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Keywords:

  • fetal growth restriction;
  • pre-eclampsia;
  • pregnancy complications;
  • pregnancy loss;
  • venous thromboembolism

Key content:

  • • 
    All the major heritable thrombophilias have been found to be significantly associated with increased risk of venous thromboembolism, but the absolute risk remains low.
  • • 
    The association of heritable thrombophilias with adverse pregnancy outcomes remains controversial.
  • • 
    Testing for thrombophilias should only be performed when this may affect management.
  • • 
    Ideally, testing should be performed some time after the acute event, when the woman is not receiving anticoagulation and is not pregnant.

Learning objectives:

  • • 
    To understand the relationship of thrombophilias with risk for venous thromboembolism.
  • • 
    To understand the difficulties in determining possible associations of pregnancy complications with hereditary thrombophilias.
  • • 
    To learn who and when to test for hereditary thrombophilias.

Ethical issues:

  • • 
    Thrombophilia testing should be performed in an expert centre where it can be supported by effective counselling and explanation of the implications of both positive and negative results. This is particularly the case when testing because of a family rather than a personal history.
  • • 
    Detailed and sensitive discussion regarding adverse outcomes and hereditary thrombophilias is important, as well as giving an honest summary of the current knowledge and a clear explanation of results in terms that can be understood.

Introduction

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

In 1990 the British Committee for Standards in Haematology (BCSH) defined thrombophilias as familial or acquired disorders of the haemostatic mechanism which are likely to predispose to thrombosis.1 However, the term is often used loosely to describe all conditions predisposing to thrombosis. This review concentrates on the heritable thrombophilias, pregnancy and treatment.

Heritable thrombophilias

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

These can be due to deficiencies of the naturally occurring anticoagulants, such as antithrombin, protein C and protein S, or to abnormalities of coagulant factors, such as factor V Leiden and prothrombin G20210A gene mutation (PTM), resulting in gain of procoagulant function.

Approximately 11% of the normal population have one of these inherited thrombophilias, which can be readily detected by laboratory tests. There are other known thrombophilias for which tests are not routinely available, such as thrombomodulin deficiency, tissue factor pathway inhibitor deficiency,2 defects of the fibrinolytic pathway3 and others that have not yet been described. Other risk factors have been proposed, including high concentrations of procoagulant factors such as VIII,4 IX,5 XI6 and fibrinogen.7 Among them, high levels of factor VIII have subsequently been confirmed by other investigators8 as being, at least in part, genetically determined, as shown by familial clustering.9 However, the value of measuring these weaker factors in assessing risk of venous thrombosis has not been confirmed.

Homozygosity for methylenetetrahydrofolate reductase (MTHFR) C677T can cause hyperhomocysteinaemia, which has been associated with increased risk of vascular events, but a recent review10 calculated no significant increased risk in pregnant women homozygous for MTHFR C677T.

Heritable thrombophilias and risk of venous thromboembolism

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

All the major heritable thrombophilias have been found to be significantly associated with increased risk of venous thromboembolism in and out of pregnancy (Table 1). However, despite the increase in relative risk, the absolute risk of venous thromboembolism remains low. The most prothrombotic condition is antithrombin deficiency, where the absolute risk for pregnancy-related venous thromboembolism is 31% if no anticoagulation prophylaxis is administered, increasing to 49% in women with previous venous thromboembolism.11 Risk is higher with the rarer type I antithrombin deficiency than with the milder but more common type II deficiencies.

