclusion, these data indicate maternal thrombophilias are not associated with pregnancy wastage prior to 10 weeks of gestation.

scholarly journals Low Preconception Complement Levels Are Associated with Adverse Pregnancy Outcomes in a Multicenter Study of 260 Pregnancies in 197 Women with Antiphospholipid Syndrome or Carriers of Antiphospholipid Antibodies

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 671
Author(s):  
Cecilia Nalli ◽  
Daniele Lini ◽  
Laura Andreoli ◽  
Francesca Crisafulli ◽  
Micaela Fredi ◽  
...  
Keyword(s):  
Antiphospholipid Syndrome ◽  
Multicenter Study ◽  
Pregnancy Outcomes ◽  
Antiphospholipid Antibodies ◽  
Pregnancy Loss ◽  
Fetal Loss ◽  
Adverse Pregnancy Outcomes ◽  
Experimental Animal Models ◽  
Increased Risk ◽  
Adverse Pregnancy

Antiphospholipid antibodies (aPL) can induce fetal loss in experimental animal models. Human studies did find hypocomplementemia associated with pregnancy complications in patients with antiphospholipid syndrome (APS), but these results are not unanimously confirmed. To investigate if the detection of low C3/C4 could be considered a risk factor for adverse pregnancy outcomes (APO) in APS and aPL carriers’ pregnancies we performed a multicenter study including 503 pregnancies from 11 Italian and 1 Russian centers. Data in women with APS and asymptomatic carriers with persistently positive aPL and preconception complement levels were available for 260 pregnancies. In pregnancies with low preconception C3/C4, a significantly higher prevalence of pregnancy losses was observed (p = 0.008). A subgroup analysis focusing on triple aPL-positive patients found that preconception low C3 and/or C4 levels were associated with an increased rate of pregnancy loss (p = 0.05). Our findings confirm that decreased complement levels before pregnancy are associated with increased risk of APO. This has been seen only in women with triple aPL positivity, indeed single or double positivity does not show this trend. Complement levels are cheap and easy to be measured therefore they could represent a useful aid to identify patients at increased risk of pregnancy loss.

scholarly journals Hereditary thrombophilia and adverse pregnancy outcomes

2021 ◽  
Vol 64 (3) ◽  
pp. 68-77
Author(s):  
Valentin Friptu ◽  
◽  
Diana Mitryuk ◽  
Olga Popusoi ◽  
◽  
...  
Keyword(s):  
Gene Mutation ◽  
Pregnancy Outcomes ◽  
Intrauterine Growth Restriction ◽  
Pregnancy Loss ◽  
Recurrent Pregnancy Loss ◽  
Fetal Loss ◽  
Factor V Leiden ◽  
Factor V ◽  
Intrauterine Growth ◽  
Adverse Pregnancy

Background: Multiple studies have found a relatively increased risk of placenta-mediated pregnancy complications in women with congenital thrombophilia, especially early recurrent pregnancy loss, fetal loss, early-onset preeclampsia, intrauterine growth restriction, and premature abruption of normally positioned placenta. However, the extent of the association and the absolute risk are very modest, but they significantly increase in pregnant women with severe obstetric complications. Conclusions: There is convincing evidence that deficiency of natural anticoagulants (antithrombin, protein C, protein S) is a risk factor for late fetal loss. Factor V Leiden G1691A gene mutation and prothrombin G20210A gene mutation are associated with a double risk for early and unexplained recurrent pregnancy loss and for non-recurrent late fetal loss. The association of congenital thrombophilia with preeclampsia is much more uncertain, being probably limited factor V Leiden G1691A gene mutation and more severe cases of preeclampsia. Fewer data are available on intrauterine growth restriction (IUGR) and premature abruption of the normally positioned placenta. There is insufficient evidence to suggest an association of other forms of congenital thrombophilia with adverse pregnancy outcomes. In addition, genetic and epidemiological research suggests that placenta-mediated pregnancy complications are of polygenic multifactorial etiology, with a risk determined by the interaction of multiple genetic variants and other risk factors.

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