Table 1.  Major heritable thrombophilias and relative risk for venous thromboembolism in pregnancy10
ThrombophiliaPrevalence in normal population (%)Relative risk
Factor V Leiden heterozygosity2–79.32
Factor V Leiden homozygosity 34.4
Prothrombin mutation heterozygosity26.8
Prothrombin mutation homozygosity 26.4
Protein S deficiency0.03–0.133.19
Protein C deficiency0.20–0.334.76
Antithrombin deficiency0.25–0.554.69

Heritable thrombophilias can act in synergy with acquired risk factors such as obesity, immobility and medical conditions, to give a resulting risk which is greater than would be expected for the sum of the individual factors.12

Laboratory investigations

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Detection of thrombophilia does not affect the initial management of venous thrombosis but may affect decisions regarding duration of anticoagulation. Detection may be beneficial for first-degree family members who are carriers of the defect but who are still asymptomatic. Relatives identified with the same condition may be accorded a lower threshold for primary preventative strategies than those without. Testing may also help to identify those individuals with combined or homozygous defects who are at higher risk of venous thromboembolism13–15 or more likely to develop it earlier in life.16

Who to test for thrombophilia

In general, laboratory testing should be performed whenever the results may influence decisions on therapy or prevention. The clinical circumstances surrounding the thrombotic event are far more important in determining duration of anticoagulation than the presence of thrombophilia. For example, a deep vein thrombosis occurring during plaster immobilisation of the lower leg following fracture will only require a short course of treatment as opposed to an unprovoked spontaneous pulmonary embolus, which may necessitate long-term therapy. Laboratory testing should be selective and considered as only one factor in the assessment of risk of recurrence. Testing may need to be extended to first-degree family members of the proband as it may influence decisions regarding primary prevention measures. Guidelines from the Royal College of Obstetricians and Gynaecologists17 and the British Committee for Standards in Haematology18 suggest testing women in the presence of:

  • • 
    history of unprovoked venous thrombosis
  • • 
    thrombosis in association with pregnancy or the combined contraceptive pill
  • • 
    a previous event due to a minor provoking factor, such as travel
  • • 
    first-degree family history of idiopathic venous thrombosis; or venous thromboembolism related to pregnancy, use of the combined contraceptive pill or a minor risk factor. If the family member has a known thrombophilia, tests can be selective.

In the first two groups of women, testing does not influence the need for antenatal prophylaxis, but may affect decisions about dosage/duration of treatment and is beneficial for first-degree relatives. Where testing is performed on an asymptomatic person as part of family studies, the risks, benefits and limitations of the tests should be carefully explained and considered. Testing is not indicated for:

  • • 
    arterial thrombosis
  • • 
    assisted conception or ovarian hyperstimulation syndrome, in the absence of venous thromboembolism
  • • 
    significant provoking factors to a thrombotic event
  • • 
    family history of provoked thrombosis.

When to test

Factor V Leiden and prothrombin mutations are detected by genetic analysis and tests can, therefore, be performed at any time. Plasma levels of protein C, protein S and antithrombin should be tested at least 4 weeks after the acute event, because of the initial consumption of factors during the thrombotic process. Free (biologically active) protein S levels fall in pregnancy because of the rise in protein S-binding globulin and, therefore, testing should be carried out at approximately 3 months postpartum. Rarely, protein C and antithrombin can be affected in pregnancy and clarification of baseline levels may be necessary in the nonpregnant state. Most of the tests are not reliable during anticoagulation, as heparin reduces levels of antithrombin and warfarin affects proteins C and S, which are both vitamin K-dependent factors. It is, therefore, preferable to postpone laboratory testing until 4 weeks after discontinuation of treatment. In summary, testing should be performed:

  • • 
    away from the acute event
  • • 
    when anticoagulation is discontinued
  • • 
    when the woman is not pregnant or on the combined contraceptive pill.

Venous thromboembolism prevention strategies

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

All women should be assessed for risk of thrombosis, either in early pregnancy or before pregnancy, and this should be repeated if circumstances change or if hospital admission is required.17 Pregnant women should be advised about general antithrombotic measures such as weight control, good hydration, leg care and mobility. Women with previous deep vein thrombosis should also be advised to wear antiembolic stockings, or class II compression stockings if still within 2 years of the thrombotic event. Women with known thrombophilia will require antenatal low molecular weight heparin if they have a personal history of thrombosis. For women with thrombophilia and no history of thrombosis, the need for antenatal low molecular weight heparin will depend on the nature of their thrombophilia, their family history and the presence of additional acquired factors such as obesity. With antithrombin deficiency, the high risk of venous thrombosis in pregnancy justifies prophylaxis even in previously asymptomatic cases with no additional factors.

During labour and delivery, attention should be given to hydration, use of antiembolic stockings and early mobilisation. Women with thrombophilia will need low molecular weight heparin in the postpartum period for at least 7 days. This will need to be extended to 6 weeks for those with a positive family history or other risk factors. Those previously receiving long-term warfarin will need to return to this regimen in the postpartum period, overlapping with low molecular weight heparin for the first few days and until the international normalised ratio (prothrombin time) is within normal limits. Both warfarin and heparin are safe during breastfeeding.

Heritable thrombophilias and pregnancy complications

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

The possible causal relationship between heritable thrombophilias and adverse pregnancy outcome has remained a controversial issue for the last two decades.

Placental development and the theoretical basis for association

From 9 to 12 weeks of gestation there is uterine spiral artery remodelling caused by the invasion of trophoblast cells into the uterine lining. Thus maternal blood is flowing over fetal tissue and hypercoaguable maternal blood could potentially contribute to placental pathology.

Thrombin plays a central role in normal placental development and the latter appears to be strongly coupled with maternal haemostasis. In animal experiments, knockout mice that do not express thrombomodulin on the trophoblast cells have inadequate placentation and there is early embryonic death. This early lethality is dependent on tissue factor expression and thrombin generation19 but, at least in animal experiments, is not dependent on fibrinogen and heparin does not ameliorate the lethal effect. The thrombomodulin deficiency does not appear to lead to fibrin deposition and placental thrombosis and, therefore, there must be alternative mechanisms causing the early embryonic demise.20 Microthrombi are a common finding in the placental vasculature of women with pregnancy loss and placental thrombosis has been described in association with individual thrombophilic defects. However, this is not a consistent finding and similar findings are described in women without thrombophilic defects.

Thus, individual maternal haemostatic and trophoblastic cell characteristics form a complex combination of factors that affect placental development and of that maternal thrombophilia may be one component.

Pregnancy complications: confounding factors

Large numbers of studies examining the relationship between adverse pregnancy outcomes and the presence of a laboratory-detectable thrombophilia have produced conflicting and inconsistent results. There are a number of reasons for this:

  • • 
    Pregnancy complications, such as pregnancy loss, pre-eclampsia and placental abruption, are distressing experiences which often have extremely traumatic outcomes. Women who have gone through these experiences are often highly motivated to try any treatment, even if unproven, in the hope of a better outcome in subsequent pregnancies. This, together with the fact that in most cases the outcome of the next pregnancy is likely to be good, has made it difficult to conduct large randomised prospective studies.
  • • 
    Different definitions, for example, for pregnancy loss, are used in different studies, which hinders the comparison or combination of studies.
  • • 
    Women with pregnancy complications are a heterogeneous group and underlying factors for early and late complications are likely to differ. Thrombophilia is only one of several factors that can affect pregnancy outcome.
  • • 
    Both thrombophilias and pregnancy complications are common, increasing the chances of finding incidental associations. Furthermore, the prevalence of thrombophilias varies among different ethnic groups, contributing to differing study results.
  • • 
    Rodger21 recently summarised the overall difficulty: to detect an odds ratio of ≥2, with a risk factor that has a prevalence of <5%, a sample size >1000 is required in the 1:1 case control studies. Although there are many studies, most have sample sizes smaller than this.
  • • 
    Finally, many of the earlier studies have been criticised for methodological flaws.

Pregnancy loss and thrombophilia

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Up to 50% of conceptuses fail before implantation and 15% of recognised pregnancies end in miscarriage. Most studies do not differentiate between very early loss (<10 weeks) and later losses in the first trimester. Interestingly, when embryonic loss has been studied, presence of a thrombophilia appears to have a protective effect.22

Table 2 summarises the results of three meta-analyses, by Rey,23 Robertson10 and Rodger.24 It should be noted that the studies included by Rodger differed from the other two in that they were restricted to prospective studies and, in general, this set of studies shows weaker associations.

Table 2.  Results of three meta-analyses of pregnancy loss and thrombophilia
OutcomeFactor V Leiden OR (95% CI)Prothrombin G20210A OR (95% CI)Protein S deficiency OR (95% CI)
Rey23Robertson10Rodger24Rey23Robertson10Rey23Robertson10
  1. CI = confidence interval; OR = odds ratio.

Recurrent first-trimester loss2.011.9122.562.714.7 
(1.13–3.58)(1.01–3.61)(1.13–3.38)(1.04–6.29)(1.37–5.34)(0.99–2.18) 
Late pregnancy loss3.262.06Pooled results of early and late losses2.32.667.3920.09
(1.82–5.83)(1.1–3.86) (1.09–4.87)(1.28–5.53)(1.28–42.6)(3.7–109.15)

Similar results were found for all three meta-analyses for pregnancy loss and factor V Leiden. Robertson and Rodger noted heterogeneity in the analysis: factor V Leiden had a stronger association with late rather than early losses. Comparable results were found with PTM: Rey and Robertson reported a strong association of late fetal loss with protein S deficiency and Robertson noted an association between hyperhomocysteinaemia and early pregnancy loss.

A recent prospective study25 evaluated pregnancy outcomes in 1700 asymptomatic nulliparous women who underwent genotyping before 22 weeks of gestation for factor V Leiden, PTM, MTHFR and thrombomodulin polymorphisms. The women had no family or personal histories of thromboembolism or thrombophilia. The primary composite outcome was the development of severe pre-eclampsia, fetal growth restriction, placental abruption, stillbirth or neonatal death. Results were similar in carriers and noncarriers. Women with PTM had increased risk of a composite outcome (odds ratio [OR] 3.58, 95% confidence interval [CI] 1.20–10.61) and, conversely, homozygosity for the MTHFR polymorphism had a protective effect (OR 0.26, CI 0.08–0.86).

The conclusion from this and the other studies is that the absolute risks are low and that screening is not indicated.

Pre-eclampsia and thrombophilia

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Results from studies are, again, variable. Robertson10 included 25 studies (11 183 women), reporting significant associations with factor V Leiden (OR 2.19, CI 1.46–3.27), PTM (OR 2.54, CI 1.52–4.23) and hyperhomocysteinaemia (OR 3.49, CI 1.21–10.11). However, Rodger's data24 from 12 401 women showed no association with factor V Leiden (OR 1.22, CI 0.89–1.66) or PTM (OR 1.24, CI 0.72–2.12) and no evidence of statistical heterogeneity. Any association, if present at all, appears to be slight.

Fetal growth restriction, small for gestational age and thrombophilia

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Robertson10 analysed data on fetal growth restriction in five studies (195 women) and did not demonstrate an association with hereditary thrombophilias. Rodger24 analysed 20 654 cases involving small-for-gestational-age babies and, similarly, found no association with factor V Leiden (OR 1.0,95% CI 0.80–1.25) or pooled PTM heterozygotes and homozygotes (OR 1.25, 95% CI 0.92–1.70).

Placental abruption and thrombophilia

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Robertson10 evaluated seven studies (922 women) regarding placental abruption and found significant associations only with factor V Leiden (OR 4.7, CI 1.13–19.59) and PTM (OR 7.71, CI 3.01–19.76). Rodger24 analysed 12 401 cases and found a more modest association with factor V Leiden (OR 2.28, CI 0.92–5.67). Pooled relative risk for PTM and placental abruption in 5672 cases was 2.63 (CI 0.15–44.6) and significant heterogeneity was noted.

Conception and thrombophilia

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Some authors have suggested associations between infertility and thrombophilia. Bellver et al.26 evaluated markers for thrombophilia and thyroid autoimmunity in women with recurrent pregnancy loss, recurrent implantation failure and unexplained infertility. They found at least one thrombophilia marker in as many as 50% of participants in all groups, including controls; there was no significant difference in the presence of hereditary thrombophilias among the study group. Although the authors suggest that thrombophilia could be an aetiological factor in infertility, the results do not support this conclusion.

Outcomes for prophylaxis and thrombophilias

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Clinicians are increasingly using anticoagulants for women with previous adverse pregnancy outcomes. This is partly from extrapolation of results of studies of the acquired thrombophilia antiphospholipid syndrome27 and partly from the intuitive conclusion that antithrombotic therapy is likely to improve outcome in those with a prothrombotic diathesis. The pathophysiology of antiphospholipid syndrome, however, has been shown to be complex and the anticoagulant treatment in this case involves other processes in addition to antithrombotic activity; it is, therefore, not directly comparable. Even in antiphospholipid syndrome, it is disputed whether a heparin and aspirin combination is superior to aspirin alone in recent meta-analyses.28,29

A prospective study by Vossen et al.30 evaluated 131 women with thrombophilia and 60 controls, all in their first pregnancies. The risk of fetal loss appeared slightly increased in those without thromboprophylaxis:7/83 in the treatment group (8%) versus 10/48 in the control group (21%), relative risk 0.3 (95% CI 0.1–1.0). The authors commented that, per type of defect, the relative risk varied only minimally from 1.4 for factor V Leiden to 1.6 for antithrombin deficiency compared with control women and that prophylactic anticoagulation differed greatly in type, dose and duration, precluding solid conclusions on the effect of thromboprophylaxis on fetal loss.

The results of the ALIFE31 and SPIN32 studies, examining the effect of antithrombotic treatment on the pregnancies of women with at least two miscarriages, were published in 2010. Neither demonstrated benefit from low molecular weight heparins and, although not powered specifically to examine thrombophilias, this subgroup showed no benefit in either study.

For recommendations for women with thrombophilia and adverse pregnancy outcomes see Box 1.

Table Box 1.  Recommendations for women with thrombophilia and adverse pregnancy outcomes
• Unselected testing in pregnancy is not recommended. Positive tests have a poor positive predictive value.
• Current national and international guidelines advocate testing only for antiphospholipid syndrome antibodies and not for hereditary thrombophilias in women with pregnancy complications, in view of the weak associations of most pregnancy outcomes with thrombophilia.
• As some adverse outcomes have been associated with hyperhomocysteinaemia (such as pre-eclampsia), a pragmatic approach may be to advise women with relevant clinical histories to take folic acid, 5 mg daily, for the duration of the pregnancy.

Conclusion

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References

Of paramount importance for the management of thrombophilias in pregnancy is careful selection of women to be investigated, the timing of testing and the tests to be carried out. This enables effective strategies to prevent future events among women who carry genetic defects but are still asymptomatic and to reduce the risk of recurrent thrombosis among those with previous events.

References

  1. Top of page
  2. Introduction
  3. Heritable thrombophilias
  4. Heritable thrombophilias and risk of venous thromboembolism
  5. Laboratory investigations
  6. Venous thromboembolism prevention strategies
  7. Heritable thrombophilias and pregnancy complications
  8. Pregnancy loss and thrombophilia
  9. Pre-eclampsia and thrombophilia
  10. Fetal growth restriction, small for gestational age and thrombophilia
  11. Placental abruption and thrombophilia
  12. Conception and thrombophilia
  13. Outcomes for prophylaxis and thrombophilias
  14. Conclusion
  15. References